Transcript for:
Comprehensive Guide to A-Level Biology

hello love is in this video Dr Edward Langley team teaching you the whole of AQA a level barges so don't be surprised when the voice changes or handwriting changes in the middle of a topic or from one topic to another topic and all of them it's her voice on the video this is a really really long video so if you're watching this just before your exam you can put it on two times three to get through it all a little bit faster or if you're looking for a specific thing and the chapters are way too close together for you actually be able to understand then everything is time stamped in the description down below along with what is in what paper and what bits you need for which to make it a little bit clearer and easier for you to navigate through all the bits you need for each paper now in this we're going to be going through all of the content all of the the science that you need if you want some advice on how to answer the exam questions how to answer the essay questions how to answer the evaluated conclusion questions then what we have for you over my website is loads and loads of resources for this and don't forget there is also the predicted papers for this year and then the video walkthroughs for the predictive papers where Dr Edwards takes you through how to do the essay how to do the evaluate questions what sort of things the examiners are expecting to see when they ask you this sort of question good luck guys don't forget Dr Edwards every single step of the way foreign [Music] [Music] thank you [Music] there is a wide range of bonding that takes place within biological molecules and this is an area that crosses over a lot with chemistry biochemistry but do not be confused this is still a bality video we have covalent bonding which is the sharing of electrons between two non-metals we have ionic bonding which is the transfer of electrons from a metal to a non-metal this will form positive and negative ions and between these oppositely charged ions there will be an attraction and there is hydrogen bonding which is a weak attraction between opposite dipoles here is water as an example the hydrogens are a little bit positive the oxygen is a little bit negative between the little bit positive hydrogen and the little bit negative oxygen we are going to get an attraction this is going to be a hydrogen bond between the oxygen and the hydrogen there is going to be a covalent bonds this is a very strong intramolecular bonds whereas the hydrogen bonds is a much weaker intermolecular Bond there are a range of monomers and polymers that you need to know about and a great thing for you to do in biology is look at the words and understand what the words mean so mono means one and Mer means bit so a monomer is one bit of something Holly means lots of and again mer means bits to a polymer is lots of bits of things the monomer amino acid can polymerize into lots of amino acids in a chain to give us proteins nucleotides are monomers which can polymerize in a long chain to give us DNA or nucleic acids glucose is an example of a monomer and that can polymerize into a polysaccharide or a carbohydrate these polymers are examples of macro molecules and macromolecules are large very large things like protein teams you need to know about hydrolysis and condensation reactions again knowing the entomology of these words will really help you work out what is going on hydrate means water and lysis means break so hydrolysis direction is one that breaks a chemical bond using water a condensation reaction is one that joins two molecules together creating a chemical bond and in the process of joining those two molecules together another molecule is eliminated this is generally water for example if we take a dipeptide which is two amino acids joined together the link between those two separate amino acids can be broken in a hydrolysis reaction and you can see in pink and light blue here where water has been added to either side of the amino acid it has been added in hydrolysis reactions and condensation reactions happen a lot in biology they go in opposite directions so polypeptides can be broken down by hydrolysis to amino acids lipids can be broken down by hydrolysis to glycerol and fatty acids and nucleic acids like DNA can be broken down by hydrolysis to nucleotides and the reverse is also true in a condensation reaction amino acids will join together to form a polypeptide and monosaccharides will react in a condensation reaction to form polysaccharides monosaccharides are one sugars single sugars Monet means one and saccharide means sugar and these are the monomers for carbohydrates they will have the general formula C H2O and this will just be expanded upon in long chains you need to know some examples of this such as glucose galactose fructose all of these have the same formula they all have the same number of carbons hydrogens and oxygens in the same amount and the same ratios but the structure is different there are a range differently in its space which means they will behave differently there are two types of glucose that you need to know about alpha glucose and beta glucose they both have the same formula C6 h12 o6 giving them both six carbons 12 hydrogens and six oxygens but they are arranged differently the difference here is to be seen over on the right hand side in alpha glucose and in beta glucose the hydrogen and the oh group I mean different places one limits up and one of them it's down there is a change in spatial Arrangement now on a flat screen on a flat bit of paper this difference doesn't look too simply from it doesn't look too important but it really is important and that's easier to see when we move into 3D I'm going to use models to build this for you I'm just going to build this bit here not all of it because that would take far too much time in Black we have carbons and the bonds are represented as gray sticks and we'll try and keep them in the same orientation so you can see them named it in red we have this oxygen here being added on and at the moment they look the same now we're going to add on the big pink bit which basically means everything else that I'm not going to make because it takes a really long time it can look really confusing and that's not the important point of this video then we have the hydrogen and this is going to go in different places you can see that it's starting to lie differently on the table now now we have the o h being added on this is oxygen this is the hydrogen one of those will be added onto the top and one of those will be added onto the bottom and if I hold them both in the same way for you you can start to see that they look very different while in 2D they look the same they are what we call non-supereasable you cannot put them on top of each other it's a bit like comparing your left and right hand they look basically the same but you couldn't fit a left hand into a right glove because they've got a different arrangement in space you'll be really to know that there is a simpler way for you to draw Alpha and beta glucose instead of the way that I've drawn it for you before this is the structure that you are expected to know much simpler much easier for you to remember and understand Alpha and beta glucose are not that any monosaccharides you need to know about you also need to know about galactose structure to Beta glucose there is also fructose fructose is slightly different I'm first going to draw it this way around so you can see how it compares to the glucose and the galactose and then I'm going to draw the way that it's more commonly represented with the oxygen at the top the difference between Alpha and beta glucose is the orientation of the alcohol group The RH group and the hydrogen on the right hand side whereas the difference between beta glucose and galactose is on the left hand side with the orientation of your age group and the hydrogen group disaccharide is another important word diet means two and saccharide means sugar so a disaccharide is two monomers two monosaccharides joint together they're going to join via the oh group and a water molecule is going to be eliminated this is a condensation reaction when we have two monomers of alpha glucose doing together we are going to get maltose and this bonds here in the middle is a glycosidic bond maltose is made from joining two glucose monosaccharides together sucrose is made from joining glucose and fructose together and galactose together poly means many and saccharides means sugar so a polysaccharide is many sugars joined together a polysaccharide is a long chain of monosaccharides joined together blood glycosidic Bonds in condensation reactions the monama of alpha glucose will polymerize into the polysaccharide that is starch these long chains can be coiled into an alpha helix they are insoluble so they will not have any effects on osmosis they can be branched so there is going to be lots of surface area for enzymes to act on and enzymes to break it down quickly this is one of the reasons that outer glucose can be used in respiration starch is only going to be found in plant cells the different properties that start has comes from the fact that it is actually made up of two molecules so it's made up of amylose which can be the coiling and it's made up of amylopectin which can do the branching if you get asked a question about em to relate structure to function the starch then these are your functions alpha glucose can also polymerize to make glycogen this is going to have a very similar structure to starch but it is going to be shorter and there are going to be more branches this is found in animal cells in liver cells and in muscle cells this is very highly branched so it can be broken down very quickly the use of alpha glucose in respiration and as it is insoluble it will have no effect on osmosis beta glucose will polymerize to form long chains of cellulose this difference in structure will lead to a difference in function between a polymer of beta glucose and a polymer of alpha glucose it forms long straight unbranched chains that run parallel to each other these are cross-linked by hydrogen bonds this makes cellulose important as a structural material it is found in plant cell walls monosaccharides and some disaccharides are reducing sugars so we can test these with the Benedict's test two centimeter cubed is your sugar solution followed by two centimeter cubic Bendix solution and heat for five minutes and we are going to be looking for a positive result here where they are turning brick red a negative result will be no color change that is going to be still blue the brick rate is going to be an insoluble reciprocate of copper one oxide this can be a qualitative test where you can see it's positive or negative or a quantitative test with the use of a column cell where you can see things are more positive less positive and try and give them a value to carry out this test on non-reducing sugars they are first going to need to be treated to break down the glycosidic bonds this hydrolysis reaction will turn them back into monosaccharides which can then be tested using the Bendix test this will give a slight change to the method two centimeter cubed is to your solution two centimeter cubed dilute hydrochloric acid to break the glycosidic bonds heating it two centimeters of sodium hydrocarbonate to neutralize the hydrochloric acid and then follow that up with the Benedict's test to test for polysaccharides we can do the iodine test for starch we can add iodine dropwise into starch and if starch is present the solution will go blue black lipids or fats are insoluble in water but they are soluble in organic solvents such as alcohol we can have triglycerides which are fats and oils or phospholipids these are a great store of energy and will release twice as much energy as opposed to carbohydrates the waxy lipid cuticles are used in plants to conserve water they're also found in the oily glands in skin we use fats in bodies for insulation as they are poor conductors of heat so will keep us warm they also are used for electrical integration around nerve cells that is used for protection around our delicate bits such as our organs we can test a solution for lipids by mixing the test solution with ethanol shaking it for roughly one minute add in water and then a positive test results will give us a cloudy solution triglycerides are made up from to roll Three fatty acids try it means three so we're looking for something that's three Connections three fatty acids coming off it glycerol is joined to the fatty acids by an ester Bond little condensation reaction there are over 70 different fatty acids it's a wide variation in the triglycerides that are produced it is saturated it will only have single carbon carbon bonds it is unsaturated there will be some double carbon carbon bonds in there a polyunsaturated triggers where it will have lots and lots of double bonds are nonpolar which means they're going to be insoluble in water have no effect on osmosis phospholipids are made up from State group it's wrong two fatty acids is all joined with Ester bonds phosphate group is hydrophilic the tail of the phospholipid is hydrophobic hydrophilic means the phospholipid is attracted to water hydrophobic means it repels the water in a phospholipid one of the fatty acids one of the Three fatty acids we would see in a triglyceride has been replaced with a phosphate group the different ends of the phospholipid very different properties and they will behave differently droplet of water the hydrophilic head will go into the droplet of the water it loves water it wants to be around it however the hydrophobic tail doesn't and will stick out of the droplet of water property can lead to emulsions of oil and water where oil and water can be allowed to mix the cause of the hydrophilic head and hydrophobic tails a bilayer of our surface that's a double layer with heads on the outside and Tails on the inside forms the cell membrane a bilayer has a hydrophobic Middle where the tails are facing together this is what prevents any water-soluble molecules from passing through the bilayer and laid pass through using special channel proteins you need to know the core structure for an amino acid start with a central carbon which on the right hand side where it's generally drawn goes in to a carboxylic acid group off the central carbonates of hydrogen and then generally over to the left we have our amino group and then finally we have our arm group we use r as a way of showing that this is the side group and it can be replaced with a wide range of other things this is the bit that changes and changes the structure and the property of amino acids each amino acid has a different R Group the nh2 is the amino the carbon double bonded to an oxygen with a hydroxy group is the carboxylic acid group which is where the amino and the acid amino acid gets its name from amino acids can be small they can be large they are responsible for forming the different bonding that keeps proteins together they can be acidic and they can be basic [Music] thank you amino acids can join together to form dipeptides and polypeptides here we have two different amino acids and they will join together in a condensation reaction and water will be lost when two amino acids join together in a condensation reaction we lose two h's and an O from it and the bond forms between the carbonyl one and the nitrogen on the other amino acid the bond in the middle is the peptide bond dye is two so dipeptide is two amino acids together poly is Lots so polypeptide is lots of amino acids joined together proteins have a wide number of roles in biology any peptide chains fold up to make proteins few examples of proteins that you need to know are enzymes which break down large molecules all builds up smaller molecules by making and breaking chemical bonds structural proteins on that parallel peptide chains strong and stable bodies involved in the immune response two short polypeptides are highly variable final proteins in cell membranes contain hydrophobic and hydrophilic amino acids you need to know how to test for proteins a test will detect peptide bonds you need to mix equal volumes of test Solutions and sodium hydroxide a few drops dilute copper II sulfate if it is a positive result then the solution will turn purple copper sulfate is blue so if it stays Blue you've got a negative result protein structure has lots of layers building blocks are amino acids they joined together to form long peptide chains the primary structure of an enzyme long polypeptide chains can then fold and twist and bond with different amino acids to form the secondary structure either be an alpha helix or a beta pleated sheet or folding will take place and we will get to the tertiary structure and then finally the quaternary structure of a protein which is going to involve multiple peptide chains folded into secondary and tertiary structures and fitted all together the primary structure of proteins is the sequence or order of amino acids in the polypeptide chain the sequence or order of amino acids is determined by the DNA based sequence so if the DNA base sequence is changed then the sequence of amino acids will be changed the r groups on amino acids and their order gives the protein its different properties the r groups and the Order of the r groups can also affect the interactions between different polypeptide chains it can the our groups can determine whether a protein is large or small or hydrophobic or hydrophilic or acid or alkaline parts of the secondary structure is an alpha helix Jordan bonds form between the polypeptide chains this is a model of an alpha Helix here you can see the carbon in Black bonded to the nitrogen in blue and the oxygens in red hydrogen in white it is helical there is a hole down the middle we can see all the different parts bonded together the hydrogen bonds here are shown in purple now the secondary structure is a beta-plated sheet this has just been folded differently to the alpha Helix you can see it is flat we have layers going across chains of polypeptides in layers after the alpha helices and base pleated sheets have formed more folding will take place to give rise to the tertiary protein structure so we'll have a large amount of bonding between the polypeptide chains we'll see hydrogen bonding disulfide Bridges ionic bonding that leading to further folding hydrogen bonding is weak individually disulfide bridges are very strong you can see ionic bonding between the carboxyl and the amino groups bones can be broken by changes in PH the tertiary structure can be the final 3D structure of a protein a protein is only made from one polypeptide chain these bonds are all determined by the sequence of our groups so these bonds occur between the r groups of different amino acids in the polypeptide chain so if the primary structure is changed so the order of amino acids is changed then the position of the r groups in the polypeptide chain also changes this means that it can alter the tertiary structure because the bonds will be in different places the top level of protein structure is the quaternary structure seeing this in larger more complex proteins involves more than one polypeptide chain someplace fibrous proteins structural Euler proteins which is enzymes funds involved in metabolic function hemoglobin is another example of a globular protein enzymes are biological catalysts lower the activation energy that is required for a reaction to take place that we have our reaction profile reaction progress on the bottom energy up the side our substrates currently have higher energy than our products and an uncatalyzed reaction the progress will go up and then down as it moves across for an uncateralized reaction the peak that we see the peak in the amount of energy that is required to start that reaction is lower so it doesn't go up as high it doesn't need as much energy to get started an enzyme acts by lowering the activation energy needed for the reaction to start enzymes don't get used up so they can catalyze a large number of reactions enzymes are specific about the substrate they will form a complex with will only work on very narrow range of specific substrates it can work by either making a new molecule building something up or by breaking one down when we say enzymes are specific it's because the active site is complementary to only one substrate the substrate has a specific and complementary shape to the active site which allows it to bind and form an enzyme substrate complex so my pink shape here is my enzyme it is a protein that has tertiary structure the active site is the shape in the middle which is a specific shape that means it's Unique or it has a shape that will only fit or match a certain shape it's a 3D structure and is determined by the tertiary structure of the enzyme which we know is determined by the secondary and primary structure of the enzyme we can also say that the substrate has a specific shape so my purple shape here you can see it doesn't have the same shape as the enzyme but it has a specific shape that is unique to that substrate and it's complementary that means it fits into or matches the active site of the enzyme think about puzzle pieces all puzzle pieces do not look the same exactly the same shape but when they match or fit together they have complementary shapes so the active site being complementary and specific to only one substrate these words are really really important in exam questions when we're talking about enzyme specificity you may be familiar with the lock and key mechanism for enzyme action this is the old model that isn't supported anymore the lock and key mechanism needs to have an exact match between the substrate and the active site only then will the enzyme substrate complex be formed a better model than the lock and key mechanism is the induced fit model that scientific models change over time based on the best available evidence limitation of the lock and key mechanism is that enzyme has a very rigid structure used fit model suggests that shape of the active site changes slightly better accommodate the substrate with an enzyme catalyzed reaction we have a number of different ways we can measure the rate of reaction we can measure the product being made or we can measure the substrate being used up we can plot all of these changes on graphs with time along the bottom and either volume of gas being produced mass of something being lost or changed a color change or a change in cloudiness or a change in pH there are two different types of tests you can do you can do a qualitative test so what does it look like that would be can you see the cross through the solution can you see the color change that will give you a yes or no answer or a quantitative one that would be an improvement that will be using a Data Logger to measure actual values pH previous in Colorimeter or a gas syringe and to find the rate at any given point we can use the gradient at a graph which is the change in up over the change in a cross the units that you give your ants in are important volume of gas centimeter cubed per second Mass grams per second color change depending on what exactly you were measuring or pH per second you need to have to describe and explain the effect of temperature on an enzyme's rate of reaction this is a little bit of a link to chemistry and rates of reaction in chemistry because as temperature increases the particles the substrate and the enzyme will move around more there will be more collisions between these two so a reaction is more likely to take place the enzyme is more likely to meet the substrate and form an enzyme substrate complex we can see that on a graph with temperature across the bottom and rate of reaction at the side there are two parts to this graph in pink we can see what is happening as the temperature increases but that is not the whole story because as the temperature rises the bonding within the enzyme starts to break down this causes a change in the tertiary structure which changes the shape of the active site this means the shape of the active site is no longer complementary to the substrate so no es complexes can form this causes the rate of reaction to decrease as you can see on my graph it has gone rapidly down and we say the enzyme has denatured it has not been destroyed and it has not been killed because it is not alive it has been denatured the optimum temperature of an enzyme can be found at the peak of grafts that look like this with temperature on the x-axis different enzymes will have different Optimum temperatures human enzymes that work inside the body will have an Optimum temperature of 37 degrees C because that is body temperature you need to talk I want to talk about the way that pH affects how an enzyme works firstly pH is the concentration of hydrogen ions in a solution and we can write it like this h plus inside the square brackets ph1 is acidic with lots of hydrogen ions or a high concentration of hydrogen ions ph7 is neutral and you will see a balanced number of hydroxide ions o h minus with hydrogen ions ph14 is alkali so we will have lots of hydroxide ions o h minus and few h plus ions the hydrogen and the hydroxide ions interfere with the ionic bonding in the tertiary structure of the enzyme and so this can affect and change the tertiary structure which causes active site to change shape here is our graph with ph on the bottom and write a reaction up the side enzymes only work around a very narrow pH within a certain range of ph's if it is too acidic it's a concentration of hydrogen ions is too high or too alkali where the concentration of hydroxide ions is too high then the enzyme won't work it will be denatured so example the enzymes that work in our stomach like a very acidic condition this is going to be different to the enzymes that are working in our intestines if we're looking at the shape of this graph we can see it is symmetrical as either to acidic or two alkaline or denature that enzyme or an enzyme substrate complex to form an enzyme needs to be able to find the substrate if the concentration of enzyme or the concentration of substrate is too low then this is going to happen slowly here we have our graph with concentration along the bottom and rate of reaction upside and I'm going to talk about three different points on this graph a b and c a is at the point where there is low enzyme concentration so at the beginning of the graph there are more substrates floated around than there are active sites available moving across the graph to a point B where we see it changing from increasing to flattening off all of that active sites are filled up and then at Point C the flat bit of the graph as we increase the enzyme concentration there are more active sites available than there are substrates to go into those active sites at that point substrate is the limiting factor we can draw an identical graph switching the x-axis from enzyme concentration to substrate concentration so for the substrate concentration graph it will be the same shape but this time it is the substrate concentration that's on the x-axis so for part A of the graph it is the substrate concentration that is limiting so there is not as much substrate as there is enzyme molecules to start with by the time we get to B nearly all of the enzymes are saturated so this is where we've got almost all of the enzymes of active sites are full and then at C this time it's the fact that the substrate concentration is limiting because and we can tell that because adding more substrate so increasing the substrate concentration isn't having any effect on the rate of reaction so it is that the enzyme concentration must be the limiting factor here there are two types of enzyme inhibition you need to know about competitive inhibition and non-competitive inhibition in competitive inhibition the inhibitor is a similar shape to the substrate so it will occupy that active site this will stop the formation of the enzyme substrate complex some of these Inhibitors will bind for a very long time and some Inhibitors will bind to the enzyme intermittently leaving an allowing room for the real substrate to bind occasionally whereas a non-competitive inhibitor will be a molecule that will bind to the enzyme not at the active site in a location away from the active site this binding will change the shape of the active site the enzyme active site will no longer be complementary to the substrate so non-enzyme substrate complexes can form here we have our graph with substrate concentration along the bottom online for no inhibition goes up and then flattens off as we would expect what any rate of reaction graph a competitive inhibitor will slow down that reaction it will get to the same level but it would take longer getting there the non-competitive inhibitor line will never make it to the rate of reaction that the other two will this is because the enzyme is being denatured by The Binding of the non-competitive inhibitor so there is a slight increase in the rate of reaction which is when enzymes are reacting with substrates before all of the enzymes have been affected by the non-competitive inhibitor but once all of the enzymes have been bound to the non-competitive inhibitor their active sites are denatured so they're no longer complementary to the substrate so no enzyme substrate complexes can form these graphs are really helpful for being able to tell the difference between whether an enzyme is being inhibited by a competitive or non-competitive inhibitor if you see a graph that looks like this and you just see the pink line so as the substrate concentration is increasing the rate of reaction continues to increase but slower than it is a compressive inhibitor if you see a line that goes up and then there's a flat line with our non-competitive inhibitor line your evidence is that as the substrate concentration is increasing it's not having any effect on the range of reaction then it must be a non-competitive interpreter there are different nucleotides that you need to know RNA is ribonucleic acid DNA is deoxyribonucleic acid they have a phosphate group a pentose sugar and an organic base all joined together the organic bases are where we see the differences we have a g c t and u adenine guanine cytosine thymine and uracil uracil is only found in RNA in DNA you will find a and t bonding together and C and G bonding together the T that is in DNA is not in RNA so in RNA you'll get a and u bonding together between a and t and a and u there is a double bond between C and G in both RNA and DNA we have a triple bond these will make polynucleotides with a phosphate group of one being joined via the pentose sugar to the phosphate group of another via a phosphodiester bond in condensation reactions this chain can be incredibly long RNA is similar to DNA but instead of having a deoxy fiber sugar it has a ribose sugar there are three different types of RNA that you need to know about mRNA which is messenger RNA this codes the amino acid sequence rrna which is ribosomal RNA this translates the RNA and T RNA Transfer RNA this is the bit that brings amino acids to the ribosomes one important difference to note that RNA has uracil as a base instead of thymine and the uracil will take place of thymine and bind to adenine so you're getting a u it is also shorter and it is single stranded and the ribosomes are formed from proteins and RNA DNA replication is an important and relatively complicated process so you need to understand that each individual step carefully for it starts off with DNA helicase breaking the hydrogen bonds between the paired bases between the two strands this results in the unwinding of the double helix and provides two single strands of DNA onto these two single strands of DNA free nucleotides will bind this will be to the complementary basis and we will get matching strands DNA polymerase will join the new nucleotides together creating the phosphodiester bonds that hold everything in place and we can see the start of replication and new cases being formed two identical strands of DNA are going to be formed at the end of this and this is in semi-conservative replication you can see the original DNA strand and the new DNA strand two scientists Middleton and star are the ones that proved semi-conservative replication in that experiment here we have a t p i don't even try phosphate now the first part you can see the big part here is adenosine triphosphate because it has three phosphates we can also get a d p adenosine diphosphate which only has two phosphates in it we also have a version with only one phosphate in it a m p adenosine mono phosphate the little bit here is a bit that will tell you how far the compound extends and how many phosphates are in it without any phosphates this is just adenosine these Bonds in here are unstable bonds meaning they're going to break easily breaking them only requires a low activation energy meaning not a lot of energy is required to put in to break these bonds and they're easily broken upon breaking of these bonds they release energy when ATP is broken down in a hydrolysis reaction it will turn into a DP adenosine diphosphate a phosphate and inorganic phosphate and energy the enzyme that will break this down is known as ATP hydrolase it can be rapidly reformed by the enzyme ATP synthase there are larger processes in cells that require energy for example metabolism movement active transports and secretion ATP can also be used to phosphorylate molecules so to add a phosphate group and this can make these molecules more reactive water is an absolutely fascinating little molecule made up from two hydrogens and one oxygen it is a bent polar molecule so the oxygen will be a little bit negative and each hydrogen will be a little bit positive because of their Delta negatives the Delta positives they're slightly negative and they're slightly positive we can get hydrogen bonds formed between molecules of water now individual hydrogen bonds are pretty weak but within water we are going to get large numbers of hydrogen bonds so water is polar and hydrogen bonds is incredibly important they were involved in a wide range of condensation and hydrolysis reactions eight large amount of energy is required to break the large number of hydrogen bonds meaning that water is a liquid at room temperature whereas you will expect it to be a gas other similar things on gases at room temperature the hydrogen bonds are responsible for their cohesion and surface tension of water and it has a very high Civic heat capacity meaning it could buffer temperature changes which is important for preventing sudden changes in temperature within our body it is also an important solvent each of these properties gives water certain functions and makes it suitable for carrying out certain processes so we see that water is an important metabolite because it can take part in metabolic reactions like colonization and hydrolysis because lots of energy is needed to break the bonds we say water has a high latent heat of vaporization this helps to cool organisms down like the way we swept because water molecules are cohesive it allows water to flow in unbroken columns in the xylem the surface tension that water creates supports small organisms that can live on top of the water such as Pond skaters high specific heat capacity means that bodies of water such as ponds and lakes can have a more stable temperature than land this helps to regulate the body temperature of organisms that live in water water is a good solvent this means it can attract and dissolve ionic compounds so that they can be transported because the cytoplasm think about um ions being transported in the xylem in the water that's what it's useful for also because it is polar it can form hydrogen bonds with other polar molecules and dissolve them such as glucose you need to know both the structure of water and Link these structural features to its properties and how it can help organisms there are a number of important inorganic ions that you need to know about and at this point we touch slightly on chemistry but not too much you need to know that an atom becomes an ion when it loses or gains an electron for example K plus is a potassium ion that has lost one electron whether you lose electrons you'll become positive O2 minus is oxygen that has gained two electrons we can see that from the two and the gaining electrons the gaining of negative charges is the minus some common ones you need to remember are sodium ions na Plus that is involved in co-transportation across a membrane phosphate ions po43 minus which is essential for the phosphate group in DNA RNA and ATP hydrogen ions h plus and with square brackets around it that means the concentration of hydrogen ions and that is how we look at pH a tongue twister here iron ions we have iron ii Plus in a respiration with iron 3 plus and this is an important reaction that takes place inside hemoglobin [Music] [Music] thank you [Music] foreign [Music] structures within a eukaryotic cell both plant cells and animal cells and the function of all of those different organelles both plant cells and animal cells have a nucleus this is where the chromosomes are located the chromosomes are made of wound up DNA and it is enclosed all within a nuclear envelope there is a double membrane around the nuclear envelope and the nucleus is in charge of controlling the cell's activity the new case also contains the nucleolus which is where ribosomes are produced both plant cells and animal cells have a cell surface membrane this is made up from lipids and proteins this cell surface membrane controls the movement of things in and out of the cell they both have mitochondria this has a double membrane and the highly one is very heavily folded it is here that the enzymes involved in respiration and the production of ATP can be found the tiny black dots in both of them are ribosomes these are very small they can be found either on the rough endoplasmic reticulum or in the cytoplasm this is a place where proteins are made both animal cells and plant cells have a Golgi apparatus this is a fluid filled membrane that produces new lipids and new proteins podding off from the Golgi apparatus you're going to have a Golgi vesicle this buds off and stools and transports the new lipids and proteins there are some organelles that are only found in plant cells the green chloroplasts are the location of photosynthesis it has a double membrane an inside membrane is a thylakoid membranes both animal and plant cells will have a rough endoplasmic reticulum very similar in shape to the smooth ear but this one is covered in ribosomes this is where the processes proteins that are made within the ribosomes the smooth endoplasmic reticulum also found in both animal and plant cells is site of synthesis and processing of lipids lysosomes contain digestive enzymes being in a lysosome keeps them separate from the cytoplasm and the cytoplasm is where most of the reactions within a cell actually take place plant cells will also have a cell wall this ensures the cell structure is maintained the vacuole that is found in plant cells contains sap and helps to maintain the cell shape from the cell structure by maintaining the pressure and keeping the cells rigid you need to be able to talk about how eukaryotic cells are adapted to their various functions there are physical adaptations to allow cells to maximize diffusion such as microvilli which increase the surface area which we can see in the ilium epithelial cells and by concave shape in red blood cells which increases the surface area available for oxygen diffusion any cell which needs to do a lot of exchanging of substances will have some form of physical adaptation to increase surface area in order to speed up diffusion some cells are adapted for storage so fat cells can have large lipid stores these and can sometimes be in vacuoles red blood cells also have no nucleus that increases the space inside of them so that they can store more hemoglobin and therefore bind more oxygen this could also be true in plant cells that are adapted to store starch stem cells are adapted for secretion so these cells often produce large amounts of a certain substance and they release it from their cells these cells will often need a large Golgi because they'll be producing many vesicles they may also need a large rough endoplasmic reticulum or many ribosomes to produce proteins for example goblet cells which secrete mucus lots of cells that are adapted to have increased energy requirements any cell that carries out a process that requires lots of energy is going to need lots of ATP this means they will be adapted to contain many mitochondria to carry out more respiration to produce a higher amount of ATP required for example in muscle cells which contract and that requires ATP they have lots of mitochondria or any cell that is carrying out active transport or a lot of active transport for example nerve cells if a cell carries out a lot of active transport it will also require a lot of channel proteins and carrier proteins so these cells also often have many of these proteins on their cell membrane and they may also have increased ribosomes to help to produce those large amount of proteins there is a hierarchy starting with cells tissues olins and organ systems because cells do not work alone if we have a group of cells with a similar function then this is a tissue in this example we have all of these cells working together to work as a muscle tissue there are lots of different types of tissues within a body for example connective tissue muscle tissue nerve tissue or epithelial tissue a group of different tissues that are working together is an organ again there are lots of different types of organs within a body and you need to be aware of these for example skin hot or liver groups of different organs working together towards a common function or a common goal or an organ system for example the endocrine system the muscular system the skeletal system or the digestive system there are a range of structures within prokaryotic cells that you need to be aware of the function of some of these structures will have common features with eukaryotic cells but not all of them they have cytoplasm but it is without any membrane-bound organelles the tiny black dots are the ribosomes involved in protein production the cell surface membrane will control what goes into and out of cells and the cell wall is important for keeping structure and containing the glycoproteins in addition to common features with eukaryotic cells prokaryotic cells may have one or several flagella these are generally very long structures and they use for motility the DNA in prokaryotic cells is not contained within a nucleus it's within the cytoplasm and it is one long coiled strand there will also be small bits of plasmid DNA these can be easily passed between bacteria helping the spread of genes these genes could be advantageous to the bacteria for example antibiotic resistance they may have capsules on the outside of secreted slime to protect the cell from Attack viruses are prokaryotic but they are very different to bacteria and they all have very different structures to each other if we look here A bacteriophage looks very different to an ebola virus which looks very different when a denovirus but within this variation all viruses have a similar overall structure on the outside they will have attachment proteins this is going to allow the virus to attach to the cell that it's going to inject itself into they will have a capsid this is a protein coat that is surrounding the nucleic acid and the nucleic acid can be DNA or it can be RNA it is important to remember that viruses are not cells and they are not living they are incredibly small we're talking 20 nanometers up to about 300 nanometers and they can only replicate inside a living host cell they will have an envelope around the outside this is a protective coat and it is only present in some viruses in biology we can work with some very small units so it is important that you understand the relationship between these and how to convert between them we can measure people and other large objects in meters but that is useless when we are talking about very small things so here is our scale we are going to start at the big end with one millimeter if you can't visualize that go and grab a ruler now and look at this with the ruler on your desk while we look at this get a smaller 100 micrometers 100 microns 10 micrometers one micrometer 100 nanometers 10 nanometers two nanometers one nanometer and then down below that we can go to picometers and femto meters but that is more the range of physics now one millimeter is very small but there are 10 millimeters in one centimeter which on my screen is this big and a hundred centimeters make up one meter now one millimeter is roughly the diameter of a grain of sand a grain of pollen is roughly 100 micrometers in diameter down at 10 micrometers we're looking at a red blood cell bacteria are roughly one micrometer whereas viruses are much smaller at around 100 nanometers proteins around 10 nanometers and with all these things there is a range whereas DNA comes in at two nanometers and that'll be the diameter of the helix a bucky ball carbon 60 Buckminster following will come in at one nanometer and then an atom will be 0.1 nanometers so these are a very small but you need to keep this scale in mind when we are talking about the measurement of cells when we are talking about a microscope calculations because these are the units that you're going to need to be using and the units you're going to need to be converting between the most common ones you'll be using are millimeters micrometers and nanometers to go through millimeters to micrometers you times a thousand and Times by another thousand to get to nanometers to go from nanometers to micrometers we need to divide by a thousand and then from micrometers to millimeters it is again divided by a thousand you are going to be using those calculations a lot when we're using microscopes so I suggest you write that on Post-It note and stick it up on your wall somewhere there are two different types of microscope that you need to be familiar with we are briefly going to go over them here but you might need to know them a bit more detail these are Optical microscopes and electron microscopes with an optimize scope you will need light to form an image whereas an electron microscope will use electrons to form the image an obstacle microscape can look at objects which are larger than 0.2 micrometers whereas an electron microscope can look at much smaller objects much smaller things and up to White Escape can see things in color and it can see living specimens whereas an electron microscope you will get a black and white image which might be Studio color by computer and it is dead because it needs to be fixed before it can be put into the electron microscope an optical microscope will have a maximum magnification of around 1500 times whereas an electron microscope will have a maximum magnification that is much higher than that this will be around one and a half million times he is a beautiful image of a drosophila eye drosophila are flute flies those tiny annoying things that are around bananas that have gone a little bit off they are attracted to this and you can see the big differences here between an optical microscope image and an electron microscape image this one is color and it is live so this is the actual color of things whereas this one has in serial colored because it will be a black and white image for the electron microscope you were getting a lot more details on the hair whereas in the optical microwave you can't really you can probably guess their hairs but it just kind of looks a little bit fuzzy here you actually pick out the individual hairs and you can pick out the root bases the the follicles that the hairs are growing out of whereas you can't see that at all over here you get a lot more structure a lot more detail with the electron microscape but the image the the subject has to be dead so you cannot take the drosophila and then look at it under the microscope look for what you're you're testing for and then potentially breed from it and you have to kill it to be in an electron microscape I think these images are both stunningly beautiful it is important that you are familiar with the different parts of an optimal microscope hopefully you've used one of these in the lab at school or seen somebody use one we have eyepiece the base this is going to be the light source down here this could be a mirror or it could be a lamp if it's an electrical microscape this large wheel here is your course focus and the smaller one is your fine focus there are some objective lenses that come here and this bit is a wheel which you can turn to switch between the different objective lenses this is your stage and your place your slide in here so that you can view it under the microscope view it view the eyepieces the slide is held in with this clip here which you can move in and out in and out to put the slide in place and keep it there obstacle microscopes are going to use a convex Glass lens it has a pair of lenses it has the eye piece and then it has the objective lenses these will generally be four times ten times 40 times maybe a hundred times you will need a light source coming from below so that you can actually visualize things otherwise it is going to be very very hard to see anything an important thing to note about Optical microscopes is that resolution is different to magnification resolution is the ability to differentiate between two spots to work out there's two things there instead of one thing in a light microscope the resolution is roughly 0.2 micrometers anything closer than 0.2 micrometers apart will appear to be a single object under an obstacle microscape the higher the resolution a microscope has it will give the more precise image there are two different types of electron microscapes transmission electron microscopes and it's scanning electron microscopes transmission electron microscopes have a very high resolution they can see very small objects but they need to have a very thin specimen to image they work on fixed samples they have to be dead because it takes place inside a vacuum and occasionally you will get artifacts of scanning for scanning electron microscopes they have a lower resolution they can produce 3D images because the electrons are reflected from the surface and again they must have fixed samples here we have two example images the first one taken with a transmission electron microscape and the second one taken with a scanning electron microscape here you can see the image taken with an optimal microscope and you can see here the much more detail you get with the electron microscape in the scan electromaxing we can see that the 3D image is much thicker than this very thin sample over here in comparison to an optimal microscope which well I have one sitting on my desk electron microscopes are very very large they will generally have their own dedicated room and their dedicated air conditioning units to keep them controlled they use electromagnets to focus the beam of electrons instead of lenses like in an optical microscope there will be a screen for you to look through but most other images you'll be getting are going to be computer generated you cannot just look through with your eye and see exactly what you're looking for the samples will go in the middle well kind of awesome third of this very large very pull it of equipment the electrons will come from the top and then be focused by various different lenses before they eventually hit the specimen and the images are then generated by the computer when you have an image under the microscope you then need to be able to determine the size the actual real size of that image and for that we need to use magnification calculations the equation that you need to be able to remember is that magnification is the size of the image divided by the actual size of the image whenever you get that magnification calculation the very first thing you should do is to highlight all of the numbers in the text and then convert them so they are the same at scale so you convert microns micrometers to nanometers so they're all in the same scale so you do not get confused if there is an eyepiece grass secure in the question or you've been using one in the lab then you can use that to measure the size of the image that you are seeing down the microscope this IP scratch cure we need to be calibrated for each individual lens magnification that you are using if you want to look at a particular organelle within a cell and not necessarily the whole thing a nice thing that you can do is separate out all of the cell components to look at them individually you can fractionate the cell components by homogenation and then follow that by Ultra centrifugation the first step is going to be homogenization to break down the cell you can break down the cells either with a blender or you can do it by vibration this is important because it breaks open the cells and releases the organelles which we would like to study step two is going to be filtration to remove the large Parts either unwanted bits that you are not looking for or parts of cells that haven't broken down for you and step three is going to be ultra centrifugation in a centrifuge when a liquid is spun in a centrifuge the components will separate out they will separate out by weight the heavier ones will go to the bottom and you will end up with layers the supinator the liquid at the top can be removed and then further spun at a faster or higher speed to continue the separating of components so that all the different parts of it in the super native can be separated out the cell cycle is the complete pathway around from start to finish interphase is from cytokinesis to the next nuclear envelope breakdown while it may not seem like it a lot happens during interface very very roughly we can see the cell cycle takes 24 hours and 90 of that time is going to be interface we have G1 this is Gap phase one where the cell is going to grow having just divided itself in half it is going to produce new organelles and proteins S phase is where we get the synthesis of a new DNA this is where the DNA is replicated so that it can be divided during mitosis then we will have G2 this is Gap phase two there is going to be more growth and more new organelles produced I'm wise is only a very short section of the sales cycle but a lot happens within this short period of time it is important that you remember the difference between mitosis and meiosis and that you spell them correctly in the exams mitosis produces two daughter cells and the stupid way that I remember it is that mitosis has a t in it and you can write two whereas myasis that produces all daughter cells doesn't have a t in it this is not the most genius way ever but it is really effective for working out the difference between mitosis and meiosis the daughter cells in mitosis have the same DNA they have the same number of chromosomes and they are identical to the parent cells there are several different stages of mitosis that you need to know the different names for followed by a prophase metaphase anaphase telephase and cytokinesis the way that I always used to remember with order when I was studying was with IP Matt I don't know what it stands for doesn't really sound that anything if you come up with something that sounds cool then leave a comment down below to help other people during prophase the chromosomes will become visible as they condense two centrioles will develop in animal cells only and these are the spindle poles they will move to opposite sides of the cell the nuclear envelope will start to break down and the chromosomes are now free in the cell within the cytoplasm at metaphase chromosomes can now be visualized as two chromatids joined by the centromere the spindle fibers will attach to the centromere on either side and the chromosomes line up in the center of the cell each side is attached to a different chromatid in anaphase the centromeres will split an individual chromatids will start to move towards opposite sides of the cell during telophase when the chromosomes reach the opposite poles they are are not coiled and a new nuclear envelope will start to form around the set of DNA in cytokinesis the cytoplasm and all the nouns will be divided between the two new cells and a new cell membrane will form around the new daughter cells these new daughter cells will then go on to enter the next cell cycle entering the G1 phase here we're going to be looking at a root tip squash under a microscope one of my favorite things to do for this practical you need to have an actively growing root which you then put into five molar acid to stop any reactions happening you then need to take a very small section of this root put it on a slide and stain it move it around a little bit to separate out all the slides pop a cup of slip on it and then look at it under the microscope this is one of my favorite things once you get your slide under the microscape and you've found what you are looking for moving around adjusting the focus ever so slightly we need to do a calculation of mitotic index so start by finding all of the cells that are in mitosis and if you can identify the stage of mitosis that layer in for our calculation and mitotic index it is going to be the number of cells that are currently undergoing mitosis divided by the total number of cells now the advantage that I've got here is that I have a picture an image which means I can actually go through and Dot the cells as I encounter them so I don't double count things so 5 divided by 185 gives us 0.03 now everyone is going to have a slightly different number for this some cells are not going to be in the focal plane of the image not all the cell membranes are clear in this but the most important thing when you're accounting is that you are consistent in your counting consistent between slides if you are comparing different conditions inconsistency in counting is going to be one of the biggest causes of error in this cancer is the uncontrolled division of cells generally brought about by mutation in the genes that control the cell cycle or control cell division and mitosis cancer is an incredibly complicated collection of disease it is growth of cells in unwanted locations and it can be caused by lots of different factors a wide range of different genes can be influenced by an even wider range of factors and these can have diverse consequences the treatment for cancer generally revolves around killing the cancer cells this can either be done by preventing DNA replication or by preventing a metaphase in mitosis the problem with this treatment is that it also kills a large number of healthy cells generally the rapidly dividing ones such as the ones for hair growth thank you cell division is slightly different in prokaryotic cells the DNA is not within chromosomes it is circular DNA within the cytoplasm there is also plasmid DNA both the free circular DNA and the plasmid DNA replicates the cytoplasm divides and each daughter cell will get the circular DNA and a variable number of the plasmids and it is these plasmines that are responsible for a lot of traits that bacteria prokaryotic cells carry such as antibiotic resistance viruses are not alive thus they cannot undergo cell division they cannot replicate by themselves they will attach to the host cell using their attachment proteins and then they will inject their DNA into the host cell the host cell will then start producing this vile DNA the viral DNA where then instruct the cell's own organelles to produce new virus particles these new virus particles will then be released into the body this kills the host cell and the body is then swamped with new viruses you need to be familiar with the with the basic structure of all cell membranes they are complex structures made up of lots of different components combined in lots of different ways we are going to start by looking at phospholipids there are two main parts to a phospholipid the hydrophilic head points towards the outsides of the membrane whereas the hydrophobic tails are internal to the membrane this Arrangement allows lipid soluble materials to move through the membranes meaning that lipid soluble materials can enter and exit the cell the hydrophobic tail stops water-soluble materials following the same path this by lay is not fixed and is constantly moving around meaning it is flexible and self-healing there are lots of proteins lots of different proteins within the structure of the cell membrane they each have different functions we can have carrier proteins or channel proteins which will help molecules move through the membrane we can have receptor proteins which will allow the cell to recognize and respond to external stimulus to recognize what is happening within that environment glycoproteins are proteins that have carbohydrate groups attached to them these can act as cell surface receptors for things like hormones and neurotransmitters cholesterol is found we in the phospholipid bilayer it helps to give the membrane strength and stability it has a hydrophobic properties which help the hydrophobic tail of the phospholipids to hold together this further prevents water loss cholesterol will increase the close packing of the phosphate lipid this reduces the movement in the bilayer making the Biola more rigid being able to break down long complex words really helps you understand what they mean here we have glycolipids glyco means sugars or carbohydrates and lipids means lipids the fat parts through a glycolipid is a lipid that have carbohydrates bound to them this helps form attachments and for Signal recognition the fluid mosaic model of plasma membranes was developed in the 1970s as a way to describe the movement of the different components within the plasma membrane it is fluid because the phospholipids and other components of the membrane are not fixed in place and can move around it is a mosaic due to the wide range of different shapes and sizes of the parts that make up the membrane the one of the require practicals we need to determine the water potential of potato tubers for this it is important you have the same size tubers so same diameter same thickness same surface area if possible they do not need to weigh exactly the same but they need to be roughly the same you need to dry and weigh these and then you need to incubate them at different concentrations of sucrose solution after the incubation you need to dry it and weigh them again then we can work out our calibration curve plotting all the points drawing a line of best fit and then working out where there is zero change in weight this probably won't correlate to one of the samples that you've tested as that would be unlikely but if we go across and down or up and across depending on which way you've drawn your graph at zero change then we can work out where the water potential would be the same in the content of the sucrose solution and in the potato tubers this will probably vary between the type of potatoes that you are using how old the potatoes are and conditions in the lab whenever you get a question about osmosis you need to be extra careful with your wording this is one of those topics where a really careful definition I really will that definition it will do you really really well because you can just write this down in the exam as the answer here is my definition from my grocery book bits osmosis is the diffusion of water molecules from a region of plywood potential to a region of lower water potential across a partially permeable membrane so here we have our water molecules and the middle are partially permeable membrane we can see that they will fit through we also have our solute in green it is very large and will not fit through the gaps in the partially partially payable membrane on the right hand side of the membrane there are no solute molecules this has a high water potential on the left hand side of the membrane there are more solute particles this has a lower water potential now since the solute particles cannot move across it is the water molecules that will move across from the area of higher Woods potential to the area of lower water potential when the water potential on either side of the membrane is equal net movement stops and a dynamic equilibrium is established so this isn't saying that all movement stops just net movement stops if we get something diffusing in this direction we will also get it if using in this direction that is your dynamic equilibrium we're going to use red blood cells as an example of looking at osmosis in animal cells the cell membranes of these are very thin and fragile if we put them into a external solution that has a lower water potential water will leave the cell and this cell will shrink if we put them into an isotonic solution which is a solution that has equal water potential there will be no net movement of water a dynamic equilibrium will be established with the same amount of water goes in that goes out if we put them into an external solution which has a higher water potential than the cell water will enter the cell and the cell will eventually burst osmosis in plant cells is slightly different to osmosis in animal cells if you put a plant cell into an external solution that has a higher water potential water will enter the cell the pretty class swells up and the cell becomes turded if you put a plant cell into an external solution that has a lower water potential than the cell water will leave the cell and the proteoplast will shrink the cell will become plasmalized one of the required practicals is looking at the effect on alcohol concentration on the leakage of pigment from cells the purple pigment will be kept inside cells by healthy membranes whereas damaged membranes will leak out the piglet for this you need to make a standard solution we are going to be using this standard solution to compare our test against you need to incubate your beetroot discs at different concentrations of alcohol and then compare the color to the standards to make this more accurate to make it a quantitative test in terms of a qualitative test we could use a Colorimeter to measure absorbance and then we could draw a calibration curve to work out exactly where things lined up simple diffusion is another example of where having a clear definition in your mind will serve you really really well in an exam setting diffusion is the net movement of molecules or ions from a region where they are more highly concentrated to one where their concentration is lower until they evenly distributed molecules or ions will move it down a concentration gradient particles are always in constant motion and that movement Is Random and at random they will become evenly distributed over time now not everything can just pass through the plasma membrane small particles and non-hole particles such as carbon dioxide and water are ones that can pass through for things that need a little bit of help passing through the membrane we have facilitated diffusion for example charged ions and polymolecules will need a bit of help with diffusion this is to avoid the lipid body layer channel proteins allow these particles to diffuse no ATP is needed for this as it is a passive process each ion will have its own channel protein so if it's a sodium ion there will be a sodium ion channel protein and another example are aquaporins which are specific channels that are designed to help transport water molecules active transports is yet another phrase that needs a careful definition it is the movement of molecules or ions into or out of a cell from a region of lower concentration to a region of higher concentration using ATP and carrier proteins a molecule will enter the carrier protein it will bind to the receptor ATP will be converted to ADP and this will trigger a change in the shape of the carrier protein meaning the molecule can be released to the opposite side of the channel one example of Transport that uses active transport is co-transport specialized Cara proteins are able to bind two molecules at once these are called co-transporter proteins these transports proteins allow one molecule to move down its concentration gradient and this movement is used to transport another molecule at the same time but against its concentration gradient into a cell an example is how glucose is absorbed in the small intestine we have to create a low concentration gradient of the sodium ion that we want to move into the cell so we need it to be able to diffuse in so in order to make a low concentration inside the ilium cell sodium is actively transported out of the cell into the blood using the sodium potassium pump so this is done by active transport and it causes a low concentration of sodium inside the ilium cell because there's a lower concentration of sodium inside the cell it diffuses into the cell from the small intestine through the co-transporter protein glucose binds and is also transported but it is going against its concentration gradient as it is often a lower concentration of glucose inside the ilium cell compared to the illuminum of the small intestine once glucose is being co-transported into the cell there is then a high concentration inside the cell and it can diffuse down its concentration gradient into the blood using a channel protein so this process of co-transport requires ATP and energy in the same way as active transport does because it requires the active transport of the sodium ions out of the cell to create the concentration gradient which drives the co-transporter protein so co-transport does require energy and is a mixture of both active transport and facilitated diffusion you need to know the different factors that can affect the rate of diffusion firstly we need to look at how increasing the surface area increases the rate of diffusion here we have some epithelial cells and these would be how long the membrane would be with at the folding however folding of the membrane massively increases the surface area that is available these microvilli are on epithelial cells of the lining of the small intestine increasing the surface area of the cell membrane this is also known as the brush order increasing the concentration gradient increases the rate of diffusion and facilitated diffusion because it prevents equilibrium from being breached which would slow down or stop the process of diffusion decreasing the membrane thickness or having thin membranes thin walls increases the rate of diffusion because it decreases the distance that the particles have to travel increasing the temperature increases the rate of diffusion as well and this is because particles have more kinetic energy so they're going to be able to move faster to increase the rate of facilitated diffusion you can also increase the number of channel proteins this will increase the rate until all of those channel proteins are being used and then the rate will slow down this is an adaptation that some cells that need to do a lot of facility diffusion it will have on their cell membranes movement of glucose against concentration gradient is via a sodium potassium pump for example when glucose moves from the small intestine into the blood here we have our epithelial cells our bloodstream and the small intestine glucose is going to want to move from the small intestine into the bloodstream active transports will move sodium ions from cells into the blood producing a concentration gradient with a higher sodium concentration in the Lumen subsequently sodium ions will now diffuse into the epithelial cells as they enter they bring a glucose molecule with them the glucose that is now in the epithelial cells can now diffuse into the bloodstream the body has a wide range of defense mechanisms the first step is to stop pathogens getting into the body in a variety of different ways this can be using skin as a protective barrier using snot to catch anything that's going in same as with the nose hair or using scabs to block up any holes step two is to fight the pathogens this QB by phagocytosis this is cell mediated involving T lymphocytes or humeral response involving b lymphocytes antigens antigens are usually proteins glycoproteins or glycolipids they are found on cell membranes and viruses they help cells to recognize each other as either self or non-self you may describe non-self or see it described as foreign which means the antigens are different to the antigens of the person's own body if a cell with foreign antigens is detected then it will trigger an immune response examples of cells that may have foreign antigens and trigger an immune response are pathogens so microorganisms that cause disease bacteria or viruses cells from another organism so this could be a transplanted organ if you have had a donated organ transplant abnormal body cells so these would be cells that could be cancerous that changes the antigens on the surface of the membrane or if the cell was infected by a virus these change the antigens on the cell surface and so the body will know that these cells are not normal and they will seek out to destroy them phagocytosis it is important to remember that a phagocyte is a type of white blood cell receptors on the phagocytes will recognize antigens on the pathogen the pathogen will interact with the phagocyte the phagocyte will move around the pathogen eventually enveloping it once the pathogen is contained within a vacuole a lysosome which contains lysozymes fuses with this vacuole and the lysozymes are released these can break down the pathogen the phagocyte will then present the antigens and this will signal to other parts of the immune system T lymphocytes are another type of white blood cell we can have helper T cells these signal to activate phagocytes and B cells we can have cytotoxic or killer T cells these will kill the foreign cells an antigen presenting cell a phagocyte is recognized by the helper T cells triggering rapid division this leads to a rapid increase in helper T cells that recognize the specific antigen these will then activate the cytotoxic T cells stimulate phagocytosis and develop into memory cells for future responses they will also stimulate the B cells cytotoxic T cells produce perforin which leads to holes in an infected cell holding the membrane that will lead to cell death there is a large range of variety within B cells as each of these produces a specific antibody a B cell will become activated when it binds to an antigen or a t helper cell or an antigen presenting cell this is called clonal selection and the B cells divide into plasma cells that release antibodies into the bloodstream this stage is called clonal expansion because the B cells are divided by mitosis and creating clones of themselves these are monoclonal antibodies they're called monoclonal antibodies because the B cells divide by mitosis so they are clones of each other and they only produce one single or mono antibody memory B cells are long lasting and responsible for the secondary immune response they don't produce antibodies that can divide rapidly when they are needed antibodies are an important part in the immune system they are made up from heavy chains the long ones and from light change the shorter ones at the side disulfide Bridges hold the light and heavy chains together and a variable region which will determine what it is an antibody against and there will be two antigen binding sites eco's antibodies are made of more than one polypeptide joined together because they have light and heavy chains they have quaternary structure Androgen binding sites also have specific tertiary structure which is complementary to the antigen antibodies are made by plasma cells which are a type of B cell as part of the human response each antibody has two identical binding sites that are specific to the antigen there is a large amount of variety allowed in this when antibody binds to the antigen a complexes formed the two binding sites means the pathogen can be plumped together leading to the destruction of the pathogen the cramping together means it is easier for phagocytes to find there are two different ways you can acquire immunity to something this can be passive immunity where antibodies are made by a different organism such as when it is passed by breast milk mothers passing antibodies to a baby or if something is given as an anti-venom injection for this protection is immediate however protection is only short term no memory cells are produced and there is no exposure to the pathogen we can also have active immunity where antibodies are made by the immune system this can happen as a result of catching the disease or pathogen or why be given a vaccine one that includes the antigen time is needed for protection to develop memory cells are produced and this provides long-term protection for the individual while vaccinations are important so is herd immunity as it is never possible to vacuole vaccinate 100 of a population a good example of this is newborn babies but if a large selection of the population is immune or vaccinated then it is very unlikely that people who are not vaccinated will get ill as it is very unlikely that they will come into contact with the pathogen in purple we have our susceptible person in blue we have our immune or a vaccinated person and in pink we have our infected person if there are lots of susceptible people surrounded one infected person then lots of people will get sick there are not enough people who are immune or who have been vaccinated to provide a herd immunity however if there are the same number one of infected people but the majority of people around them are either immune or vaccinated then a few people in the population who would still be susceptible to infection are going to be protected because there is no way of directly transmitting to them they are surrounded by a nice little protective bubble of immune or vaccinated people there is little to no pathogen transmission with vaccines there are some ethical issues animals are used in testing and development of vaccines there are some possible side effects human clinical trials are generally needed putting human lives potentially at risk and then there is a decision of who would get vaccinated first and finally should any vaccines be compulsory human immuno deficiency virus and acquired immune deficiency syndrome are more commonly known as HIV and AIDS the HIV virus will have a capsid it will have an envelope around that there are attachment proteins all over the outside and this is an RNA virus and the RNA is in the middle in the center along with it there is reverse transcriptase this virus can make DNA from RNA it is a retrovirus the HIV will attach to the CD4 proteins and will frequently infect T cells the capsid is injected in to the cell and the reverse transcriptase turns the viral RNA into DNA which is inserted in to the cell's own genetic code this means the T cells make more HIV which are then released into the body since T cells are important for immunity and fighting viruses a decrease in their numbers since the host T cells die when they release new viruses means that the body can't put up a defense against pathogens leading to AIDS or required immune deficiency syndrome HIV itself does not cause death it leads to other diseases which cause death there are a wide range of uses for monoclonal antibodies firstly in Elisa tests Eliza stands for enzyme-linked immunosorbent assay these are incredibly useful because they can detect very low concentrations of molecules these sample being tested is on the slide a specific antibody to the sample is added this is a really important step once you've added your antibody to your sample it should bind to any antigens that are present in the sample then you have to wash away that antibody if it's not bound so after adding your antibody you let it bind and then you need to rinse it or we do a wash step to remove any Unbound antibody that means that if there's no antigen present in a sample nothing will happen but if there is antigen present in the sample then the antibody will bind the first antibody and then the second antibody will bind and so on we will get a reaction a second antibody binds to the first antibody the second wash step is also really important so after you've added your second antibody we wash again this is to remove any second antibody in the sample so that then when we add the solution that contains the enzyme it won't react with any Unbound second antibody and give us a false result or a false positive so we need to remove that second antibody if it's not bound and the Unbound second antibody is not bound to the first antibody so that we don't get a result if there is no antigen present an enzyme reaction happens which generally leads to a color change or a result you can see often the intensity of the color change is measured because the darker the color change the more antigen was present in the sample because more antibodies bound and there was a greater concentration of the product formed through the enzyme reaction this is an indirect Elisa you can also get a direct Elisa test which will only use a single antibody and what I call in antibodies are used in these because they are all identical not only are they used in elisas but they're used in diagnostic tests for example in pregnancy tests or in cancer treatment [Music] [Music] thank you [Music] [Music] surface area to volume ratio cells need to move things around from A to B generally across a partially permeable membrane there are certain ways that we can take a short distance here in purple and actually fits quite a lot of membrane on it the more membrane there is the more opportunities there are the things to diffuse across one example would be cells need to take in oxygen and need carbon dioxide removed nutrients need to be moved to the correct location urea needs to be excreted and heat needs to be evenly distributed to ensure that this exchange is as effective as possible the surface area needs to be as large as possible in comparison to the volume smaller organisms have a larger surface area to volume ratio the substance is to move from the outside to the inside of a larger organism this is why large organisms bigger than a single cell or flat worms very very small organisms they need an internal exchange system for things which reduces the distance and increases the rate of diffusion to make sure that all the substances get into all of the cells as fast as possible here we can use cubes as an example we're going to look at a large animal and a small animal this large animal has a surface area of 86 centimeters squared and a volume of 48 centimeters cubed dividing this gives us a surface area to volume ratio of 1.8 a small animal represented by a one Cube will have a surface area of six centimeters squared on that centimeter cubed so the surface area of the volume ratio here is six which is much higher than 1.8 the smaller animal has a larger surface area to volume ratio a few maths hints to take note of here that there are no units for a ratio if the question is talking about cells think sphere and use four pi r squared for a circle it is pi r squared or for a cylinder it is 2 pi r h plus 2 pi r squared all exchange systems have the same three adaptations in common these all help to increase the rate of substance exchange inside organisms they have thin walls to create short diffusion distances they have a large surface area to increase the amount of membrane or Surface that's in contact with the substances that need to be exchanged they have a good blood or Air Supply which we call ventilation to maintain concentration gradients all of these are obviously factors that affect the rate of diffusion and that's really what we're talking about here so some examples are the fact that leaves are thin so there's a short distance between the air and the inside of the leaf we've got the folds of villi in the small intestine which increase surface area and structures like the alveoli which have lots of capillaries around them which is a form of good blood supply which will help maintain the concentration gradient so as we go through this topic and the rest of these slides you'll notice these same features coming up again and again because these are adaptations for gas exchange or digestion and the movement of substances across membranes gas exchange in plants plants need to exchange oxygen carbon dioxide and water and this all needs to be done via bad leaves the balance of photosynthesis and respiration creates concentration gradients so these diffuse into and out of the leaf depending on which is happening at a faster rate transpiration is the evaporation of water vapor from the leaves through the stomata this also moves down its concentration gradient guard cells control the opening and the closing of stomata smarter are generally on the underside of leaves there are internal connecting air spaces that will allow the rapid diffusion of gases this is because they create a large surface area around the edges of the cell membranes that's in contact with the air the opening and closing of stomata controls the rate of diffusion of gases and water gas exchange in xerophytic plants is slightly different these need to control water loss plants can be adapted for hot environments cold or dry environments or very windy environments in all of these loss of water is an issue they could have hairs on the epidermis to trap water a thick or waxy cuticle curved or rolled up leaves the stomata could be in pits or grooves or they could be fewer estimator they can also have a reduced surface area to volume ratio these adaptations reduce transpiration by either reducing the effects of wind such as curving or rolling up the leaves or having your stomata inputs or grooves or they can increase humidity and therefore reduce the water potential gradient which reduces evaporation such as hairs on the epidermis to trap water the other adaptations reduce evaporation opportunities so a thick waxy cuticle is waterproof so no water evaporates and fewer stomata mean there are less holes for water to leave a gas exchange in single-celled organisms because they are very small they will have a large surface area to volume ratio meaning substances can easily diffuse from one place to another so there is no need for a specialized system gas exchange in insects using a grasshopper as an example they have a small series of tubes called tracheals these extend the whole way throughout the insect's body air is brought directly to the tissue allowing for a short diffusion distance gases will move according to that Fusion gradients this is Health by the rhythmic movements of the insect's abdominal muscles to move air in and out gas enters and leaves the system via spiracles on the surface of the insect these open and close via a valve gas exchanging fish skills is something you hopefully looked at in class while I sit in a fish skill might be one of these similar practicals that you do it really helps you to see how the Gill filaments separate out when they're appear in water compared to when they're in the air same three rules apply that we've mentioned a lot already the Gill filaments and having many of them creates a large surface area they have a good blood supply or lots of capillaries which helps to maintain the concentration gradient and they have thin walls which helps to reduce the diffusion distance if we look closely at a single Gill filament we can see there is deoxygenated blood on one half and an oxygenated blood on the other this is a single Gill filament blood will flow in this direction and water will flow in the opposing Direction this counter current system maintains a constant gradient the important thing to note here is that this counter current system maintaining this concentration gradient is what makes sure the diffusion happens across the whole length of the ill filament the respiratory system is where gas exchange in humans takes place we held the alveoli these are tiny little air sacs right at the end of the system they are surrounded by collagen and lined with epithelium we have bronchials these are subdivisions of the bronchi they have wolves made of muscles the bronchi are two subdivisions of the trachea and the trachea this is made from cartilage to protect it the rib cage has a protective function over all this is contained in the lungs the large structure where you'll find all the abiola and bronchioles the diaphragm moves up and down to draw a in and out and all of these work together so if we follow the pathway of air as it moves into the lungs it would follow the nose and the mouth then into the trachea then into the bronchi then into the bronchioles then into the alveoli and then across the alveolar aetherium across the capillary endothelium and then into the blood this is obviously the journey for oxygen and this would be reversed if we were talking about the diffusion and movement of carbon dioxide as it leaves the lungs when we think about the mechanics of breathing we need to compare breathing in with breathing out this can also be referred to you as inspiration and exploration breathing in is an active process that requires energy the external intercostal muscles contract the internal intercostal muscles relax the diaphragm contracts the volume of the lungs increase the pressure within the lungs decreases and subsequently a is forced in conversely breathing out is a passive process the external intercostal muscles relax the internal intercostal muscles contract the diaphragm relaxes the ribs moving it down and inwards direction the volume decreases the pressure within the lungs increases and subsequently a is forced out here we can see the alveolar epithelium this is where gas exchange in the lungs takes place these are tiny air sacs approximately 100 to 300 micrometers in diameter but with a total combined surface area spunning tens of meters squared we have the oviolis cavity the epithelial cells the capillary surrounding it and the air inside oxygen-rich air will move into the lungs to the alveoli down a pressure gradient red blood cells in your penis will slow as they move around the alveoli oxygen will then diffuse down its concentration gradient across two layers of epithelial cells in to the bloodstream red blood cells are flattened against the capillary walls to reduce the distance needed for diffusion carbon dioxide follows the opposite pathway the movement of air in and out of the lungs maintains the concentration gradient we need to think about our three factors that our adaptations to efficient gas exchange for the lungs as well so many alveoli is the reason that we have this large surface area the narrowness of capillaries are the fact that they cause blood vessels to slow down as they move around the alveoli increases the diffusion time the thin walls of both the capillaries and the alveolari which means we only have to go through two layers of epithelial cells one cell layer for each reduces the diffusion distance the constant ventilation of air in and out of the lungs maintains the concentration gradient but also the alveoli having lots of capillaries providing a good blood supply also maintains the concentration gradient lung disease affects a wide number of people the impact of disease on the lungs can be reduced volume it can affect the number of breaths per minute it can affect the change in expiratory volume risk factors for lung disease include smoking your occupation local Air Pollution any infections you've had and your genetic makeup examples of lung disease could be tuberculosis fibrosis asthma or emphysema when I was working in the lab the risk factor that I had was my occupation so every three months we used to have to go and do a test where we breathe as hard as we could and they measured our expiratory volume to check our lungs basically digestion in humans involves a number of organs worth all together we have the tongue the salivary glands the esophagus the stomach that produces enzymes and digests feed the liver the large intestine where water is absorbed the small intestine where food is digested by enzymes and the products of digestion are absorbed this has adaptations on the walls microvilli to increase the surface area and thus the rate of diffusion physically broken up with your teeth or chemically with enzymes so we need to look again our three main adaptations for exchange surfaces and how these adaptations are formed in the small intestine so the first one you can see the tube here and then you can see a zoomed in of a couple villi so these folds inside the Lumen of the small intestine increase the surface area each inside of each villus we have lots of capillaries which again helps us to maintain that concentration gradient if we look at each individual epithelial cell around the edge of that Villi then they have folds on their membrane as well and that's the surface that points into the Lumen of the small intestine and that further increases the surface area these small folds are called microvilli you'll also notice from the diagram that the walls of the Villi only one cell thick again this decreases the diffusion distance as we've previously mentioned with cell adaptations these cells will also be adapted for facility diffusion active and co-transport by having extra proteins in the membrane that faces into the Lumen of the small intestine carbohydrates is one polymer that needs to be digested the monomers the glucose the monosaccharides I held together by a glycosidic bond enzymes can break the glycosidic bond by hydroysis amylase will break down starch into maltose and amylase is produced in the mouth and in the pancreas maltes will break down more toes into outer glucose and this is produced in the ilium or small intestine Secrets will break down sucrose into glucose and fructose and lactase will break down lactose into glucose and galactose larger molecules larger carbohydrates will need more than one type of enzyme to fully break down into the substance sugars and this is one area where spelling and handwriting is going to be vitally important because if the examiner can't tell whether you Vision superas or sucrose you're not going to get the marks lipids or fats also need to be broken down here we have our triglyceride and he is the estebond lipases will hydrolyze the triglycerides into monoglycerides and fatty acids and water liposes are made in the pancreas behind the liver and they work in a small intestine bile salts which are made in the liver and stored in gallbladder emulsify fats increasing the surface area thus increasing the rate of digestion biocytes also help to neutralize the stomach acid this is important as it creates the pH that is needed in the small intestine for those enzymes that work best at those Optimum PHS after digestion has occurred and we have monoglycerides and fatty acids present in the droplets the bile salts form smaller droplets of these mixed and broken down lipids called micelles These are going to help the absorption of these fatty acids and monoglycerides proteins also need to be broken down to be digested here we have a dipeptide made of two amino acids held together by our peptide bond here is a representation of a long polypeptide with the amino acids and the petried bond endopathases increase the number of terminal ends available for the other enzyme that breaks down proteins exopectinases so they create a larger surface area for the exopeptidases to work on the combination of these two enzymes therefore increases the rate of digestion of proteins will hydrolyze Central peptide bonds exopectidases hydrolyzed peptide bonds at the end this creates smaller chains and then single amino acids from the end of the chains and dipectadizes will hydrolyze the peptide bond in a dipeptide these are membrane found these are on the cell surface of the epithelial cells in the small intestine these can be made in the pancreas and in the stomach once products have been broken down they need to be absorbed here we have a close up view of the small intestine the tube going through and then a close-up of the surface area of that tube once the carbohydrates lipids and proteins are broken down they need to be absorbed glucose galactose and amino acids are absorbed through co-transport with sodium ions fructose is absorbed by facilitated diffusion monoglycerides and fatty acids travel to the cell membrane in my cells the micelles breakdown and the monoglycerides and fatty acids diffuse into the ilium cell they then get transported to the endoplasmic reticulum where they recombine to form triglycerides again in the Gogi they then bind to cholesterol and proteins to form something called chylomicrons these enter the bloodstream and also the lymphatic system the lymphatic system is made up of capillary-like structures called lacteals you can see them here kind of underneath in between the capillaries in the Villi we have a closed double circulatory system it is a double circulatory system because the heart will pump to the lungs and the hole pump to the rest of the body the heart the pump is needed due to a low surface area to volume ratio the benefit of having a double pump also helps to increase the pressure and therefore the speed of the delivery of oxygen to all of the cells and tissues not all organisms have this double pump and so their circulation system will be slightly less efficient and a bit slower as well as the blood vessels to and from the heart you need to know that the renal artery and the renal vein are the main blood vessels that serve the kidney and remember the heart has its own coronary arteries that feed the heart muscle whenever you see a heart right right then left on the correct opposite sides just to remind you when that you are labeling things blood will enter through the vena cava and exit to the lungs it will come in from the lungs by pulmonary vein and then exit by the aorta to the rest of the body the path that blood takes I'm going to teach you a little trick to help you remember it so it comes in through the vinegar clavo to the right atrium then down to the right ventricle out to the lungs via the pulmonary artery back to the Heart by the pulmonary vein into the left atrium down to the left ventricle and out to the rest of the body via the aorta now I've written them in like this so you can see the pattern it goes V i v i v i v a if your flow of blood does not follow that for example if you've got two A's next to each other or you've got two v's Next original either you've mislabeled something or you've drawn the path from thought required practical five we are going to be looking at the dissection of an organ within a Max transport system in this case the heart if you want to see all of the Gory details then you can go and watch my heart dissection video but here we're just going to use an image within the heart you should be able to find the aorta the vena cava the pulmonary artery going to the lungs the pulmonary vein coming from the lungs the left ventricle and left atrium as well as the right ventricle and the right atrium notice I've written right and left as the first thing whenever I see a heart's diagram we have deoxygenated blood coming in through the vena cava in to the atrium down to the rental core and then being pumped out by the pulmonary artery to the lungs oxygenated blood will come back from the lungs via the pulmonary vein in to the left atrium down to the left ventricle and then pumped around the rest of the body via the aorta when looking at the heart you will find valves these are very thin but very strong these open and closed do you control the direction of blood flow the walls of The ventricle are much thicker however on the left hand side of the heart they are noticeably thicker than on the right hand side this is because instead of the right hand side just has a pump to the lungs the left hand side has to pump the whole way around to the body so instead of just pumping to the lungs it pumps to the whole body and needs to be a thicker muscle hemoglobin in humans consists of four polypeptide chains this is a protein's quaternary structure they have heme groups which contain in2 ions in and the heel roots are the part that actually combines with oxygen hemoglobin will combine with four oxygen molecules in a reversible reaction oxygen will readily associate with hemoglobin and readily dissociated meaning that hemoglobin can change its affinity for oxygen in a different conditions this is done by changing shape when other substances are present this will happen at gas exchange surfaces for example in the lungs there is a high oxygen concentration and a low carbon dioxide concentration we say this means there is a high partial pressure of oxygen meaning there will be a high affinity for oxygen and oxygen will load at respiring tissue in the body there will be a low oxygen concentration a high carbon dioxide concentration this means there is a low partial pressure of oxygen there will be a low affinity and oxygen will dissociate you need to be able to interpret and sketch oxidant Association curves at point a on this curve it is very hard for the first oxygen molecule to bind so at low oxygen concentrations they read little oxygen will actually bind for example this could be within respiring tissues at point B after the first oxygen binds the shape of the quaternary structure changes making it easier for subsequent oxygens to bind or we can see this as it is only a small increase in partial pressure whereas a steeper radian happens at this part of the graph there is positive cooperation at Point C after the third oxygen molecule binds it is harder to bind the fourth and the last oxygen to talk about with this graph is the bore effect so the concentration of carbon dioxide can also affect the loading of oxygen onto hemoglobin a low partial pressure of carbon dioxide for example in the lungs the Affinity of hemoglobin is increased within the lungs there is a high concentration of oxygen so oxygen is readily loaded onto hemoglobin where there is a high partial pressure of carbon dioxide for example in muscles or spiraling tissue the Affinity of hemoglobin for oxygen is lowered this could be in the muscles so oxygen easily dissociates and goes to where it's needed when affinity for hemoglobin is lower we say the graph is shifted to the right this is why this is sometimes known as the bore shift and sometimes you'll be asked to explain this difference and the word you need to use here is by saying that at the same partial pressure of oxygen there is a lower Affinity of hemoglobin which means that there is less or a lower percentage saturation of hemoglobin with oxygen because more oxygen is dissociated from the hemoglobin hemoglobin isn't the same in all animals I have a little bit of a soft spot for Horseshoe craps because when I worked in America for a few Summers it was in a lab that kept horseshoe cracks and you have your gas tab you'd have your water tap and you would have your salt water tap all the horseshoe crabs anyway the reason they are so interesting in science is because they have Blue Bloods because they use copper instead of iron in their hemoglobin so differences in genetic code can lead to differences in quit ternary structure of hemoglobin thus different animals will have differences in oxygen affinity this is one example of adaptation to an environment there can be variances based on size smaller animals will have a higher surface area to volume ratio thus they lose heat quickly so we'll have a high oxygen affinity this is because they have a higher metabolic rate in order to keep warm if an animal lives in a low oxygen environment it needs hemoglobin with a high oxygen affinity if an animal has high activity levels it needs to be able to quickly dissociate oxygen so the hemoglobin is a lower oxygen affinity you need to be able to recognize the differences in these graphs when we have these different hemoglobins or different environments so I always try and use this way to remember it so low oxygen environment will mean a left shift on the graph so from the normal dissociation curve we have a left shift because we've got low O2 concentration the example of this that is one of the most common is fetal hemoglobin so fetal hemoglobin has a higher affinity for oxygen which it needs to because otherwise at the same partial pressure of oxygen the oxygen would not dissociate from the mother's hemoglobin and associate with the fetal hemoglobin so it needs to have a higher Affinity than adult hemoglobin because otherwise oxygen would not transfer from the mother's blood to the fetus's blood in the placenta as we said this was a low oxygen environment so a left shift so the other example is animals that live either at high altitude so up in the mountains where there is a low partial pressure of oxygen or in a low oxygen environment such as in sand for example where they aren't getting a lot of ventilation or flow of air or water this again ensures there's enough oxygen that's going to bind their hemoglobin even at low concentrations of oxygen to make sure they get enough to survive the opposite graft shift is when the graph shifts to the run so we can remember this by saying right shift means High respiration so high respiration right shift it ensures that when there's more respiration occurring so there's going to be a high carbon dioxide concentration more oxygen will be released to help maintain High metabolic rates so this is the example like we said for small organisms that have a high metabolic rate they'll be doing more respiration and so they will need more oxygen to dissociate even at low partial pressures of oxygen there are distinct parts to the cardiac cycle in diastole the heart relaxes blood will enter the heart via the pulmonary vein and vena cava as the Atria fill up there is an increase in pressure when atrial pressure is higher than ventricular pressure the valves open and blood begins to flow from the Atria to the ventricles in systal contraction of the atrial walls moves the rest of the blood down towards the ventricles after the ventricles have filled up the walls will contract ventricular pressure increases and the atrioventricular vowels close this further increases the pressure and blood is forced into the aorta and pulmonary artery the aortic pressure Rises as blood is forced in and then Falls as the blood leaves ventricular pressure is low at first and then Rises this Rises quickly after the valves close then Falls as blood is forced into the aorta and pulmonary artery atrial pressure is always low ish as the walls are very thin and this drops when the valves open ventricular volume increases as the Atria contracts and they fill with blood it then drops as the blood moves to the aorta and pulmonary artery we can look at cardiac output as a calculation of stroke volume multiplied by heart rate there are three main types of blood vessels that you need to know about arteries carry blood away from the heart arterials are smaller arteries these help the blood vessels to contract which can control the flow of blood and also help to withstand the high pressure walls a thick elastic layer the elastic layer helps the blood vessels to stretch and recoil which allows them to maintain blood pressure which is needed to keep the blood pressure high and they have no bounds veins carry blood towards the heart they have thin muscular and elastic walls the elastic muscle layers are thinner in veins because pressure is reduced bounce at regular intervals to stop the blood flowing backwards and capillaries these carry blood to the organs and they allow exchange to take place they are one layer of cells thick the one layer of cell thick walls creates a short diffusion distance for substances they are highly branched and very narrow to allow for the rapid diffusion of gases nutrients and ions into and out of the bloodstream being highly branched slows down the blood flow as well as being narrow allowing for greater time to be given for diffusion a capillary blades we need to be able to explain how tissue fluid is formed at the arterial and high hydrostatic pressure is caused by ventricular contraction this forces out plasma and dissolved substances through the walls of the capillary large plasma proteins and red blood cells stay behind in the capillary because they are too big to pass through the walls this reduces the water potential of blood and because we've lost liquid or fluid we also have decreased the volume of blood this means at the venule end of the capillary water potential is higher which creates a higher osmotic pressure than the hydrostatic pressure because we've lost volume and therefore lower hydrostatic pressure this High osmotic pressure forces water to return to the blood by osmosis from the tissue fluid any excess fluid that does not return to the capillary is drained into the lymphatic system through lacteals or lymphatic capillaries cardiovascular disease affects a wide number of people atheroma is a buildup of fatty material under the epithelium resulting in reducing capacity of the lumen making it harder for blood to pass through most cardiovascular diseases are the result of atheromas first example is aneurysms is a buildup of blood behind a blockage which can be caused by an atheroma it weakens the artery wall and it can burst due to the pressure these are often fatal thrombosis a blood clot forms due to an atheroma coming or bursting through the endothelial vessel and causing a rough surface to be created then a blood clot forms around and on this rough surface and it can cause a complete blockage of the vessel angina and atheroma can form in the coronary arteries which reduces blood flow and oxygen transport to the heart anaerobic respiration in the heart then causes pain and breathlessness a myocardial infarction this is just a fancy name for a heart attack and obviously that is when there is a complete blockage in the coronary arteries so angina is just reduction of blood flow whereas a heart attack is caused when no blood flow and no oxygen can reach the heart muscle and therefore the heart stops beating strike a strike is caused by an atheroma or blood clot or bleeding which could be caused by something like an aneurysm it leads to reduced blood flow to the brain this can be mild or it can be severe depending on the vessel and depending on the part of the brain and depending on where the stroke occurs and how fast treatment is given there can be different outcomes in terms of symptoms you need to understand the risk factors that can increase someone's chance of having cardiovascular disease lifestyle based risk factors include a diet that's high in saturated fat and salt being overweight or obese and having extremely high alcohol intake the first one in the diet is a risk factor because it increases the cholesterol in the blood which increases the amount of fat in the blood and the other three are a risk factor because they increase blood pressure an increased cholesterol and increased or raised blood pressure both contribute to being a risk factor for cardiovascular disease because they both increase the chance of forming atheromas there are other uncontrollable risk factors which are not able to be controlled by the person due to their lifestyle and these include genetics age gender ethnicity and other disorders such as type 1 diabetes these are factors certain parts of these are factors that can increase your risk factor for cardiovascular disease but they are outside of your control water will move around the plants via the xylem water will enter plants Violet roots and needs to move around the plant to where it is needed evaporation of water from the leaves creates a force that pulls water up via the xylem this is a passive process hydrogen bonds between water molecules ensure cohesion and thus a continuous flow of water across the mesophyll cells and the xylem transformation pool means the xylem is under pressure if this is broken an air enters the xylem then this pool is also broken the way water moves through the xylem in a plant is known as the cohesion tension Theory cohesion because of the cohesion between water molecules which creates this unbroken column of water and tension which is the force that's applied to this unbroken column of water that's created by the water potential gradient as water is being lost from the leaves it needs to be replaced you need to be able to explain the factors that can affect the rate of transpiration increasing light intensity increases transferation rate this is because more stomats are open due to more photosynthesis occurring at higher light intensities increasing temperature also increases transpiration rate this is because water particles will have more kinetic energy so it is easier for them to evaporate increasing wind or air movement also increases transpiration rate this is because the water particles are being blown away from somata and they reduce the water potential gradient between the inside of the leaf and the outside air increasing humidity decreases transpiration rate this is because it reduces the water potential gradient because water vapor will be in higher concentration in air around the stomata so the difference between the inside of the leaf and the outside of the leaf is reduced we can measure transpiration how well the xylem is working with a potometer an air bubble is introduced and we can follow that movement and measure the movement of the air bubble the stem of the plant needs to be cut underwater so that we don't introduce any air bubbles and the mean volume of water loss can be calculated a few variables you could change in this experiment are humidity temperature light intensity and air movement or wind remember this experiment is only an estimate of transpiration rate because it is assuming that all water taken up by the shoot is being transpired the phloem is responsible for the transportation of inorganic ions from the roots and sugars produced by photosynthesis to wherever they are needed we say the flow is from source to sink the best theory we have for this at the moment is the mass flow Theory sucrose is actively loaded into Civ tube elements this creates a low water potential in phloem at the source and causes water to move in by osmosis from the xylem this increase in volume creates high hydrostatic pressure mass flow of solids then occurs down the pressure gradient to six where sucrose is being used up this is a very brief summary of the mass flow Theory remember if you want more detail go to the topic video there is some evidence for this safe Chiefs are under pressure there is a concentration gradient another piece of evidence is that ATP is needed for the active loading of sucrose into the sub tube elements if ATP production is stopped or respiration is inhibited then mass flow also stops another final piece of evidence is that mass flow increases in daylight especially from the leaves down the phloem and this is clearly due to more photosynthesis producing more sucrose in the leaves and creating that pressure gradient and there is some evidence against this not all solutes move at the same rate and a sieve by its structure would appear to be a barrier to movement [Music] [Music] foreign [Music] [Music] there are a number of different locations within a cell where DNA can be found in prokaryotic cells DNA is short and circular and it is not associated with any proteins in the eukaryotic cells DNA is linear and long and it is associated with histone proteins these make chromosomes mitochondria and chloroplasts also have their own DNA this is short and circular and not associated with any proteins similar to that in prokaryotic cells within DNA we have coding and non-coding DNA this slide is going to be basically a summary of the keywords that are needed please make sure you can use them all properly to show The Examiner you really know what you're talking about a gene is a section of DNA that codes for a polypeptide chain or functional RNA the locus is that position of Gene within the DNA an allele is different versions of the same gene introns are bits of a gene that don't code for anything and exons are bits of the gene that do code something homologous chromosomes are matching pairs that contain might contain different alleles a triplet is a three base pairs that code for an amino acid DNA has a degenerate code so more than one triplet can code for an amino acid the code is non-overlapping so each base pair is only read once The genome is all of the genes in a cell whereas the proteome are all the proteins that a cell can make there are lots of words here so what I've done is I've written you a glossary you can see this is massive at 223 Pages I've written this because it is so important that you have and can use accurate definitions for these key words some of these definitions I've written for you are really long and make perfect three or four Mark exam answers but unless you use the language needed for a level biology properly The Examiner will never know that you know what you're talking about so the language you use a new use of keywords is vitally vitally important in a level biology this is a short slide and transcription mRNA please remember this is just a revision video so if you want more details on the full process then the teaching videos where this is going to be doing a lot more detail is the place to go now messenger RNA is a single polynucleotide chain smaller than DNA but larger than TRNA Helicon shape and manufactured in nucleus during transcription but found throughout the cell here in blue we have we had DNA background and in pink or RNA strand the big green blob is our RNA polymerase all the bases will be color coded so green is going to be a diamond is blue Euros is Pink cytosine is purple and for League one in is black already polymerase works on a section of DNA of the DNA helicase has separated the strands nucleotides free in the nucleus pair with their complementary base on the template strand and the RNA polymerase moves along forming the phosphodiester bonds that connect the nucleotides forming the pre-mrna only a small section of DNA is exposed at any time afterwards it coils back into a double helix when it reaches a stop signal the RNA polymerase falls off and the pre-mrna can exit via nucleopause splicing will occur in eukaryotes to remove introns creating the MRNA translation and TRNA is another slide where you're going to see my poor animating skills if you want more details or confused about this then the longer teaching video is the place to go here we have our mRNA and our pool of tea organize translation occurs in the cytoplasm ribosomes attach to the MRNA chain and the TRNA is being complementary amino acids the ribosome moves along the MRNA collecting more tRNA molecules the first two amino acids are joined by a peptide bond this is an active process that requires ATP the ribosome can then move along to the next triplet the third TRNA joins and a peptide bond between the second and the third amino acid is formed again the ribosome will move along calling another TRNA and another amino acid is joined by peptide bond to the chain until we have a long amino acid chain formed 15 amino acids each second can be connected together and there can be a large number of ribosomes acting on the same mRNA strand at once meaning a lot of identical polypeptide chains can be produced very quickly from the same mRNA strand this whole process stops when a stop codon is reached any change in the DNA base sequence is a mutation if it happens in genes it is a gene mutation these mutations can arrive spontaneously or because of mutagens such as infrared radiation if they occur in the germline they can be passed On to the Next Generation one example is base substitutions here we have a sequence and the three amino acids that it codes for in this second sequence you will notice that one of each of the bases in the DNA has been substituted with something else but because the genetic code is degenerative these substitutions have not changed the amino acid that is being coded for we often say these are silent mutations because they have no effects so they go unnoticed another trip is a base deletion here we have our DNA and the proteins that it codes for deletions will always cause mutations in the polypeptide chain as they change the reading frame here A T is being deleted this inserts a stop codon and stops the protein early meaning that it might not work or it might not function be produced at all and we have chromosome mutations that occur during my excess these can lead to polyploidally commonly apparent implants where three or more complete sets of chromosomes are used or non-destruction where we have one more or one fewer chromosome for example in Down syndrome there are three copies of chromosome 21 and in Edward syndrome there were three copies of chromosome 18. it is important you are very clear between the differences in meiosis and the differences in mitosis here is my sneaky little way of remembering mitosis has a t in it so it will produce two identical daughter cells meiosis will produce four not identical daughter cells these are your gametes this is one topic where you're spilling and your handwriting is very important if the examiner cannot tell what you've written down myosis or my choices these can be really hard for them to give you the marks so make sure you can spell these words and your handwriting is clear meiosis is two nuclear divisions one are said the other leading to happy weight cells these gametes can then fuse together to produce viable offspring crossing over an independent segregation are two ways that meiosis increases genetic variation the stages in yss are very similar to that in mitosis in that we'll have metaphase and anaphase and telophase the DNA is duplicated so the chromosomes get copied to become chromatids they will arrange themselves in the homologous pairs we will get crossing over the chromatids will line up and are pulled to the opposite sides of the cell the cell will divide and the new cell membrane will form and cytoplasm is divided this is Moises one followed unsurprisingly by my ex is two the two daughter cells will start the process over division again they will line up just as before but this time the chromosomes are separated with each arm being pulled in a different direction here each daughter cell will be haploid and will not be identical this is the second Vision in meiosis during lysis one we will have crossing over this leads to an increased in genetic variation homologous chromosomes line up and then we'll twist around each other part of it will break and then we'll rejoin the other chromatid the point where the chromosomes join and break is known as the chiasma leading to a mixture of maternal and paternal genes being in the same place another way to increase the genetic variation is independent segregation homologous pairs are lined up at random so a mixture of paternal and maternal chromosomes will end up in the daughter cells subsequently there are a large number of different combinations of the chromosomes within water cells we can determine this by using 2 to the power of N squared n being the number of pairs of homologous chromosomes now this calculation doesn't truly reflect the genetic variety is an undressed race it doesn't take into account the crossing over that cats causes a variation causes of variation can be genetic these include mutations meiosis and we've looked at independent segregation and crossing over and the random fertilization of gametes the causes of variation can also be Environmental these can include large or rapid climactic changes the availability of food or water if you are an animal or the intensity of light availability of water or soil nutrients if you are a plant environmental changes and causes of variation make sense because if organisms get different amounts of nutrients or water they're going to grow and develop differently so this is what causes those types of variation the theory of evolution and natural selection explains why we have so many different types of pets pets and other things within any population there will be a range of alleles not all of the alleles or individuals have the same chance of reproduction or passing them by alleles to the Next Generation random mutations means that some individuals are more likely to survive in that environment and thus more likely to reproduce and pass on that genes those alleles that have provided an advantage are more likely to be passed on over time this advantageous allele will become the most frequent one in the population and other alleles will die out these advantages can be behavioral physiological or anatomical genetic diversity is all about the number of different alleles for something that is in the population for example if we look at our adorable furry little friends down at the bottom here the allele for coat length will vary for the color for the length of the coat we can get short head cats or long-haired cats it will vary by the texture of these all code for the coat having a range of domestic University in a population means they're able to adapt to sudden changes in the environment it will prevent the whole population being wiped out by a single event genetic diversity can be reduced if there is a genetic bottleneck when a large number of population die and there are only a few alleles left it can also be small due to the founder effect where a small number of the population split off to become a separate population or a separate group or species they would only take a small number of alleles with them restricting the genetic diversity there are two different types of selection we are going to look at directional selection and stabilizing selection directional selection is where it takes an extreme adaptation to survive this is generally due to a sudden change in the environment for example bacteria that reproduce after an antibiotic has been applied here we have a graph and we can see that there's a low influences characteristic or high incidence of this characteristic and the number of individuals so if we are thinking about the ability to reproduce after antibiotic use these individuals will be highly likely and these individuals will be very unlikely in the original population you can see we've got a bell curve with a mean at the middle after the sudden change in the environment only these ones here were able to reproduce so you can see The Offspring is shifted shows there being a high prevalence of that characteristic in the population only the individuals that can survive the new extreme environments can survive to reproduce the populations normal distribution curve and the mean are shifted to the right in this case stabilizing selection tends towards the middle of the range this will generally occur during periods without sudden changes in the environment birth weight of babies is one nice example of this here we have our bar charts with very tiny babies over here and over this end we are going to have our very large babies you can see that the majority babies are clustered around the middle if we compare that to a percentage of infant mortality in the first four weeks you will see that very tiny babies are less likely to survive this may be because the very tiny babies or the premature babies on the other side of the graph very large babies are also less likely to Vibe than those born in the middle of the range this could be due to complications during birth and those complications will cause the death of them he is me when I was pregnant there is my very large baby in there because all of my babies all two of them will right over this end of the graph antibiotic resistance is one easy to look at example of natural selection or Evolution because it happens very quickly we can investigate this in the lab if we put a law of bacteria on a plate or technicians might have done this bit for you already but antibiotic discs onto the plate leave it to grow for a few days and then we can measure the clear zones always good to measure it in two different places and work out the average of this the closer that the bacteria can grow to the antibiotic disc the more resistant they are to that particular antibiotic anti-fungal or antiseptic that you've put on there there are lots of reasons that antibiotic resistance develops and is developing quicker these days this could be the overuse of antibiotics for example putting into animal feed this could be the inappropriate use of antibiotics for example giving out antibiotics when timid has a viral infection or it could be due to the incorrect use of antibiotics if you have a cause of antibiotics but when you feel better you stop taking that antibiotics that will allow the small number of anti-bacteria that are resistant to the antibiotics to continue to grow the increasing prevalence of antibiotic resistance is leading to a big problem the world as a whole is running out of antibiotics that actually work meaning that in a few years time the leading cause of death in the world may be due to a simple bacterial infection there needs to be a large investment into researching new antibiotics and developing new antibiotics however this is expensive for one of your required practicals you need to be comparing the effects of different antimicrobial substances on the growth of bacteria on a lawn plate there are a few things you need to pay attention when you do this because if you don't do this practical carefully it will show up in your end results work as closely as possible to the flame here I have the little ethanol burner you might have a Bunsen burner or a little camping stove in school this will prevent any cross-contamination getting onto your plate and growing you need to incubate your plates for a few days and then you need to measure the zone of inhibition or the clear Zone around each of your discs it is best to measure this in two different places as the clear zone is unlikely to be a perfect circle you can then work out an average of these two different things and remember it is important to know whether you are measuring the radius or the diameter we can then use pi r squared to find the area of the circle or the area of the zone of inhibition this is a semi quantitative experiment because you're just going to get the area we can see that this one has a bigger area or this one has a smaller area compared to something else we can also look at measuring the effects of antimicrobial substances on the growth of bacterial populations in broth culture this is a quantitative experiment again you are going to need to work as close to the flame as possible flaming everything when you open it flaming your Loop to make sure you do not cross contaminate things to make sure the bacteria from the air doesn't get in to your cultures once you have your cultures set up leave them to grow for a few days you can also spread them on a plate you can have dilutions and then you can actually count the number of colonies alternatively you can use a calorimeter and this will give you the percentage absorbance so you can tell how cloudy the broth culture has gone and because of these two things this is a quantitative experiment the definition of a species is a group of similar organisms that can breed together to produce fertile offspring for example here we have a lion and a tire these can reproduce to create what is called a liger however a liger isn't an individual species because these are generally not fertile classification and taxonomy can seem like a little bit of a mouthful if you've never done any Latin I have never done in Latin so please excuse my horrific pronunciation phylogenetic trees such as this one can show how closely related things are for example we can see that animals on slime molds are actually much more closely related than animals and green filamentous bacteria however you would think that slow molds and filamentous bacteria would be much more place related based on how they look there are Branch points every so often where a new species or new section branches off from the rest of them and if we measure these in an accurate diagram we can see a time scale when reading or interpreting phylogenetic trees organisms that share a branch will be more closely related to each other and the point at which which branches separate or the branch points that is the last point where two organisms had a shared common ancestor taxonomy is biological classification he is one of my favorite animals again the Horseshoe crowd when it was named it was called a crab however it is more closely related to spiders you need to be able to remember the order of properly namely things we start with the domain and then the kingdom the phylum class order family and the genus finally the species if we compare horseshoe crabs and humans we can see that they are both in the domain of eukaryotes they are both in the Kingdom of animals see I'm not even going to try and pronounce the Latin you just need to know how to understand what it is but we start to see differences when we get down to phylum and class we generally refer to ourselves as Homo sapiens this is the binomial system it is much less of a mouthful when you are writing this in the exam remember to have a capital letter for your Genius if you are reading this then the binomial system will be written in italics classification and taxonomy creates a hierarchical system of organisms based on shared characteristics a hierarchy is a series of large groups split into smaller groups with no overlap between those groups so that means you can't be in more than one of these groups at once so for example the large groups here like the domain and the kingdom and as we go down and further down the taxonomic list we get into smaller and smaller groups the no overlap between groups means that organisms cannot be in more than one group at once what's useful about the system is that more closely related organisms share the same groups so you can look at taxonomy of an organism and work out what is most closely related to by working out how many groups it shares with another organism As you move further down the groups there's fewer organisms in each group but they become more related to each other so in a various family there will be a smaller number of species or organisms than in Kingdom but all the ones that share the same family group will be closely related to each other let's have a look at our horseshoe crabs again and this time I've put the taxonomy next to them for spiders so you can see that they share that first four groups and then they split at the order whether in separate orders this would be their Branch point on a phylogenetic tree because they would have separated from each other and now be in different groups but the more groups that an organism shares with another organism the more related they are so this is why taxonomic hierarchies like this are useful there are a number of different ways that scientists can discover illuminously relationship one that has always been very easy to observe before modern technology allowed us to experiment a bit more was courtship of behavior this also allows animals to easily recognize members of the same species for example a peacock a male peacock is very very easily to recognize a female peacock which is a p hen is going to be very attractive to these feathers whereas a female duck is not going to be very attracted to these feathers able to classify these to say that these have an evolutionary relationship however modern genetics allows us to go further we can compare the DNA or the rna-based sequence we can compare the amino acid sequence you can look at Immunology which is where we see if they have similar proteins because they should bind to similar antibodies from other organisms all of these including courtship Behavior we can look at and the more similar the genomes or the amino acids or the Immunology or the courtship Behavior the more closely related the organism here is my favorite again the horseshoe crab it doesn't look very much like a horseshoe and honestly it doesn't look very much like a cramp either if we think about it a little bit the horseshoe crab has blue blood it has 10 legs it has an armored skeleton so a bit like a crab and it breathes with gills so again I can see why they initially thought it was a crab now it's fossils of this are 450 million years old so we can see that the branching Point came a very very long time ago however in 2019 it was approved using genetics that the horseshoe crab is actually a member of the arachnid family it is more closely related to spiders than it is to crabs biodiversity within a community is going to be the populations of all of the species in the habitat and the variety of living organisms the number of different species can be referred to as species richness genetic diversity is the range of annuals within all of the different habitats around so if we look at this example here we can see we've got a number of different species of fish we've got fish species richness we're also going to have invertebrates in here and plant life there is going to be a range of alleles among the to our previous which I don't know the actual name for and then there are lots of different types of coal lots of different habitats all of them species richness can be used to measure for example the biodiversity of the fish in this Coraline so our species richness would just be four because I can see four different species of fish black orange stripy and green this doesn't take into account the number of different individuals of each species of fish there are because for my black fish and my green fish there's only a couple whereas there are loads of orange and stripy fish so this is actually a poor measure of biodiversity on its own we need a better measure of biodiversity which takes into account the number of individuals of each species as well having a high biodiversity in an ecosystem is really important because it creates a stable ecosystem these are more likely to be able to adapt to changing environments because there's greater variation within the populations if we want to give an actual number to diversity we can make a calculation of index of diversity this is the equation that we need to practice using when we are calculating the index of diversity lowercase D is our index of diversity we have the sum of capital N being the total number of all organisms of all species and lowercase a being the total number of organisms of our single species the higher the index of diversity the more diverse an area is if a single species is dominant in that area then the index of diversity the D will be lower human impact impact there are three main ways that humans can reduce biodiversity by reducing the number of food sources this happens when animals or plants are removed from a habitat when habitats are moved or destroyed which reduces shelter and food sources so this is like when hedgerows are removed for example those are those first two points involve the removal of species so actually digging up or cutting down trees or plants or removing animals for some reason by hunting killing them the last point is then the impact of that so the removal of habitats and food sources also causes the death or migration of other species in the habitat so either organisms die because they don't have enough food or they don't have enough shelter or they migrate they move away from the area so all three of these produce biodiversity because they've reduced the number of different species in a habitat what are the main activities that actually cause these reductions in biodiversity the main ones are deforestation removal of hedgerows pesticides and herbicide use which obviously kill plants and animals and then monoculture farming conservation we need to be able to explain why it's really important to conserve biodiversity and also ways that we can do that conserving or maintaining biodiversity should be done to prevent Extinction of organisms we have a moral duty to make sure that species are able to survive and be around for future Generations there are many species that guide us with food medicines textiles and building resources and some of these we may not even have discovered yet so it's really important that we keep our plant species in particular around so that we can have these resources for the future and pollinators not just bees other insects and animals as well are really essential for pollinating our crops and our as part of the food chain so we need them to stay around so that we can continue to grow our food conservation schemes and practices that can help to improve or conserve biodiversity such as legal protection for endangered species to prevent them from being hunted protecting areas of land particularly ones that have high biodiversity that we'd like to conserve and and not reduce but also places where endangered species might live to make sure that farming or building does not take place on that land rewilding or replanting encouraging the growth of native species if trees or hedgerows have been removed replanting them allowing areas to re-wild and be Wildflower Meadows to increase plant species diversity especially around agricultural land modern farming techniques can reduce biodiversity and there needs to be a balance between conservation and farming here we have a picture of what could be considered a very traditional Farm in the British Countryside we can see there are lots of different types of crops going on I'm not a farmer I could tell that because they're different colors some of it is crops and I believe these little white blocks down here are sheep so we've got a mixture of different types of farming going on as well in between all of these we can see hedgerows which are fabulous habitats for insect and bird life and there are lots and lots of trees where again birds and insects and potentially deer and other small mammals live in contrast this here we have a different type of foam this only has one crop in it and these probably all came from seeds that are identical so these are basically clones of each other there are no hydros there's no different crops there's no animals in there this is a very very different habitat there is a lot less diversity because there's a lot less animal and plant species here finally here is a picture of the Amazon rainforest or at least this bit over here is the Amazon rainforest and this bit here the trees have been cut down to plant a single crop field of soybeans now the Amazon rainforest is a massive unexplored area of wide-ranging biodiversity it is important that we have these massive areas of biodiversity for discovering new medicines as an example and keeping this diversity of species alive in there there are animals in there that we haven't even discovered yet however if all of that animals and rainforest is cut down the plant's single crop Fields like this soybean then we have lost all of that biodiversity when we are looking at investigating the genetic diversity within and between species there are a number of ways we can measure this but it could be measured by observable characteristics such as Peak shape these are influenced by a wide range of characteristics but they can also be influenced by the environment for example someone's weight we can measure it by the base sequence of DNA all of RNA and improvements in technology are allowing us to do this more and for us to be able to compare sequences alternatively we could look at the amino acid sequence different DNA sequences can code for the same amino acid sequence and this could potentially be an advantageous mutation closely related species will have similar DNA sequences it is likely that you will need to do some quantitative work with diversity random sampling is an important technique it would be impossible for us to measure the whole population so we look at a small sample and estimate to find the final value it's important we avoid sampling bias so it must be random areas or samples that are taken for example here is a picture of a beach say we wanted to investigate variation in things on the beach if we took these three samples here we wouldn't actually get the impression there were any umbrellas on the beach just a little space increasing the number of samples and making it more random will give us the impression a better impression of the total value however one way you can ensure that you're looking at random areas is by drawing grid lines over your example and then using a dice or pulling numbers and letters out of a hat to ensure that you do get a truly random sampling going on as well as making sure any samples we take are random to remove bias we also need to make sure our sample is large enough to ensure it's representative of the whole population which we're going to be estimating the larger your samples so for example the more quadrats you place down or the more areas in the grid you sample then you're reducing the probability that any patterns that you're going to find are due to chance we can do quantitative investigations of variation here we have a normal distribution with the mean shown by the dotted line in the middle the main is the sum of all samples divided by the number of samples the mode is the most common number and the median is the number in the middle in an ordered set of values standard deviation is how far away from the mean that something is so if we have a small standard deviation there is not a large variation but if we have a large standard deviation then there is a lot of variety there are two ways that standard deviation can be shown or represented to you in the exam it could either be in a table format as numbers or they could be as error bars on a graph so here we have three woodlands and there's that index of diversity values plus their standard deviations in the table they're represented as plus or minus the number which is the distance from the mean and then the error bars that plus or minus is above and below the mean which is the top of the bar the reason standard deviations are important in these questions in the exam is because they're a good indicator as to whether there is a difference or not between the means of these different groups so if standard deviations overlap then it's a good indicator that there is no significant difference because it means that the range either side of them means overlap which suggests that their mean itself is not significantly different from each other so in our graph here we've clearly got an overlap between a and b and A and C but potentially no overlap between B and C the standard deviations cannot actually prove or tell you if there is a difference between your groups the only way you can do that is through a statistical test so there are three tests we have to know and we have to know when you would use them so chi-squared test is used for categoric data so non-continuous data when you've got things in groups the t-test is used when you're testing the difference between two means a correlation coefficient such as spearman's rank is used when you're checking for a relationship between two variables this data is normally plotted as a scatter plot in any of these statistical tests you're looking for this magical number which is when the p-value is less than 0.05 this is like the golden number in science because it means that we do have some significant difference between our results which is normally what we are hoping for the way we would describe a p-value being less than 0.05 and what that means in the exam is we have to use very specific language so this phrase if the p-value is less than 0.05 this means there is a less than five percent probability that the difference or relationship is due to chance so that suggests that whatever the pattern we've seen is clearly being caused by whatever we were changing in our experiment [Music] [Music] [Music] all right foreign [Music] so different solvents will pick up and dissolve different molecules in different amounts they're Affinity to the stationary phases so how well the interact will bind to the stationary phase if they're really strongly interacting with it they won't move as far and their Maps so this one of the molecules are the further they'll travel this is less important but it partly something you should know as a way that we can separate molecules by their mass as well so each photosynthetic pigment in this case will have a specific RF value when run under those conditions so these can be compared to their known RF values and database to try and identify the pigment however as I said it's under those certain conditions that that RF value is produced so more than one substance can have the same RF value for a particular solvent and whether you use chromatography paper or thin layer Crematory or whatever the stationary phase was so the different mix of solvents and the different stationary phase can have an effect on the RF value okay so we're gonna have a look at trying to analyze our results now and calculating the rf30 now as you can see from the picture my results were a little bit of as much so this can be due to multiple things it can be due to having too much concentration on the spot using the wrong running solvent a lot of solvents actually take into account different chemicals in the pigments that can actually interfere with the chromatography and you sometimes need a mixed solvent to be able to get a really good achieved separation and so that is what I've got here this is one that I did on a thin layer cremator cookie plate using spinach again so it's the same same plant and so I've measured my solvent distance which is 36 millimeters so now I can start calculating the RF values but all of those really nice separate distinct points and then we can use their colors as well as their position and their RF value to try and work out what pigments we've got separated in these leaves so that was measured the distance from the bank sign to the middle of the spot was five millimeters so using our formula 5 divided by 36 millimeters which was the distance that the solvent has traveled gives us an RF value of 0.14 okay so now I've got all my RF values I can start trying to identify the spots the nice big bright yellow spot right at the top the six dots clearly going to be a carotene because it's yellow and orange bright a bright yellow deep yellow and it's right at the top and it's a 0.9 RF value which fits right in the fear fighting is quite easy to spot because it's great and there aren't any other gray spots that it would be responsible for that even if the iron value isn't exactly the same then we've got chlorophyll a normally comes before chlorophy if we're going kind of down from the top and we've got the blue green and you can see that we've got a blue green spot and then we've got like a sort of a bright light green spot so we've got two greens sort of close to each other and we've got that blue green so I think that blue greens most likely would be chlorophyll a and then obviously Chlorophyll B underneath and it could be a couple of chlorophylls that are more than just the two chlorophylls as well so there can be some other chlorophylls in there now I'd say we probably don't really have any anthocyanins at all because there's no purple but we'll look at what that looks like in a second when I show you my chromatogram that I got from my purple leaves that feels we could have some examples that yellow green very very early kind of yellowy brownie spot we could have down 0.14 and 0.15 has been shown to be an rf3s bear in mind obviously we can't necessarily use these armor values and directly match them up these three different columns are all from RF values that were done with completely different running solvents in completely different conditions they will never be exactly the same unless you run it in exactly the same way okay so I said the windows xantha feels present on that chromatic arm we just measured but there were some present online so you can see where I had my purple leaves I've got very very clear purple runs that have gone up and you can see how they've started to separate and then they're going to Green so there's two interesting things here is that we can see what anthocyanins look like on a chromatogram and we can see that they're there and they do sort of separate out quite early on down the bottom which is as expected and also we can see the difference between the two running solvents so one very clearly separated out this green and the purple has two sections whereas the other one there was only a little bit of green here it clearly traveled a lot slower and it wasn't necessarily going to spread it out as far but it's also very nice to show that those very purple purple leaves did have obviously chlorophylls present because that what gives us the green colors and obviously it has to have those because it will have to have those in its four plus to be absorbing the wavelengths of white that we need for photosynthesis and most of those other colored pigments sort of the purples the reds are those accessory pigments that can help to get extra wavelengths first of all let's look at parts of the chloroplasts and their functions and what happens there so the stroma is fluid inside is where the light independent reactions happen it means it will contain enzymes including ATP synthase and obviously also rubisco and it will be the place where proteins lipids and starch are all stored inside the chloroplus and you can see I've got some starch grains and a lipid droplet labeled here okay so then we have our double membranes we have our inner and our outer membrane chloroplast a double membrane and then one of the double membrane organelles along with the mitochondria and the nucleus so the inner and the outer membrane control the entry and exit of substances into and out of the chloroplast they're semi-permeable and they will allow in carbon dioxide and oxygen and obviously allow them to diffuse back out as well chloroplasts just like mitochondria contain their own ribosomes and their own DNA and they can use them to make proteins that they need for photosynthesis they have 70s ribosomes and their own small kind of Loops singular Loops of DNA is evidence for the endosymbiotic theory like the double membrane this idea they were once Free Living bacteria that then were absorbed to make eukaryotic cells it also means that they aren't relying on any of the other cell processes in order to carry out photosynthesis they've got everything they need to make from the proteins they need inside the chloroplast itself and finally we have the internal thyroid membranes so these are formed into specific shapes we have the thylakoid discs so they're like kind of 3D kind of sacs or coin shapes and they are then stacked on top of each other in piles known as Grana one granum multiple Runner and then these have some of them have joining strips of thyroid membranes which are called lamene the arrangement of this membrane creates a large surface area for enzymes ATP synthase again and also the electron transport chain proteins which are all needed for the light dependent reactions so my independent reactions happen in the stroma light deep and it happens and take this in this style of blood membrane the Grana on right next to and surrounded on all sized by the stroma which is really useful because it means the products and the reactants of the photosynthesis reactions can be exchanged easily between the two sections so between the light dependent and the like independent reactions okay so let's have a look at photosystems and pigments so how are plants going to harvest the light that they the light energy so that they need for photosynthesis so a photo system is a protein complex found in the thylakoid membrane and it harvests light energy from photons and it uses that light energy to excite electrons and specifically electrons in a chlorophyll molecule or chlorophyll a molecule which is found in the reaction Center at the kind of very middle of the photo system there are two types of photosystem in Plants phone system one and photo system two we normally put them the other way around so first system two first and first system one first just because that's the order in which they were discovered in both system 2 has Optimum wavelength of absorption 680 nanometers and photosystem 1 has an Optimum absorption of 700 nanometers they both absorb away blanks of light using chlorophyll a it's just that they have a slightly different Optimum wavelength that they can absorb and obviously as well we know that photo system 2 and photo System One have different kind of roles in the like independent reactions as well um because we have cyclic non-cyclic photophosphorylation happening and that happens at certain protein systems inside the photo systems as well as our chlorophyll molecule we have other pigments known as accessory pigments they absorb light at different wavelengths because they are different colors and they pass the energy down to the chlorophyll in the reaction Center by having these accessory pigments they allow the plant to absorb different wavelengths or an increased range of wavelengths which therefore helps us to increase the rate of photosynthesis and how much for instance this happens because the more like we absorb the more light energy we have to carry out photosynthesis so you can see from my action Spectrum graph here that the blue light and the red light produce the greatest photosynthetic rate the highest peaks because those two colors are absorbed by chlorophyll but there is this dip in the Middle where mostly green and yellow light is reflected and that's why portal and plants often appear green so lastly the kind of thing that's related to these pigments is that we can use chromatography to separate and identify the pigments in different plant leaves they the pigments will move up the chromatography paper at different speeds because they can be separated by their Mass their size their charge and therefore you can look at the pigments and identify the pigments that are in in Plants it could be shade tolerant plants or UV resistant plants or just plants that have different colored leaves you should be able to spot the differences and then be able to talk about the fact that having more pigments is an adaptation and why it's an adaptation because they can absorb the different wavelengths okay so moving on to the light dependent reactions so stage one is where light energy is hitting our photo system and it's exciting electrons in the chlorophyll molecule at the reaction Center of both system two so the electrons move to a higher energy level that's what we mean when we say that they are excited and so they are then able to leave the chlorophyll and because the electrons have left the chlorophyll it becomes an ion so light energy here is being used to ionize chlorophyll so we say it is photo ionization because we've made chlorophyll and ion we need to replace those electrons it will be positively charged now but it will be needing electrons and wanting electrons to replace it that comes from photolysis remember photolysis means splitting using light and what we're splitting is water and this happens early at furniture system two because it's the only one that has the enzyme so an enzyme uses light energy to split water into oxygen gas and hydrogen ions and electrons these electrons are going to replace the ones lost from the chlorophyll the hydrogen ions are going to be used to make ATP and also to help us reduce our nadp later on and the oxygen will then just diffuse out the chloroplasts we know it's a waste product it can go on to be used in respiration or it will just leave and diffuse out of the leaf next stage is where are these electrons going to go so once they've left the chlorophyll they move through a series of protein carriers called the electron transport chain they move through a series of redox reactions remember that is alternating production and oxidation so as they join the protein they will be reducing it and then as they leave they'll be oxidizing it will not be reduced in the next one and so on because each protein has a lower energy level they lose energy as they move down the electrical transport chain that energy that's lost is used to produce ATP and we're going to look at that on the next slide so then once they've moved through the electron transport chain these low energy electrons find their way to throw system one and they'll be really excited by light energy and then they lead the chlorophyll again and then they'll pass down a couple more protein carriers remember the electrons are constantly coming from the electron transport chain for photosystem one so they do not need photolysis to happen here to replace electrons that's why fertilizes only happens at both system two and also because there is no enzyme for it to happen at photosystem one So eventually the electrons and some hydrogen ions are used to reduce nadp which is what is the final electronic sector in this kind of small electron transport chain at photosystem one nadp is a coenzyme or an electron acceptor or a hydrogen carrier all of those names can be used but it's now been reduced and so the reduced nadp will then travel into the stroma for the light independent reactions is where we look into a little bit more detail about how we actually make ATP in the light dependent reactions to start with electrons move down the electron transport chain and as we've said they lose energy because each protein is at a lower energy level so they move through these redox reactions down the electron transport chain losing energy the energy lost is used to actively transport hydrogen ions from the stroma into the thylaboid space so remember that means thinking about those discs those sacks of thylakoid membrane a thylakoid will have outside and then inside because it's like a sac this movement of h plus ions to moving them from the stroma into the thyroid space inside the thylakoid creates a concentration gradient across that thyroid membrane so we've got a low concentration of the stroma High concentration in the thyroids this gradient then causes the hydrogen ions to diffuse back down their concentration grid but through a specialized protein Channel which is attached to an ATP synthase enzyme and as they move through they cause the adobe's enzyme to turn ADP to ATP because we use light in order to end up adding a phosphate to ADP to make ATP this is known as photophosphorylation and the process of using a chemical gradient of h plus ion is known as chemiosmosis the ATP produced is then used in the like independent reactions so it's one of the products of light dependent reactions that then travels into the stroma to be used in the light independent reactions okay so we're halfway through voted to this point done the light dependent reactions that have taken place in the thylakoid membrane they have produced oxygen gas which has come from photolysis and that leaves the chloroplast although it could be used for respiration we have made some ATP through photophosphorylation and chemosis and that travels into the stroma for the light independent reactions and we've reduced nadp so we've made some reduced nadp which are going to It's the final electron acceptor in the electron transport chain so it's taking the hydrogen ions and electrons and it travels to the strainer with them for the light independent reactions as well so now we're going to look at the light independent reactions they obviously are taking place in the stroma so not in the thylakoid membrane they use products from the light dependent reactions the ATP and the reduced nadp and they're going to fix carbon dioxide and use it to produce organic molecules including glucose okay so now we're on to the light independent reactions so the first stage is carbon fixation and it's where atmospheric carbon dioxide which is diffused into the leaf and then into the cup the chloroplast is combined with a five carbon molecule called rubp or ribulose bisphosphate combination of the carbon dioxide and the ruvp is catalyzed by the enzyme called rubisco and it produces two lots of GP which is a three carbon molecule this is because it initially makes a six carbon molecule because one carbon dioxide plus the five Carbon on ubp is unstable breaks apart so it creates two three carbon muscles the next stage is reduction so we are going to reduce our GP to turn it into a molecule we can use so GP is reduced using the energy from ATP and the hydrogen plus ions from the reduced nadp from the light independent reactions this still produces a three carbon molecule because we haven't changed at any carbons but it is now called gout or triose phosphate the glp or TP is used to build lipids amino acids glucose nucleic acids all of the biological organic molecules that are plants going to need in order to function they're going to have to combine it with things like nitrogen and phosphorus that they're going to have to get from the soil as ions they can use this one molecule to build all of the molecules that they need for life the third stage is the Regeneration stage of rubp most of the molecules of TP or gout they're actually five out of six of them you can see in the diagram are used to regenerate five carbon molecule iubp and the rest of the ATP from the light dependent reaction is also used to do this and then our uvp can go back and start the cycle all over again so it stays in the stroma ready to be reused and combined with another carbon dioxide this whole cycle is named the Calvin cycle after Dr Calvin who discovered it using his lollipop experiments if you need to learn more about the lollipop experiments go and look at the more detailed video online independent reactions the ADP and the nadp that are left over after we've used them are then passed back into the thyroid membranes for the light dependent reactions and then the cycle will continue redox indicators change color when they are reduced so when they gain hydrogen ions or electrons in this case we're going to be using DC pip which will turn from a blue solution to a colorless solution one is accepts the electrons and it accepts those instead of the nadp and it is reduced so it kind of plays a role of energy p in this reaction the speed of this reduction in various conditions can be used to measure the rate the light dependent reactions of photosynthesis so we're going to look at ammonium hydroxide which is often used in weed killers because it disrupts the electron transport chain and prevents the reduction of nodp and the production of ATP because if no electrons are moving along the electron transport chain they won't be there to be accepted by the nadp and therefore reduce it and the lack of electron movement is going to reduce the amount of ATP we can make through chemical osmosis this will have a knock-on effect then on the light independent reactions because GP will not be reduced to TP because no reduced energy fee is moving into the light independent reactions and so then we're going to get a few organic molecules and ultimately this can prevent growth and eventually cause death of the plant in this experiment we're going to use availing hydroxide to show that this disruption of these UTC occurs and in this case it's because the ammonium hydroxides that affect the pH of our solution light reactions working properly reducing DCP removing the color what happens if we remove light or what happens if we add this weed killer does that show us that the electro transport chain is stopped or not working and therefore we don't get that reduction of the juicy bit so we don't get a color change that's what we're looking at here gcp water and the chloroplast was in tube a and we put that in the light and here's it compared to tube D now we know it was very close for the color room is reading and also visually we can see that it's very close here so the reason this happened was that the light dependent reactions took place because light was present and so were four blasts the DC pick was reduced by the electrons from the electron transport chain and therefore after 10 minutes the DC Pit All Event had decolorized because all of it has been reduced into B so we can see here it's obviously very very blue same color pretty much as the DC bit started out so here there was no light because we covered it into a bottle so there's no light energy to absorb to excite electrons and so they do not leave the chlorophyll molecule to move down and along the electron transport chain so therefore they aren't available at the end of the end of the excellent transport chain to be accepted by the DC bit so the DC poop has not been reduced and what we've ended up with is the most like neutral doing all the juices is stayed this is when you could have used instead of comparing this tissue D you could have also used uh tube e that we talked about so the other control tube where you put the DC pipin and water with no chloroplast so that would definitely obviously not have changed color and then you can use that in the color room set and then come also to as a comparison to compared to be what a complete no change conducive it would look like I didn't do that but you can obviously do that it's very easy you can just dilute the juicy fix and do something with the same amount of water as you would use for the water in the club bar solution and then you can use that as a comparison oh probably we've got cheap seats so you can see hopefully much better here in this image than you did on the video about the different color between say two c and Tube B so we said earlier on that the ammonium hydroxide weed kind of disrupts the electron transport chain which it does so although it does disrupt it it's not instantaneous and so obviously the chloroplastopolis synthesizing as soon as I put the DC pip in so some of them will some of the deals of it will have been decolorized and reduced by some electrons that were initially got through the electron transport chain before the ammonium hydroxide completely disrupted it but because there is a disruption to the electron transport chain the electrons stop moving through it so fewer electrons are then free to decolorize and reduce the DC pick at the end as the graph shows you what rate of photosynthesis on the y-axis and light intensity is our Factor on the x-axis now to remember make sure that when we have these kind of straight up and then across graphs that are the outline so on the angle going up and the x-axis is a limiting factor there so light intensity is increasing the rate of growth since this is increasing up until the flat line when we get to the flat line the plateau at the top the Factor on the x-axis is no longer a limiting factor so at that point light intensity is no longer limiting because we're increasing the light intensity but the rate of photosynthesis isn't going up so something else must be limiting it that's how we interpret these graphs so light intensity is a limiting factor as we increase the light intensity we increase the rate of reaction Plus plant grow once there wants the greater than rate of respiration which is what we call the compensation point and you can see there on the graph that we have to get above that compensation point so above that kind of horizontal dotted line for us to be making enough sort of biological molecules that where the glucose that we're actually using to grow instead of just using it to respire at low light intensities the GP is going to increase but iubp and gout and TP will decrease the light wavelength it needs to be red or blue there to be the maximum rate of photosynthesis as you can see in the action Spectra because green to kind of orangey or green to kind of yellowy light is reflected by the majority of the pigments in plants which is proportional onto temperature the graph shows that obviously we've got two rates of photosynthesis where we've got two different temperatures so here up until we get to here remember that light intensity is the limiting factor and then obviously once we get past that we get towards the flat point then we have the two temperatures are the limiting factors and the rate is obviously higher with 30 degrees than with the 20 degrees so increasing the rate of the temperature so increasing the temperature has increased the rate of photosynthesis so at low light intensity down here the two lines are basically the same because the temperature is going to have little effect if there's not enough light for photosynthesis to be happening at fast enough right temperature is not going to make any difference but when the light intensity is no longer limiting so when we get to those flat lines increasing the temperature is going to increase the rate of for instance it's up until about 45 degrees and then we get our usual issues with enzymes and proteins denaturing light independent reactions are most affected by temperature because they're most reliant on the enzymes for example the visco and so GP rub anti-people all fall and all start to decrease if the temperature gets too high for carbon dioxide concentration we have the same thing so it's only has an effect it's only limiting up until this point when it's low light intensity back to the limiting factors up until there but then you can see if we concentration of carbon dioxide we increase the rate of photosynthesis up until about 0.4 higher than 0.4 percent if you remember this demand to close and so that if smart is closing then we're not going to be taking any carbon dioxide and said that will then affect the rate of photosynthesis low levels of carbon dioxide means our ubp is going to increase but GP and Gap or TP are going to decrease and that's because our ubp is no longer combining with the carbon dioxide so it's going to be there but not being used up and because there's going to be no combination there's going to be no formation of the GP and the Gap 14 greenhouses maximize the rate of photosynthesis because they can control all of those limiting factors and they can make sure that they're all at their Optimum they can additional lighting they can use heaters and they can increase the carbon dioxide concentration artificially inside the glass houses this is going to speed up the rate of growth because we're doing more photosynthesis but these measures can be expensive and they must be balanced with the profit or the increased profit that could be made from either growing more or being able to produce the same amount faster just a note on water so water stress doesn't directly affect the rate of photosynthesis so it is not known as a limiting factor because if the plant didn't have enough water and for photolysis to take place then the plant would already have been wilted and probably dead but in drought conditions when there's limited amounts of water they often close their stomata so they prevent water loss and then therefore less carbon dioxide is being absorbed which obviously does reduce the rate of photosynthesis so that is how water is linked let's have a quick overview of what we're going to go through when we talk about respiration there are four main stages so in this video we're going to look at glycosis it happens in a cytoplasm it doesn't happen in the mitochondria I'll explain it all in a second it splits glucose and it creates a small amount of ATP now remember the whole point of respiration is to produce as much ATP as possible so at each stage there is some normally some ATP made but overall that's going to add up to a large amount and much larger than photosynthesis so that's stage one stage two is called the link reaction it literally links glycolysis with the next stage the Krebs cycle and it's how we get the products of glycolysis into the mitochondria it does not produce any ATP but it happens in the mitochondria the Krebs cycle is another cycle it's going to be similar to the Calvin cycle that we've already learned it sort of does this similar job we're producing a lot of coenzymes so nadh and fadh so lots of reduced coenzymes which are going to carry electrons and hydrogen ions all the way to the ETC very very similar to what we had previously in photosynthesis so we're producing coenzymes that are reduced because they have the added height plus and electrons which again go to the GC in electoral transport chain in order to produce ATP and then lastly we have oxidative phosphorylation now we've spoken about what phosphorylation means it means adding phosphate so we're making ATP by adding lots of phosphates to ADP using ATP synthase in exactly the same way as we talked about infosynthesis but we're not talking about photophosphorylation here because there's no light so we're talking about oxidative because we're going to be using oxygen which is what the main reactant of respiration is so it happens in the membranes of the mitochondria similar to how the electron transport chain happened in the membranes of the chloroplast and so it's going to be a very similar story and that will be where we make the most like the majority of our ATP from respiration first part of respiration which is glycolysis glycosis takes place in the cytoplasm of cells it is a shared or the only shared stage between aerobic and anaerobic respiration the point of glycosis is to split glucose literally glycolysis means splitting of glycogen or glucose into pyruvate and it produces some ATP F1 glucose is phosphorylated to hexo's bisphosphate sometimes also called fructose 6-phosphate using two ATP to do that so two ADP are made because we have two ATP and the phosphate from each is removed and used to phosphorylate for glucose and then we get to stage two the exposed business phosphate is going to split to produce two molecules of triosphate or GP so um the hexadeus phosphate is a six carbon molecule and it splits into two three carbon molecules which is the triosphate in the GP and then stage three we've got the TP or GP is going to be oxidized to form pyruvate and during that process we also form some reduced NAD and this energy from that reaction is so the oxidization of pyruvate and the reduction of NAD releases some energy and that energy is enough to produce four ATP so to phosphorylate two more ADP into ATP okay so what does glycosis produce so per glucose we get two reduced NAD and that's going to diffuse into the mitochondria carrying the h plus and the electrons to the electron transport chain we're gonna make two ATP net which remember means overall because we make four in total but we use two in the first stage so they get used for processes nearby um for example they can get used to help actively transport pyruvate into the mitochondria so the pyruvate we ate two of those and they get actively transported into the mitochondria for the leak reaction but only if there's enough oxygen if there isn't enough oxygen the pyruvate goes through anaerobic respiration which is either lactic fermentation or alcohol fermentation okay so second part perspiration is the link reaction but first we'll have a quick look and reminder about the mitochondrial structure because this is the first part of respiration that starts actually taking place in the mitochondria so we've got the outer membrane which controls the entry index of substances including oxygen carbon monoxide pyruvate and ATP then we've got the inner membrane which is folded into cristae that's what we call the Folds One Krista mini cristae and that makes a large surface area for the ATP synthase and for the proteins for the electron transport chain to allow oxidative phosphorylation to happen which is what produces ATP which is the last stage of respiration then we have the Matrix which aside similar to the stroma in a chloroplast or the cytoplasm in a Cell it contains enzymes specifically the decarboxylases and the dehydrogenases that are going to remove carbon dioxide and remove hydrogen and this is where we need those to carry out the link reaction and the Krebs cycle it also contains DNA and ribosome so they can make its own proteins similar to the chloroplast the whole point of the link reaction is to try and connect glycolysis to the Krebs cycle so there's no ATP made here it's just basically a transition stage it takes place in The Matrix so we've moved from outside into the mitochondria now and it happens twice per glucose molecule so the first step is that pyruvate is decarboxylated and oxidized to form acetate so carbon dioxide is removed and we also oxidize it and that means that we end up producing A reduced NAD the acetate that's made is going to combine with the coenzyme a to form acetyl Co a or acetyl coenzyme a the carbon dioxide is going to diffuse out as a waste product from the mitochondria the reduced NAD is going to take the hydrogen ions and the electrons to the electron transport chain and then the acetyl COA is going to enter the Krebs cycle the Krebs cycle part three so the Krebs cycle takes place in The Matrix It produces lots of reduced coenzymes that take h plus and electrons to the electron transport chain and it also produces the main DP so to start with we're going to need the acetyl COA that we made in the link reaction and it's going to combine with a full carbon molecule called oxaloacetate they're going to combine to make a six common molecule called citrate or citric acid and this is stage one so we've got a two carbon molecule combining with a four common molecule to make a six carbon molecule we are going to regenerate that six carbon molecule back into oxalo acetate through this cycle the first thing that happens to the citrate is that it needs to be oxidatively decarboxylated which just means oxidizing and decarboxylating at the same time so we're going to remove hydrogen ions and electrons which is oxidizing and that's done by the dehydrogenase enzymes they are going to be accepted by NAD so we're going to make some reduced NAD and then we're going to decarboxylate which means to remove carbon dioxide so we're going to take two carbon dioxide molecules away from the citrate so we've gone we go from a six carbon molecule down to a four carbon molecule this happens in two stages so we initially go from six carbon to five five come to four you don't need to know the names of those intermediate molecules the five carbon and the four carbon you just need to know that this is what happens the final stage is going to be the Regeneration of oxaloacetate so we oxidize again so we remove some more h plus ions and electrons and these are used to reduce NAD and fad so remember they are both coenzymes that are or hydrogen carriers and they're going to take those to the electron transport chain also at this point we have another example of substrate level phosphorylation which produces a molecule of ATP okay so like the link reaction where we have two molecules of pyruvate which means it happens twice this is the same thing so because we have Technologies of pyruvate we get two molecules of acetyl-coa and so therefore the Krebs cycle is going to have to turn twice per glucose molecule so let's see what we get from that we get per glucose four carbon dioxide which as we've said are waste products so they're going to diffuse out to reduce fads which goes to the electron transport chain six reduce nads which go to the electron transport chain and three lots of ATP which can provide energy for whatever's happening nearby so we are producing a little bit of ATP but realistically we've managed to produce eight coenzyme reduced coenzymes which are going to take those hydrogen ions and electrons to the electron transport chain so that means that we can make more ATP using that oxidative phosphorylation so the main things to remember here is the stages that happen in the cycle what gets produced at the end remember that with the acetyl COA is just kind of bringing the coenzymes bringing the acetyl group to the start of the cycle the cycle regenerates IT background to make oxalo acid which you need to start the cycle so it's a self-sustaining process and as long as we have the acetyl COA arriving then and we don't really need much else we need some ADP to do the phosphorylating we need the coenzymes without it to help with those enzymes to do those reducing and decarboxylating okay I'm on to the fourth and final stage of respiration now which is the oxidative phosphorylation so it takes place in the inner membrane of the mitochondria the cristae it uses chemosis to produce large amounts of ATP it requires the electrons and the h plus ions from the reduced care enzymes NAD and fad that we produced in all the stages up until now and it also requires oxygen to be the final electron acceptor and allow electrons to keep flowing down the electron transport chain so the first stage is where the hydrogen ions and the electrons are released from the reduced NAD and The Fad when they are oxidized as they reach the first proteins in the electron transport chain you'll notice the fad goes to the second protein in the electron transport chain and not the first one it can only bind there and so it only starts at slightly lower energy level than if it was to go to the first protein where NAD combined and that means that fad just produces a slightly less amount of ATP because the ends the electrons moving down the Electoral transport chain won't start as a higher energy level so they won't produce as much energy to so they won't remove as much hydrogen ions so that's what we were just saying so part two is that the electrons move down the electron transport chain proteins in this series of redox reactions losing energy this is exactly the same as what we've already spoken about with photosynthesis the energy released from the electrons moving down the electron transport chain is used to pump or actively transport the hydrogen ions from The Matrix to the intermembrinal space so that's the space between the membranes so between the inner membrane and the outer membrane there is a gap and that's where we're sending these hydrogen ions and we've created a chemical gradient hence chemiosmosis so there's a greater concentration of hydrogen ions in the intermembrane space than in The Matrix of mitochondria and so the hydrogen ions diffuse back down their concentration gradient across the membrane through ATP synthase which is a modified protein Channel and therefore as they go the movement of those h plus ions causes the 80 piece of this to turn and make ATP from ADP and inorganic phosphate at the end of the electron transport chain electrons leave the final protein and combine with oxygen and some other h plus ions that are being pumped back across in order to make water so oxygen here is final electron acceptor and it accepts those electrons in it without that without those electrons being having somewhere to go at the end of the electron transport chain we wouldn't maintain that constant flow of electrons through it and so we wouldn't get respiration happening this is where we need the oxygen that is one of our reactants for respiration and it's also how we produce the water that is one of our products of respiration think about our general equation so in total we have to be able to think about add up the total amount of ATP produced by respiration so each reduced NAD can produce two and a half ATP and each reduce fad can produce one and a half ATP and we said that this was because of the lower energy level that fad starts at in the electron transport chain so if we add this up about how much reduced NAD and reduced fod that we produce throughout the whole of the stages of respiration we make two reduced NAD and glycolysis so 2 times 2.5 gives us 5 we make two in the link reaction that gives us another five we make six in the Krebs cycle that gives us 15. we make another two reduced Fad in the Krebs cycle which gives us another three aerobic respiration but alcoholic fermentation is what it's called in Plants yeast and in some bacteria not all they use the reduced energy to convert pyruvate into ethanol and this process also produces carbon dioxide so pyruvate first get some decarboxylated so carbon dioxide gets removed to form Ethan now and then we use our reduced NAD to oxidize the ethanol into ethanol so we produce a carbon dioxide and we produce NAD that's important and we'll come to why in a second so in animal cells it's called lactate fermentation because we're making lactate or lactic acid so again we're using our reduced NAD that we've produced at the end of glycolysis to convert our pyruvate to lactate which otherwise known as lactic acid so why is this important why does this link back to glycolysis and and why do these organisms do anaerobic respiration in this way well both of these fermentation processes allow the Regeneration of NAD so we're using the reduced NAD and therefore we're creating the NAD so what we do then is we allow glycosis to continue because if we've got more NAD and we've we can go back and do the same process again we can do glycolysis to make more pyruvate and then we can go through the same conversion stage to get fermentation so it allows small amounts of ATP to be continuously made through glycolysis and it allows it to continue happening so the ordin's concerned for a short time without oxygen because the energy is going to be able to be used to do some basic fundamental processes so often there's questions about how does fermentation or how does anaerobic respiration allow small amounts of ATP to be produced or why is it important that NAD is regenerated in fermented version and that's the kind of answer they're looking for linking a little bit back to GCSE here how do we get back from lactate or lactic acid so in animal cells after some time then we can re-oxidize that lactate back to pyruvate but we have to use oxygen to do that and that oxygen is what we say the oxygen debt is so the amount of oxygen we used to say needed to convert lactate back into or you to break down the lactic acid that's what we're saying here what we actually mean is we're saying we're oxidizing the lactate back to pyruvate then that can go back to the start of the link reaction and therefore we can continue with our respiration reactions some lactate can also be converted so that's another way the way we store it is something that can be used so glycogen can obviously be used to be broken down to resupply the cells with glucose for respiration as well okay so I've got my table of results so initially I've got my temperature and I've got my time taken for the DC event to colorize so if I plotted that as a graph I'd get this kind of bucket shaped graph which is not the type of graph we're used to seeing for an enzyme reaction because we're used to seeing it with rate up measure the time taken but in order to have the rate calculation we will need to calculate rate from that it's related to obviously the time that it took the rate of respiration can be characters from the data because it's inversely proportional to the time taken to decolorize the redox indicator whichever one you've used so in order to calculate the rate we need to do one divided by the time in seconds and that will give us the rate so I would need to do one divided by 11 1 divided by 3 1 divided by 2 1 divided by nine one divided by 14 and 1 divided by 24 and that will give us our rate and then if we plot that on a graph then it would look a little bit more like the rate graph we're used to seeing with an enzyme reaction so here we go so now I've added my rate column so in seconds minus one because it's the inverse and then my rate numbers so I put it to three decimal places because obviously uh it's a bit more accurate to show that because we're not if we just had it to one decimal place or to zero it wouldn't be very much difference between them but also it means that plotting the graph is kind of a bit easier for you as well okay so let's have a think about how we explain this graph you could be asked to explain a scrub again it's very simple because it's very similar to any other enzyme and rate of reaction crops that we've looked at because it's the effects of temperature so in my stretch a on my graph then as the temperature is increasing the rate of respiration or the rate of reaction is increasing and that's because we've got increased temperature so we've got increased kinetic energy so there's more successful collisions between the substrates and the enzymes and therefore we get an increased rate of reaction because we get more successful enzyme substrate complexes and therefore Albright reaction has increased so the very peak of the graph and you can say that this is that um sort of 0.5 seconds minus one this is the optimum temperature it's the fastest or is the highest rate of reaction so about 40 degrees is the opulent temperature here of our enzyme and then if we think about what starting to happen at B we've got as the temperature is increasing past 40 degrees we've got a decrease in the rate of reaction this time and so we're going to explain that by saying that obviously increasing temperatures can cause enzymes to denature they can cause protein other proteins as well as to denature if we're thinking about respiration then that's going to be our examples could be something like ATP synthase enzyme it it could be the proteins in the electron transport chain of denaturing and because this is happening we're getting a decrease in the rate of reaction because the reactions are slowing down in respiration and you can also talk about the fact that it's 80 percent days for example the active site is going to change shape because the enzyme will denatured and so that leads to fewer enzyme substrate complexes and that's probably going to decrease in the rate of reaction and in this case there would be a decrease in the rate for ATP production people talk about ATP symptoms as an example just to recapping some ecosystem Basics stuff we've done at GCSE so an ecosystem is made up of different populations of organisms so remember our population is a group of one species in an in an area in a habitat or in the ecosystem interact with each other so we know obviously that organisms are interdependent and that means they rely on each other for things like food shelter pollination see dispersal that type of thing the main theme we're looking at here is obviously going to be feeding relationships so food chains like the one I've got on the right show simple lines of energy transfer between organisms so don't forget the arrows in the food chain show the transfer of energy from one organism to another orphanous sun to plants for example and then food web so a more complicated version of this with different animals and plants in that feed on each other and aren't interlinked would show how something like different food chains would overlap with each other and interconnect we're just going to look at food chain for now though to make it a little bit easier so the Sun at the start of my future on here is the source of all energy in the ecosystems so without the sun that's the starting point for the where the energy comes from that gets into the producers and then is transferred to all the other organisms the energy from the Sun is harnessed by producers so the plants and things like algae and cyanobosynthetic bacteria in the oceans they will all absorb that light energy and through photosynthesis as we've already talked about produce organic molecules which includes things like glucose but also amino acids and lipids and other carbohydrates Etc that those molecules that energy that they've harnessed and those molecules that they've built with that energy become used to build tissue so new cells new cell walls new material that the plant obviously creates as it grows that living material those tissues are known as biomass or the plants biomass so the biomasses tends to be we say all of the living material of an organism once that energy is stored from the Sun by producers into their biomass their living material of the plants then the rest of this energy transfer that occurs is actually a transverse biomass because the chemical energy that has been stored in those molecules in the bonds that make up the molecules that have made up the tissues of this organism that is what gets passed on when an organism eats another organism so when the rabbit eats that grass it's ingesting the biomass the living tissues of the plant and it's breaking those Bonds in the chemicals and the molecules down through digestion where it's going to absorb some of those nutrients and use it to make its own molecules and biomass and living tissues so we can it isn't an energy transfer that's going on we can also think of it as a transfer of biomass because the biomass is the part that gets eaten by the organism each time in the food chain remembering that as well as passing into all of these organisms when organs eat each other then as well some of that biomass is going to end up coming to decomposers so some of that energy is going to end up not necessarily being passed onto the next trophix level because sometimes not all of the organisms gets eaten we're going to talk about this in the next video but just to remind you and make sure that you're aware that obviously some of that biomass is going to also go to decomposers they are part of the food chains as well they are obviously they do the breakdown they do the Decay process where they break down the molecules in dead organisms which they use for their own nutrition not sure remember that's called saprophytic nutrition which means they're breaking down and dissolving dead autisms they are going to take some of that biomass as well so some of that energy some that biomass is going to pass into decomposers so bacteria and fungi and they are also part of the food chain these labels here the primary consumer the secondary consumer and the producer these are all trophic levels troph literally coming from the word mean to eat so these are all trophic levels they're the levels that we talk about in the food chain so if you're a primary consumer you're often a herbivore because you're often eating plants only then if you're a secondary consumer you tend to just eat animals etc etc um and then the third they just mean in first the second and third primary secondary test shoot is the mass of the living tissue in organisms so we can measure that because realistically it's the equivalent of the dry mass of an organism so removing the water because water will vary from organism organism and the water inside an organism is not a part it's biomass it wasn't made energy wasn't used to make that water in there it's there to help keep the orgasm alive so to remove the water we will need to dry the tissue in oven until the mass is constant so this confirms that all the water is evaporated and then what is left is just the dried tissue which we can whey and then that gives us our biomass we can then use this biomass to make pyramids of biomass so we can do this drying and weighing of organisms in each traffic level of the food chain and then we can use that to kind of make a diagram of the kind of levels or amounts of biomass in each trophic level it's more reliable than doing a period of numbers just how many produces how many insects how many frogs but it's only going to be estimated as a small sample we're not going to kill and dry and weigh all of the animals from each of the populations in the traffic levels so we won't doing that because that's unethical and also would take time but if you take a small sample then to do that because you don't want to kill a lot of organisms then your sample might not be representative of the whole population in that trophic level alternatively as well we can take that biomass once we've won watch that out and we can learn a bit of that biomass that dry tissue and that will allow us to work out the chemical energy stored within that biomass so we use a calorimeter to do this be careful about the spelling of calorimeter make sure you're aware that it has an A in it it's not a Colorimeter and do not get them confused because in the exam if you misspell then you may not get marks for it because it could they could think you could mean a tolerant which is obviously a different machine that looks at light absorption so the biomass is burned a sampled by myself so again not all of it you take a couple of grams so you know what the mass was you burn it so you set fire to it in the presence of oxygen in this special machine called parameter and the energy that's used to heat up the water around the area the metal box where you've burned that sample of tissue is measured so we measure the change in temperature of the water the increase in temperature and that's the equivalent of the heat energy that's been released so that will tell you how much energy chemical energy was in that biomass sample you need to know a diagram of what a calorimeter looks like and you might need to interpret some of the reasons why it has some of the parts mainly the stirrer so that circulates the water to make sure that it's an even temperature so it gets a need a distribution of heat which makes sure that the thermometer reading is more accurate so then once we've calculated our energy that's in our biomass we can use this to make a pyramid of energy this time instead of a pyramid of mine so we're now using kilojoules per meter squared and it can be per year so if you've grown a set amount of crops in a set size of a field in a year then you can use this to say that in that year this amount of energy per meter squared was produced and we'll talk about that in terms of productivity so most accurate this is as in terms of all the period of biomass pyramid of numbers there's all different types but pyramids of energy the most accurate because two different organisms could potentially have the same biomass and so that would mean they would say like register the same as the same amount of biomass from the Pyramid of biomass but actually if you look at the chemical energy stored in that biomass in those tissues two different organisms with the same biomass can store different amounts of energy and that's normally because fat is stores more energy than carbohydrates for example again they're only representative because they have the same issues as pyramid of biomass and also it's only the energy that is in those organisms at that specific time point which can vary So Different Seasons different times of the year different temperatures outside and the amount of food the organism has had recently all of that is going to change the energy availability in their biomass in their tissues so it's a snapshot of one time Point um in in one part of the year energy transfers and how we can measure energy transfer and calculate energy transfer efficiency so not on the energy from the Sun or biomass is available to each traffic level only around 10 is transferred each time and we're going to talk about how we work that out so each time you're moving up the future and there's only 10 of the energy in biomass or chemical engine biomass from the total energy that was put in from the Sun for example at the start of the food chain that's available to the next traffic level so it decreases each time we go up so to start with is because most of the energy 60 of the energy total that's available so from the start from the Sun for example isn't actually ever absorbed by the organisms in the that stress so there that's for a number of reasons so for plants and the light energy transfer and how not all of that makes it into plants it's because they're likely reflected it could be the wrong wavelength so only red and blue light is absorbed so the rest can be reflected some will pass straight through the leaf and not be absorbed at all and some could hit parts of the plant but the plants those parts aren't photosynthesizing so the bark or the trunk of a tree where there's no portal to absorb it so animals and plants as well not all of the parts of the plant or the animal is going to be digested such as the roots of the plant or the bones often animals only eat certain parts of the plant and they won't eat all of it same animals won't necessarily always eat the bones of other animals and also some is lost in feces as well so some is undigested and passes through the system and all of that ends up then going to decomposers so all of that energy and all that biomass will eventually be broken down but that will go to decomposers and they are not part of this food chain and they don't go to the next traffic level so we're only interested in hearing about what parts of the energy and then what parts of the biomass are actually making it into the organism in the next traffic level that they can then use to produce their own biomass so we call the part the available and you're the potential available energy to be absorbed by at each traffic level the growth primary productivity so that's all of the energy that could be available to the organisms of the next traffic level but not all of that GP is absorbed okay because only some of that becomes biomass and then only some of that gets absorbed or taken in by the consumer so what we call the biomass that actually gets eaten that actually gets taken into the next animal or the next organism is the net productivity or if you're a plant the net primary productivity and so that's the actual amount of energy that would pass from one organism to another organism between the traffic levels so you can see here I've got my net price my net productivity or my net primary productivity that's been transferred at each traffic level so now let's look at what actually happens so what gets lost is due to what we call respiratory losses so because it's being used the energy from respiration is being used not always for growth not always to make new biomass but in things like movement to create heat energy so we lose our respiratory losses at each level of the food chain so those are my respiratory losses so we can work out using some equations what NP is going to be so we've obviously can use the technique that we've talked about so by getting the biomass and calculating the chemical energy to find out what energy is being passed or what energy is available if you pass on to the next traffic level so that would be able for us to work out so we can work out NP by taking GP and taking away ah obviously the same works for primary productivity as well net primary productivity is just gross productivity takeaway the respiratory losses and that is out how you can work out Network to the team and if you're doing it the other way around and you're wanting to work out GDP obviously you can take and put those two together that's how we can look at working out what is being absorbed what's being lost what's GP what's NV and now we have to think about efficiency so to calculate the efficiency of the energy transfer between the traffic levels we can use the numbers we already have so the energy that's transferred to the next the next trophic level divided by the total energy available times 100 to get a percentage will tell us the efficiency of that energy transfer between each traffic level from producers to the primary consumers is the least efficient because there's actually a lot of indigestible material implants and then from between each consumers and primary consumers to secondary and secondary territory there's actually a slightly increase in efficiency because there's more digestible material and more of it can be absorbed so you need to know how to work out Energy Efficiency you need to know how to work out MP or MVP or GP using these numbers you might get given a food chain or a diagram that looks similar to this and have to use those numbers to work it out you also need to be able to give reasons why only 10 of energy is available in each level of the food chain and the reasons why not all that energy is transferred and reasons why energy is lost so you need to know how farming tries to improve net primary productivity of crops and also the net and productivity of livestock by increasingly how much they grow and also by increasing their energy transfer so by reducing their energy losses through respiratory losses so that increasing NPO MVP and then reducing are in order to try and make sure we get more yield out the end so for farming of animals that means controlling their movement or reducing heat loss giving them more hydrogen food and then slaughtering animals before they get to adulthood so that all of the energy that's been put into them has been used for growth and then once they stop growing they are killed and used for meat or and also this accounts for things like eggs and milk as well the amount of engines going into there and the production of those plants we care more about preventing anything from reducing their biomass so increasing their yield by making sure that they don't suffer any competition that they don't get eaten or destroyed by tiny pests or diseases and also by adding nutrients to the soil and giving them the maximum amount of minimal islands in the soil that they need in order to be able to grow as quickly as possible okay so the phosphorus cycle let's go through it quickly so you must remember that most phosphorus on Earth exists in the Rocks so the phosphorus cycle always starts with weathering and the weathering erosion of rocks through acid rain and rain over time and caused it to leech down run down through mountains into lakes and rivers and we also have to remember that fertilizer runoff can cause phosphates to leach into waterways as well so it can come from phosphates and nitrates that you both and obviously that could have implications for things like eutrophication but that's another way that phosphates can end up in the water the water is then going to leach into soils we know that obviously that water drains into soils and that's how we will get the phosphate present in the soil plants are then going to take up the phosphate ions from the soil through active transport in The Roots which we've done since GCC and in the same way as we talked about in the nitrogen cycle and remember that they have this ability they have these mycorrhizal fungi and what they do is they provide the plant with an extended surface area of their Roots so they they're high fee stretch out and give them more surface area in order to absorb more water and more phosphate but they also form a symbiotic relationship so they can literally exchange phosphate ions which the height you're able to get and swap that for carbohydrates that the plant produces in photosynthesis very similar to the nitrogen fixing bacteria but obviously this is a fungus this time and it's evolved because there's really low concentrations of phosphate in the soil so plants can grow better and grow larger if they have this association with this that lives inside their roots and then obviously we have the process of feeding so animals will eat the plants in the food chains and the food webs and that's how they get and phosphate transferred into their bodies and then they can use it to make their molecules and in the same way as we talked about with the nitrogen cycle animals and plants are going to die or excrete waste in the form of fetus in urine and the saprobiants the microorganisms in the soil that carry out that sacrobiotic nutrition where they break down the organic molecules and they're going to release those phosphate ions back into the soil to be taken up again by plants by active transport So that's its own little cycle going on there but obviously that it's got to link to the water system as well because water is where a lot of these phosphates are going to run off and end up being dissolved in aquatic systems so phosphates both from the fertilizer leaching and also the weathering of rocks also enters the aquatic system so as much as that water the North Sea seeps into soil and that gets into the kind of land side of the food chain this is also happening and the food chain is also happening in the water so aquatic Marine plants like algae here they will take up those they'll absorb those um mineral ions from the water and then use them as part of their growth and then those plants will be eaten by marine animals so fish in particular and other organisms and then that and then obviously they die and that cycle goes around we'll talk about in a minute but there's another element to this that we need to talk about which is birds so there's a link here between the aquatic system and the land system of where phosphate can get from the water or the marine environment into the land or the terrestrial environment and that is because of birds so birds will come along and eat fish most birds consume fish as part of the food chain so they will be eating these marine animals and then their waste specifically it's called guano and obviously when they die as well when the birds die and when the birds release their waste it gets broken down by decomposers the same as other land mammals and other land animals that are consuming plants on land it's going to then go back into the soil in the same way and guano is incredibly rich in phosphates and so in some areas it can actually be scraped off of rocks from coastal areas or collected in large forms and used as a natural fertilizer by Farmers so sometimes this guano this bird feces is actually really useful for fertilizing soils and putting phosphate back into places where there isn't a lot to help plants grow and then finally as we've said so Marine plants and marine animals they also are going to die and when they die they're going to release sort of dissolved phosphates they're going to kind of release those or dissolve and sediment into the bottom of the ocean so they drop down broken bits of shells broken bits of organisms dead organisms dead plant material tends to sink down to the bottom of the ocean and it forms there in layers of sediments and over millions of years if you remember from geography from key stage 3 sedimentary rocks are then pushed up over time over geological time and through forces of the tectonic plates they're pushed up and formed these mountains or Hills or rocks above the surface of the of the water above sea level and so then they'll be exposed again ready to start the weathering process so that's how we get to being in a cycle there's a couple of smaller Cycles happening here but overall we start with weathering and we have to end with sedimentary rock containing phosphate being pushed up in order to be weathered again and so that is a summary of the phosphorus cycle it's mostly remembering about the different sources and how it can be slow over time this idea of a marine food chain happening and then the terrestrial feature happening but ultimately ending up with this idea of death and the recycling of those phosphates back into the soil in different forms so this is the nitrogen cycle as a diagram summarizing the stages so let's go through each stage and talk about what happens and what bacteria and are taken by in that process so a modification is where organic nitrogen that just means like nothing is trapped in amino acids or proteins and DNA is turned into ammonia or competitive ammonia or ammonium compounds and that those proteins that source of nitrogen comes from dead organisms and the waste that they excrete so including urine pieces is done by sacrobites or saprophytes which are decomposers and they carry out this process of taking that protein and turning it into ammonia or ammonium compounds I remember obviously the amino acids and the DNA have passed through from plants into animals through feeding and then obviously they continue into or they stay in the bodies when they die and they can also be found in the waste products as well and all of this empty the soil or when the organisms die and then that is what the decomposition happens on then that ammonia or ammonium compounds is turned into nitrates through the process of nitrification is where we take ammonium compounds we turn them into nitrites and then nitrates it's done by nitrifying bacteria and those nitrates that we're producing can then be taken up the rainbow plants it's a two-step process and remember we've got two types of nitrine bacteria we've got the naturalness and the nitrobacter okay so the next stage is denitrification which is where we're taking nitrates that we've just produce in nitrification and turning them back to nitrogen gas it's done by denitrifying bacteria which live in the soil it's only done in anaerobic conditions so so only when we've got water logging or we've got lack of oxygen in the soil that's when these denitrified bacteria will carry out this process obviously farmers and I think people who are growing plants do not want this to happen and do not want to lose then nitrogen from the soil so they do try and prevent this by plowing which allows more air to go soil they aerate the soil and if that should hopefully maintain good drainage and good high levels amounts of oxygen that can then prevent this diet rification so moving on to the final stage which is an action fixation so this is where nitrogen gas is able to be taken from the atmosphere and fixed into ammonium compounds and it's done by nitrogen fixing bacteria there's two kind of types of these bacteria rhizobium is an example of a genus of these bacteria that live in the root nodules of laguinous plants that do this process and also azobacter which is found in soil if we're talking about the nutshell fixing happening in the root nodules of plants it's forming a mutualistic symbiotic relationship because the bacteria are going to exchange carbohydrates from the plants that they make through photosynthesis with their proteins or amino acids or the ammonia that they're making from nitrogen fixation so they're both benefiting which is why it is mutual and farmers can then obviously use plants that can do this process to enable them to get nitrogen back into this world that they use when they grow in plants in the field and then Harvest them without there being this Decay protest which takes up most of this nitrogen cycle so if the farmers are not using um natural fixing plants or legumes in order to put nitrates back into the soil then when they've harvested their crop and or they've removed their organisms for the animals that they're using for Salter rather than letting them die and decay in the natural way then they would need to put nitrogen back into the soil somehow and to do that they use chemical fertilizers and obviously we need to know the impacts of them using those chemical fertilizers on biodiversity and on other surrounding wildlife so we've explained why we need the nitrates to leave the back of the soil and why chemical fertilizers are potentially a good thing and we need them to make sure that we have the nitrates that plants can take up the problem is is that there are some negative impacts of this so lots of fields lots of farmers using lots of chemical fertilizers can cause some problems so the excessive use of them can actually change the balance of nutrients in the soil so it can cause to die because if you put too many mineral ions and think about the fat level book charges into the soil it reduces the water potential and so then water could actually start leaving plants to go into the soil if you've over fertilized it and sometimes Um this can also look like 35 a burn so some actual chemical burns if the chemicals are too strong and they've hit the roots directly or the leaf or even plant directly if they're spraying them it can cause kind of actual damage to the plant so that's obviously an issue for the farmers and growing the crops and it is the industry for the crops themselves and sometimes plants that are near and surrounding the fields the other main problem and you may have also done this at GCSE is eutrophication so the soluble fat that they're in they can be dissolved in water so they can be sprayed means that they can leach into waterways so they can be washed away by Heavy Rain or watering systems if you over water or too much water in the soil it can Leach out because they can dissolve in the water very easily and they'll end up in nearby ponds and rivers and then that's how we get eutrophication so let's just have a quick recap and reminder of what the stages of eutrophication are so first of all we've got the fertilizer runoff or the leaching the fact that it runs off or it leaches out into the waterways means that we've got this massive increase in Mineral ions in nutrients so nitrogen and phosphorus thing nitrates phosphates that wouldn't be in the water normally and that's the first stage that starts the whole process off that really large increase in nitrates and phosphates causes algae so these are plants that are floating around in the water types of plants these have now got access to way more minerals and nutrients than before and so they start to grow rapidly and so we get what we call an algal bloom where the algae divide and grow really quickly and cover the surface of the lake or the river that which ones that we're talking about if they're going to cover the surface often what they end up doing is blocking out light from getting to plants underneath and from getting to the lower layers of this algal bloom and so if plant so I'm going to have the light blocked and so they're not going to be able to do photosynthesis they start to die in quite High numbers and so we get this kind of floating scum of green algae on the top and everything underneath all the plant matter all the plant life in the pond and the liberal the lake underneath starts to die because it can't get enough micro photosynthesis so all this dead matter has to go somewhere so bacteria and decomposers are going to start the Decay process and start breaking down all of this dead plant matter and during that process obviously they're using it as part of their nutrition so sacrific nutrition as we've been talking about and they're going to do respiration as they carry that out so lots of dead material means lots of decomposers carrying out um Decay process which means that they're going to take oxygen out of the water so all these bacteria carrying out respirations they carry out this Decay because they're going to have loads of food to feed on as well so they're going to be able to multiply and grow really quickly and since then we have loads of bacteria doing loads of decomposition they're doing a lot of respiration which means they're taking a load of oxygen out of the water and ultimately that shifts up we create this imbalance where there's not going to be enough oxygen in the water dissolved for large organisms that need a lot of oxygen with every kind of bulb of water like fish frogs and other kind of large organisms amphibians are just going to have to they're just going to die because there's going to be no oxygen left in the water and this process creates what we call dead zones where we've got rivers or lakes or ponds where everything is just dead there is not enough oxygen in the water to support life anymore and we just have this Decay process that continues and obviously this is a serious problem it massively decreases biodiversity in the area it can cause it's causing the death of a local fish species or species that live in these specific environments around places where there weren't previously Fields so there wasn't this runoff before or but as we've kind of expanded and take up more and more land farming this becomes more and more of an issue [Music] foreign [Music] [Music] [Music] foreign plants can't move away or towards as doing as they can't get up and physically move themselves they're not mobile organisms but they can change the way they grow in response to changes in their environment so if it's a movement towards or away from the stimulus that involves the whole organism moving then that is then a taxes if it's something where a plant is obviously just changing the direction of growth towards or away from a stimulus then it's a tropism and in the same way as the other responses the taxes and communities these can help plants increase their chances of survival so for things that plants need again before it was thinking about Predators food and mates going towards resources that they need similar for plants so obviously they need more light because if they have more light they can do more photosynthesis if they have more water minerals obviously they need minerals various minerals for growth and more stability so I'm thinking about roots in the ground so having a greater kind of connection to the soil and therefore holding their own if it's windy if it's very exposed and if they're likely to be pulled up very easily or knocked over very easily and therefore if they're on the ground they would get less light so being able to be supported is very important so we're going to look at how different trophisms can help them achieve this they are directional so they are still directional which is why they are atropism so they either grow towards or away from the stimulus so that's the same thing as before so towards there'll be a positive tropism whereas a way will be a negative tropism but just in case make sure this time we're talking about growth towards the wrong way we're not talking about movement towards or a way because that would suggest the orgasm is physically moving okay so in the same way with taxes the prefix in front of the tropism describes the stimulus that causes it and again remember we can have positive and negative trophisms describing the movement towards or away so we're going to have a look at four examples of plant cell business again most of these if we get to learn because you are going to be given these as examples there aren't many trophic responses in plants so the more you can learn the better you'll be able to identify them and then justify them so the first one is probably the most obvious one those territoryism so photo again that prefix meaning light so we're going to talk about shoots and Roots as separate entities when we talk about this tropism because they often have different responses so shoots are positively phototropic they grow towards the night and that makes sense because they want to maximize the life of synthesis roots are negatively phototropic so they grow away from the line which encourage them to grow down into the ground that makes more sense there are no chloroplasts in groups and they need to grow down because that means that they'll be growing away from the light which suggests they're growing into the soil and that's when they're going to need to grow to get more water and nutrients Etc geotropism sometimes also called gravity tropism so geotropism or gravity tropism is the growth towards or away from the field of gravity or the gravitational pull so sheets are negatively geotrophic or gravitrophic they grow against the gravitational field they make sure they're growing above the ground towards the sky so away from the center of the earth to make sure there's more light because again they need more light but those consists so if you're growing with gravity and you'd be growing into the ground which is not what we want if we are a shoot Roots other than the opposite they are positively geotropic or gravitropic that means they grow down into the ground and the deeper they go the more likely they are to find more water mineral ions and also Roots being sort of deep into the ground helps to stabilize the plant as well so it means it's less likely to fall over get knocked over in high winds it gives this stability so we've got negatively geotrophic geotropic shoots and positively geotrophic roots okay this is probably a new one you may well have heard of the others in when if you talked about plant responses at key stage three but big monotropism is interesting it's talking about mostly feeling inclining plants not all plants can do this but they have the ability to sense touch so when they sense that they're touching an object their shoots or their roots are touching an object the growth of those can be stimulated to change so there are specialized shoots called tendrils you'll have seen these kind of they grow in a spiral and then when they touch something that they could grab onto they are able to sense where that is and grow in the spiral around it so they grow around the object which enables the plant to grip on and use that in order to reach high up and get more light so these plants don't have tall wooden stems like trees that enable them to grow up with really tours straight that they have is they have a race or floppy bendy stem but they kind of grow in this little techno that can kind of creep up and grab onto you've seen things like ivy for example will grow up and grab onto bricks and grow up the front and side of a house that's able to do this because it can grab onto the it can sense where the brick is the kind of kind of growing and around parts of the brickwork hold on to it put out more shoots go up a bit higher do the same go abortions go up probably the same and that makes sense you want to be able to grow up and get more light if you can if you're a shoot if you're a root they tend to grow away from objects to touch so they're negatively stigmotrophic you'll see sometimes if a root grows down and hits a rock it'll turn to the side and carry on growing until it can grow down again it won't try and grow through things if they can't or aren't able to they'll tend to move when grow in the opposite direction through substrate that they can get through and lastly hydrotropism this is another one that kind of makes sense so roots are positively high durotropic so they grow as water inside this helps to make sure that they get enough water even in dry environments so you can see here my roots of my plant are bending towards that cup of water they can sense increased water content in soil or in substrates and they will grow towards it in order to try and maximize the amount of water the plant can get this makes sense so all of these are tropisms because they are all directional and the growth of the plant is changing and his implant responses are controlled by growth factors and we use the term growth factors here but they behave in similarities of hormones so they're hormone-like chemicals they are produced at the tips of roots and shoots in the meristem there's different classes of them and they can travel around the plant in diffusion active transport or even in the vascular tissue if they need to and we've got different groups including auxins gibberellinsic acid E3 IAA is the example we're going to look at which is endo acetic acid and it's an example of an auxin so it's within the group of auxins and it controls your own photo and geotropisms or gravitropisms in both roots and shoots so let's look at photosarapism in shoots first so the way it works is that IAA moves to the more shaded part of the sheet so in this case we've got the Sun moving throughout the daytime and changing direction so the size initial going to come straight down so we have none of the tip is shaded any different to any of the rest of it and then as the sun moves across the sky during the day then we get a shaded side and a sunny side of the sheep tip what happens is the IAA gets moved to the Shaded side and that promotes the growth of cells on that side of the elongation of those cells and so that causes the shoot to bend towards the light because the same illumination is not happening on the sunny side of the shoot so we get that bending that bending the shoe tip towards the direction the light is in so this is obviously a tribalism where positively pressure turbic here we're moving the growth towards to make the growth coming towards the stimulus which is the light okay so moving on to Native Photoshop there's no roots so this is where we're obviously going to be growing away from the light and we've said that roots are negatively photos so they're going to be growing away from the light because so they're going down into the ground so in this case I am moves to the more shaded side of the root still but it inhibits growth so because it inhibits growth on that side the cells on the unshaded side elongate whereas the Shaded side does not and therefore we're going to be bending down and Away in from the direction of the light okay so then if we think about grabbing trophies or geotropism as well it happens in the same way so positive geotropism works in the same way as negative phototropismal Roots because the IAA is going to move to the side that is lowest to the ground or closest to that gravitational pull again it's going to inhibit elongation in those cells whereas the elongation occurs in the sort of the side that's furthest away from the gravitational pull and so then we get that movement down sort of bending down and growing down towards the gravitational pull so that's how the roots kind of go further into the ground so mainly the remembering sort of fact here is to kind of think about where is the Ia going and if it's moving it's always moving to the Shaded side of the side that's pulling down with gravity but in shoots it's promoting the elongation so it will bend towards the light in Roots it's inhibiting elongation so then we Bend oh from the light or we bend down towards gravity so that's the kind of thing to remember so in shoot IAA is causing elongation or promoting elongation in Roots it's inhibiting elongation on that side and therefore the elongation occurs on the opposite side and we get bending away taxis and Kinesis are animal responses to stimuli so first of all responses are still might help to increase chances of survival by helping animals to avoid pretors avoid aimatic stresses and increasing access to resources so avoiding Predators literally just means they can run away or they can move away from an area they can spend more time in someone that's covered or shaded or something so that helps to protect them avoiding abiotic stress by responding to their environment surrounding so they'd be able to detect temperature humidity water availability light and move in accordance to how they need to depending on those factors and then increasing access to resources so get more water get more food go towards where there might be maintenance opportunity because all of these will involve some form of movement thinking about like migrations and things like that happen as well with things like this so they make sure they move to where they know there's going to be more water but what we're talking about here in terms of responses we're going to be talking about some innate responses so all animals have to respond to their environment and so do all plants but we're going to be talking more about innate behavioral responses so taxes and communities than kind of just general behavioral choices so if you remember hopefully from GCSE a change to an internal or an external environment is what we mean by stimulus so there'll be some kind of change and the behavior will need to be altered in response to that and that's going to be their response so in animals obviously animals have motility they can move they are able to move towards or away from favorable or unfavorable conditions they can get us to walk around or they can swim or they can fly and so that's most of what we measure or we're measuring these responses in animals is we're measuring their movement and there's two kind of focuses one is Direction and one is frequency of movement and we'll look at those in a minute in more detail with plants plants can't get up and walk away that's not to say plants don't move or can't move they obviously can move various parts of them and really what we mean by that is that they alter their growth so they can change the direction or the type of growth that's happening at the root tips and tips in order to respond to changes in their own or respond to stimuli they can't physically get up and move their whole organism um but obviously they have methods some things in seed dispersal that can move seeds further away from them and potentially move the seeds to a more favorable environment when that happens but as an individual plant living they can't just get up and move around so that's kind of going to affect the differences between the responses of these two types of organisms we're going to look at animal responses in this video and then we'll move on to your plant responses in the next one okay so in Mobile organisms there are two types of innate responses which help them to survive taxis and Kinesis as we've said sometimes you'll see this word motile or they have motility instead of the word mobile and obviously that just means they can move around they have the ability to move and so we're thinking about anything that can move it's not just going to be animals we're talking about things like swimming bacteria and even it can be the case of individual cells so obviously there are some cells in your body that can move around white blood cells for example are another example that display taxes of some kind because they can move in response to a stimulus so let's have a look at the two different type of responses they are both innate responses and that just means they're not learned so these are responses that you're born with or an animal or an organism is born with it's encoded in their kind of DNA to respond to certain conditions in a certain way when they are detected that doesn't mean to say these aren't necessarily choices but they're going to be ways of behavior that have not been taught by another orders and two they're more or less they've learned it from watching other organisms it would have been ingrained in their DNA and that they would have been born with okay so taxes the taxis is the plural so you have a taxes or the plural is taxis a tactic response is directional so taxes or taxis a taxes is a directional response so the movement has to be in a direction the direction that the stimulus is coming from will determine the direction of the movement in response so if the stimulus needs to be coming from a certain direction or you can be able to tell which direction it's coming from then the response will either be to move towards that stimulus or away from that stimulus and that means that the response is also directional so the stimulus will have to be coming from a certain direction and then the responsibility to move towards it or away from it so the response has a direction if an organ is used on the stimulus that is counted as a positive response by positive taxes if they move away it's a negative response very negative taxes and that's how we describe the direction Kinesis or Kinesis plural is slightly different they are somewhat more random and they are non-directional and this will make a bit more sense when going through some examples but they do not rely on the direction of the stimulus coming from one place it's about the intensity of the stimulus and how it affects the speed of the movement in response so if this is what more examples of things like light if the light can be directional but things like temperature humidity but it can be in the whole environment in an area where it's not going to just be you wouldn't have a temperature coming from a certain direction most likely you'll have hot areas in cooler areas and there'll be a gradient there saying for humidity so they're more likely to be able to follow a gradient of change but there isn't necessarily going to be a direction for them to follow so in those certain conditions High Community low Community high temperature low temperature how intense system this is whether they want to be in that high temperature or want to be in that low temperature will affect how fast their response is and this again will make a bit more sense when you go through examples but basically if you think about it you're moving around in a random motion more often if you're in an area that you don't want to be in that is going to increase your chances of you being able to get out of that area faster so if you move around slower in an area you want to stay in you're less likely to accidentally wander out of that condition okay so let's have an example for taxes so I've got my euglena here which is a single-celled photosynthetic organism so it has the ability to present size it's single celled it's free living it has a flagellum so it is able to swim and move around it has a photoreceptor or an eye spot which allows it to detect light and it demonstrates positive phototaxis which means obviously it moves towards light and this makes logical sense if my torch is shining in this direction the movement of direction will be towards the light it's positive photos axis and this makes sense it has chloroplasts it can photosynthesize so if it's going to move in a direction it's going to move towards light to enable it to carry out more photosynthesis so that's my description of it and my explanation of why that phototaxis and that positive response makes sense then so that's what color with taxes itself identifying it's a taxes because the light is a directional stimulus and also the movement of the organism is in a Direction and it's in response to it and it makes the response make sense we can explain why they will demonstrate that response okay so an example for Kinesis so this is going to be with wood likes I'm going to look at this in a second with the practical but for example we put wood lice in a chamber like a choice chamber that's called where there's two conditions light and dark and you can track their movements so the movement is random it doesn't appear to be in a direction often then we'll just go around around the environment but it's more about their speed and how much time or how long they spend in each condition so you can see here their speed and their amount of turning and their movement is faster in the light than it is in the dark and that makes more sense they are showing it's a random response but the intensity of the light so the light intensity is dictating the speed of the movement so in the light they are moving faster they are moving around more than they are in the dark and that makes sense because if they're moving around slower when they're in the condition that they want to be in or vice versa if they're moving around faster in the condition they don't want to be in then that will allow them to move away and find a condition that's better suited and when they do when they're in the dark they're moving slower because they're in a condition that is better suited to what they need it allows them to make sure they spend more time in conditions where they're able to not lose water so for example woodlice obviously have a solid exoskeleton they can't lose water they need to retain water to make sure it stays in but they also need to respire and open their sphericals so what they want to do is open that in a dark cool moist area in order to be able to not lose water loss and water too much so therefore this explains this Behavior this is the time you're going to be able to hear the responses of invertebrates so things like maggots or wood lice or flatworms especially in the exam questions you're going to get asked as well what we're going to look at an example is looking at taxes in woodlice by putting them into a choice chamber or a choice chamber-like setup where they're going to have different conditions and it'll be monitoring their movement and in theory if they are going to be moving towards or away from a stimulus like we've talked about then we should be able to predict where they're going to end up what conditions they would prefer and that would suggest that they are able to sense those conditions and then move accordingly obviously Roy will repeat this especially with animal behavior experiments or something where you're relying on organisms to do something the more repeats you can do and the better because they're not always going to behave in totally expected ways okay so I am making up my little choice chamber here um I've got four quadrants and that'll make more sense once I put the little in a second but you can see we've got dry here and dry here this will be dry in the dark because when I put the lid on this is covered by the dark green paper and then I've got the light Square here as well and then in these two I've put some kitchen towel and I've just made them wet so it's in kitchen task so it's going to be a damp environment and again I've got a dark this side and light this side put a thin layer of cloth inside the choice chamber for the wood lice to walk on top of so they they're not actively walking on the charcoal or walking on the wet areas okay so I've placed my cloth in and you can see hopefully the price spin it down but there's actually now a gap so there's a gap between the cloth and the lid so there's enough space there for them to walk around on but crucially my kind of surface isn't touching the wet and so it's not going to absorb that water but it's going to be near enough to it that they'll be able to sense the human environment versus the dry environment and then you can see my lines on here and what we'll do is I'll put the wood lice in the center and then put the lid on leave it recording and watch what happens and time it okay so that's me taking off the lid at the end so we can literally see which wood lights are in each quadrant at this point in time recording and making sure that you kind of if you record it and film it at this time and you can kind of be accurate because obviously with the black covering it's kind of hard to tell who is in the black sections so this is a good way of doing it and sort of filming it or taking a picture straight away having someone else to help you to make sure that you can no they're not always going to stop moving and this is one of the Perils of working with moving organisms Okay so we've got our results we move on to the analysis I've drawn a really simple bar graph to help us kind of visualize our results and the null hypothesis for this investigation would be that there'd be no difference in the number of word lice in each section after 10 minutes it's and that's that's what being it's a null hypothesis is always that there is no difference or no change or no relationship so however obviously we can see that there is a slight difference and this is expected because we know from taxes behavior and what would I nice environments they prefer they're going to hopefully directionally move away from light so demonstrate negative photo taxes because they prefer dark damp cool environments so anything that's light and dry they're going to want to move away from and they will demonstrate that behavior it's also likely that the wood lights are going to slow down or spend more time in The Damp areas as dry environments they're more potential water loss they obviously have hard exoskeletons and they need to be able to respond through sphericals and so when they open those they do not want to lose water so if they're in a dry environment that risks losing water so they would spend more time in human environments so being able to sense their environment and we expect them to move to where they will be more comfortable or demonstrate negative photo taxes away from light again because it could be due to predation but also because it means that they would end up in their favorable environment of being dark so in order to test to see if these differences are significant we need to do a statistical test we can't just have on heart say okay yeah look more woodlice went to the dark and damp and therefore they were demonstrating protection photo taxes and they spent more time in the dump than in the dry and so therefore that demonstrates and improves our hypothesis we can't say that this dose of backs up that suggestion unless we do a current Square test in order to prove it and we're doing a chi-square test because we have categorical data they were either in a section or not there was no in between there are sensory receptors and these are specialized cells that can detect stimuli and remember stimuli is just meaning changes in the environment so most can be described as transducers because they convert one form of energy into electrical energy in the form of a nerve impulse so receptors in your ear they detect changes in air vibration so that's the movement of the air so kinetic energy to electrical energy you've got stretch receptors in your muscles and they also detect the movement or stretch or elongation of muscle fibers again kinetical movement energy to electrical energy you've got lots of different types of receptors in your skin most of them respond to things like changes in temperature changes in pressure whether it's light pressure or hard pressure pain again so there's pain such as again hard pressure and these then take those changes in say temperature so thermal energy or movement or pressure energy into electrical energy as well and then lastly your eye hopefully this one's quite an easy one so we have photoreceptors in the back of the eye in the retina and they detect changes in light intensity so making sure we're talking about changes as the stimulus so it's things that change and then how they turn that into an electrical impulse so changes in light intensity generate electrical impulse and we'll learn more about specific types of receptors including some that's found in the skin compressor and the eye as well others detect the presence of chemicals so in your nose and your mouth it works slightly differently so in your nose you have something called olfactory receptors they detect chemicals in the air that you breathe in through your nose and then in your mouth you have receptors in your taste buds and these are both they detect stimuli but it's more that the chemicals bind to The receptors and that causes an electrical impulse to be generated so it works slightly differently it's not responding to a change in a type of energy they are just responding to the fact that a receptor something will bind to those receptors and that will cause the impulse to be triggered so we need to think about and be able to explain how these sort of changes in a stimulus actually then leads to an electrical signal or what we mean here is that the change in ion movement and that change in ion movement create an electrochemical gradient so what we mean is that the main way you describe is potential difference so in the same way we talk about voltage so when there's a potential difference in charge cross the membrane so we've got more positive and more negative either side of the membrane the cell membrane of the neurone then we have a potential difference so that's a voltage and remember charge is carried by ions that can move and so that's that counts as electricity so in this example we've got the cell membrane of a neurone we've got just a small section of it the outside is more positive known has a greater positive charge because there's more positive ions outside and the inside is more negative then it has more negative ions or fewer positive ions inside and so it's about minus 65 millivolts it's the potential difference across this membrane we've got potassium channels sodium channels and then the sodium potassium pump these are obviously all ion channels that are used to allow charged particles to move across the membrane and when we're at resting potential which is where no stimulus is happening this is just the resting state the neuron the sodium channels and the potassium channels are both closed and just the sodium potassium pump is working as normally as it would using some energy to move three sodium ions out for every two potassium ions in so overall we are moving out more positive ions that are being moved in so three sodium are going out two potassium coming in so that gives us and helps us to maintain that overall difference in the membrane where there's more negative inside and more positive outside or we can say more positive outside less positive inside and then that helps us to remember where there's more positive ions okay so then what happens when the stimulus is detected so the first the series starts to happen and its first starts to be detected by The receptors we start creating what we call a generative potential so you'll see here we've gone from minus 65 millivolts to about zero millivolts so that means we've got more positive or we've got less negative and the way that works is that sodium channels are opened somehow by the receptor so there is the stimulus is detected by the receptor and that opens or leads to the opening of sodium channels so more positive ions are coming in so the inside of our neuron cell the inside of the membrane becomes more positive and that's how we get from my 65 up to zero so basically it means that we end up being about the same either side of the membrane and the sodium ions remember have stopped being from being coming in up until this point because their channels were closed so by allowing them in they're just diffusing in down their gradient because there's a lot more of them outside than inside currently so they're just going to diffuse it until we get equal and then we move on to the action potential itself so once we get to a point where with potentially created a large enough stimulus to get over the threshold value so the threshold the generated potential has to be high enough and there has to be enough depolarization to get above the threshold value which if we got to zero we definitely would and you can see the threshold on the graph down the bottom right so if we reach this stimulus of the threshold potential because the stimulus is strong enough and then enough depolarization of the membrane has happened then even more sodium channels will open and even more sodium will diffuse in sometimes we say it's an influx sodium because it just means that there's monitorium ions coming in to the cell the nerve cell so that means our membrane potential has passed the threshold level even more sodium channels open the membrane depolarizes even further and then what happens is those sodium ions diffuse across they diffuse to the right or to the left depending on which way the signal is traveling they all diffuse along inside the cytoplasm of the cell and create generator potentials further down by making the membrane potential depolarize as it goes down the later on and we'll look at that in a bit more detail when we look at nerve structure and how that happens but the point is is that once this action has started if the threshold value is met it just goes we can't stop it at that point so then we have to re-polarize so we have to return back to our resting potential by re-polarizing the membrane which basically just means excessive positive ions are removed and we get back down to being down below about minus 50 minus 65. and we've gone from plus 40 at this point so we've had such an influx of sodium during the action potential that we've gone all the way to plus 40 millivolts very very very very very positive and now we need to get back to minus 65. so to do that we have to open the potassium channels and we close the sodium channels so we don't let them diffuse back in and the sodium potassium pump gets back to work putting out three sodium ions for every two potassium ions that are coming in and then the potassium ions are also able to diffuse out of their own channels down the diffusion gradient so they're able to just leave so in total that means we're kind of pumping out and diffusing out more positive ions than we are keeping and so that works to eventually make our membrane potential go back down to about minus 65. and the important thing is to know obviously the sodium channels are closed so at the peak of the action potential around three on the graph down the bottom the sodium channels will close and the potassium channels will open and then that will allow us to start getting back to resting potential okay so this is something we have to learn this sequence this order we need to know how resting potential is maintained through the sodium potassium pump and Which ion channels are open and closed and for each stage would be able to describe what happens and this graph you might be able to match it to the graph or you might need to look at it as the diagram sometimes I've seen it as a table where you've got open closed open close depending on which ION channel you're talking about or it could be the membrane potential numbers so if y65 0 Plus 14. but the other thing to know is that this action potential is an All or Nothing response so it's the same size it always goes from about minus 65 to plus 40. it's never any higher than plus 14 and then it goes back down again and always threshold there's no stopping it if such will travel along the neuron if the stimulus is too weak and we don't reach the threshold it won't happen so it is either it will happen because the threshold has been reached or the signals too weak it will not happen there isn't an in-between and there isn't kind of a stronger action potential or a weaker action potential there is no such thing as that they're always the same in terms of the change in membrane potential it's just about whether or not the threshold is reached by the generator potential and if it is great then an actual potential happens if it's not then the membrane potential just goes back down to resting potential and we don't have an actual potential traveling along the nerve cell did we look at the Brazilian corpusal this one is found in the skin quite deep in the skin and also in some joints as well it's a mechanoreceptor which is another way of saying it responds to movement or kinetic energy like we said and it's attached to a single sensory neuron which will then link up and join up with others potentially to pass on the signal we have the neuron on the nerve ending at the center of this kind of world of layers of connective tissue they're called lamella we've seen the word lamella before it's just to use a word used to describe layers of things there's gel between those layers as well which helps with the transport of ions and then on the actual kind of micrograph you can see at the bottom you can kind of see these little dots they kind of look like nuclei but these aren't individual cells they're kind of they're called fibroblasts they are parts that are secreting these connective tissue layers at micrograph that is a cross section and you'll see that the outermost layer lays very thick and darker than the others that is sometimes called the capsule so they're very outermost layer of obsidian cup so it's called the capsule and then this is quite circular this image because actually this is a cross section so that very very central part is the axon that's been sort of cut through a pressure stimulus pushes on the Novelle which deforms the membrane of the sensory neuron so you can see I've gone redraw my diagram with these layers that have been pushed down to form pressed down which is what happens when the pressure is applied and this opens stretch mediated sodium ion channels which is basically saying that when the membrane is pushed that physical kind of pushing pressing moving of the membrane stretching of the membrane literally when it's stretched they kind of push open or pull open those sodium ion channels and that's how they open so that force is going to physically open sodium ion channels which causes the influx of sodium ions and they sort of push they rush into the cytoplasm of the neuron cell that acts on in the middle so at that point where it is depressed that is going to cause depolarization of the membrane and then hopefully a generator potential and the greater the pressure so the more areas of these lamine that are pressed down and pushed down the more membrane is going to gonna get deformed and stretched the more sodium channels will open and that makes sense because if you're going to deform more memory or push or stretch more membrane more of the channels will be pushed or pulled open and therefore you can get more sodium coming in which means we're more likely to get a thresh meet the threshold potential and cause an action potential and if an action potential is then generated the impulse is going to move down the neuron in this where it's got it in this direction here so down and away from the receptor and then it will drone up and link up and that signal will be received as pressure okay so today we're going to look at visual receptors so many organisms across the kingdoms have photoreceptors to detect light and in most cases they're found in some sort of eye or an ice spot so we're going to look at the human eye the furniture receptors in your eye can be considered transducers because they are converting light energy into electrical energies when light enters the eye it passes through the pupil through the lens all the way through the eyeball and hits the back of the eye which is obviously the retina it doesn't stop when it hits that first layer of the retina but it carries on through that layer until it hits the photoreceptors which are at the back I'll show you with an arrow in a second so that's the optic nerve at the front all those bundles of nerves that join up to be the optic nerve so it's going to pass over or through that past that past all of these nerve neurons to the very back where you've got the ends of all of these photoreceptor cells so the light passes all the way through this and goes when we say to the back of the eye we don't mean it just hits the retina it hits all the way to the back of the retina as well and that's where we have the light detecting the pigments that are in these photoreceptor cells so that's where the light gets absorbed so the two types of photoreceptors we have are both rods and cones so you see in this diagram where it cones are red and my rods are blue so these are photoreceptors in that sort of end part the kind of long cylindrical part of the end of their cell that's where the pigments are the light when it hits those pigments causes a chemical change and Alters membrane capability to sodium ions if that generative potential is high enough if enough light hits the nerve cells then we'll create the threshold potential and then that impulse is going to be sent along the bipolar neuron and then to a ganglion cell and then to the optic nerve so we've got our rods and our cones if you follow them down they're attached to either these blue or sort of red orangey bipolar bronze so they're the cells that directly attach to the photoreceptors and that's the Gene and that electrical impulse is going to take in order to send that electrical impulse to the brain for our body to be register that we've detected light and turn that into images okay so we need to know in detail the two types of photoreceptors that we can find in the retina so rods and cones are the two options that we have rods are mostly found around the retinal edges and the cones are found closely densely packed together in the fobia rods contain rhodopsin which is the photosynthetic pigment that they have in the sort of pointy parts and part of those cells cones contain a different type of iodopsin red green or blue wavelength sensitive so it detects that wavelength colored wavelength of light so you have red kinds green cones and glucose rods because they only can change rhodopsin they only detect what we say monochromatic Vision otherwise sort of known as black or white Vision so shades of light and dark and Grays whereas the cones allow us to have our colored Vision our trichromatic vision the different wavements detected red green blue can mix and blend together so if red and green cones are stimulated because the wavelength of light is yellow and that crosses over into both red and green wavelengths then the brain will detect that as yellow this is one of the structural things so there are many rods multiple rods joined to one bipolar neuron they share in cones each can is connected to just one bipolar neuron because many rods share about bipolar neuron they have low visual Acuity so it means that they cannot separate light from close objects that bounces off those rods or object is detected by those rods the light because they can't continue as separate objects because all three of those rods are very close together but they only share one neuron so they can only produce one action potential between them cones are the opposite because each cone has its own bipolar neuron they are able to detect light from two close together objects and see them as separate objects allow you to see them as separate objects because they can send individual Action potentials for each object even though they're close together this is what we call Visual accuracy so your ability to see kind of in high resolution in a similar way to light microscopes rods give us High light sensitivity because all three of those rods can detect the low light intensities they can combine their weak Action potentials or their weak signals into that one bipolineuron which will be enough to trigger an action potential this is known as summation low light sensitivity is what happens with codes they don't aren't able to detect really sort of low levels of light because they don't have any subnation so when light intensity hits it it can't amplify the signal if it's a low light intensity because it can't combine signals to join to one by polynomial because there's only one attached to it control of heart rate and we're going to focus on Barrow and chemo receptors the main part that you will be familiar with is the central nervous system the CNS so that's made up of the brain and the spinal cord we have our central nervous system and then we have our peripheral nervous system your peripheral nervous system is then split up into the autonomic and somatic nervous systems in the autonomic nervous system we Branch out again into two separate systems one is the sympathetic nervous system and one is the parasympathetic nervous system so sympathetic is active when the body is stressed so for example it is responsible for part of the fact or flight response and so for our example because we're looking at heart rate that part of the nervous system is going to be responsible for increasing heart rate parasympathetic nervous system then does the opposite okay so sympathetic and the para is the opposite so this is active when the body is at rest and calm okay so the parasympathetic nervous system works to slow things down and in this case in our example it's going to decrease heart rate so if our stimulus is that the stretch receptors of the barrel receptors have detected high blood pressure then the impulse is sent to the medulla are going to say we need to reduce the heart rate and then the medulla is going to respond with after it's coordinated this response by sending parasympathetic nerve impulses to release noradrenaline at the cyanole node that's in the right atrium and as we said they'll be using the parasympathetic nerve or the vagus nerve to do this and that's going to release that inhibitory neurotransmitted neurodrenaline which is going to decrease the frequency of impulses from the cyanoatrial node and then that's going to decrease the frequency the impulses go into the AVN or the H of ventricular node and so they're going to decrease the heart rate okay so if we think about the opposite then low blood pressure happens so that's detected Again by The receptors the impulses are sent to the Madonna again this time saying to increase the heart rate and then we have the same response to the Madonna is going to use the sympathetic nerve this time to send impulses and release acetylcholine at the sign of atrial node in the right atrium and because it's releasing acetylcholine that's an excitatory neurotransmitter so it's going to be increasing the frequency of impulses leaving the sinum atrial node and therefore we're going to increase the frequency of impulses going to the atrioventricular node and therefore we're going to increase heart rate why is this important why is it useful well it's useful because it's going to prevent things like fainting so if your blood pressure suddenly drops then your your wouldn't be getting enough oxygen to your brain and that's obviously a bad thing and can cause you to pass out or faint and so in order to remedy this we can increase our heart rate in order to try and prevent that from happening most of the time this is going to happen when you've got exercise occurring because you've got increased rates of respiration which means we need more oxygen going to our muscles and we've got more carbon dioxide being produced that needs to be removed so it could be building up and causing that carbonic acid to increase which will lower the ph or obviously we've got low oxygen levels because a lot of it's being used up so if that is detected by these chemoreceptors then we're going to send impulses again to the Madonna organ to increase the heart rate the medulla is going to use the sympathetic nerve to send impulses and release acetylcholine again at the cyanoatrial node in the right atrium again we're using acetylcholine so that's an excitatory neurotransmitter which is why with its results in a speeding up of the impulses and again we're saying to the cytometrial node is going to increase the frequency of impulses that are sent to the avian and therefore we increase heart rate we increase heart rate we increase blood flow to the lungs which means a lot of oxygen levels can increase but also it helps to remove the excess carbon dioxide so this is a slightly different picture of a neuron we can see the cell body in a bit more detail they have lots of mitochondria and lots of ribosomes because they do a lot of active transport and movement of ions so obviously the active transport of sodium potassium pump needs 80 feet in order to carry out that active transport the membrane then is adapted because the cell membrane around the cell body and all along the axon is going to have lots of iron channels as well and they're very long so they've got this long stretched out thin axon and also they need that to carry impulses over long distances this diagram has the myelin sheath on the axon and so these are special cells or special sections made up of cells and they actually insulate the axon so about a third of all peripheral neurons are myelinated myelin is just made up of layers of Highly lipid Rich membrane that is released from these cells called Schwann cells and they I've got an example at the top so they kind of wrap around they produce the myelin and it wraps around spirals around this axon in layers and so then we get layers and layers of layers of that membrane built up and it wraps tightly around the axon and what it does is it actually insulates the membrane so if that means it acts like an electrical insulator so there are gaps between these areas of Mind sheath or between these Schwann cells and they are called the nodes of ranvier and that's what he named after a French person who discovered it and these gaps are important because it's where Action potentials actually occur because if the Schwann cells are insulating that means there's no iron movement where they are covering the axon so no sodium ions can move in around and so therefore we've got no depolarization so depolarization can only happen at the gaps at the nodes of Rabia where there's a concentration of sodium ion channels and so that allows the impulse to actually travel quite fast along the neuron and these are kind of adaptations to increasing the speed of impulses along the neuron okay so this is an action potential graph and we need to make sure we can describe what's happening at each point and explain what's happening at each point as well so at point one when we see the membrane potential start to rise above resting potential is because it's stimulus has been detected so the sodium ion channels are going to open and the membranes can become more permeable to sodium so the sodium ions will start to diffuse into the axon and into the neuron and so that's going to start making our membrane potential less negative or more positive whichever way around you want to say it then we get to part two so if that generated potential so that influx of sodium ions that causes our membrane potential just becomes slightly less negative or more positive is large enough and hits that threshold level of about -55 millivolts then we've reached a point where we can make an action potential trigger an action potential because we've hit that threshold and that's because what happens if we get to that voltage of that minus 55 as I said the voltage-gated sodium channels are going to open so the sodium ion channels that are triggered to open when a certain voltage is reached so in this case minus 55 they will open and so more sodium ions are going to rush into the cell into the neuron and that's going to cause us to trigger depolarization where we get rapidly more positive inside the cell so our membrane potential has got all the way up to about almost plus 40 millivolts now so part three is where we then transition from depolarization to repolarization so remember every action potential will hit the same level so we'll hit the same about plus 40 millivolts and then the sodium ion channels are going to close and the potassium channels are going to open and this allows us to make the membrane impermeable to sodium ions and more permeable to the potassium ions so they will diffuse out down their concentration gradient and allow us to bring that membrane potential back down more negative back down to the resting potential now we have something called hyperpolarization so you can see here at point four our membrane potential actually dips below the resting potential it goes a bit more negative than we would expect and that's um because the potassium channels close but they tend to close quite slowly and so what happens is too many potassium ions diffuse out of the cell so the membrane becomes a bit more negative than resting potential because we've lost two Humanity too many positive ions and so we go into what's called hyperpolarization so we go the opposite way to depolarization and that's okay it can be fixed and it's quite normal and so that kind of delay in going past resting potential and coming back up to resting potential is a good thing and it's partly what helps us to stop more action potentials from happening too quickly after one is finished and all that that we've because I've looked at from about 0.3 all the way to 0.4 so between that four to six millisecond time limit that's what we call the refractory period so this idea that sodium ion channels are closed and we have this time delay before another actual potential can start because another one cannot be triggered in this time window because this already my channels are closed because we've got hyper polarization happening it allows us to kind of create a separation between Action potentials so then we get back to 0.5 so we've returned then our membrane potentials returned to resting potential so the sodium ion channels are closed the potassium channels are open and the sodium potassium pump is doing its job and working to maintain that approximately minus 65 millivolt resting potential by making sure that more positive ions are going out so three sodium ions for every two potassium in and that keeps us in that nice negative resting potential that we need okay you need to be able to talk about a wave of depolarization and how that act one action potential isn't going to create a response to you to create multiple Action potentials that move along the axon of the neuron as a wave so the stimulus gets detected at one end of the neuron and then we have to change from resting potential which will be occurring across the whole of the axon and we have to create this wave of depolarization where we kind of a wave of action potentials that move along the axon body away from the stimulus so once an action potential is triggered those sodium ions that are diffusing in because of that action potential and that leads to that action touch being created once those sodium ion channels are closed they are going to diffuse down the concentration gradient along the axon and in this case it's going to be to the right this is because they cannot diffuse back to the left because once an action potential has happened we have that what we call we've just talked about the refractory period we have that repolarization stage where the sodium ion channels are closed and so we can't go backwards so they will diffuse to the right and then they move along and because they refuse to the right they start to trigger the action potential along the neuron in the next section so they start to depolarize it they cause a generator potential which reaches the threshold potential and then more sodium ion channels open again more sodium floods in and we get an action potential and so this refractory period of time is where an action potential can't be triggered because the sodium ion channels are closed and it acts as this time delay to make sure that we only move this wave of depolarization in One Direction away from the stimulus and towards the other end of the neuron okay so there are a couple of factors that can affect the speed of this impulse conduction the action potentials can only happen at the nodes around here in a myelinator neuron so we have an action potential at where a node is the ions will have to diffuse through the inside and then another actual potential will happen at that node diffuse across another action potential will happen at that node the ions diffuse across inside underneath the Schwann cell and then we get another action potential in each node this is known as saltatory conduction and it's very very fast so because you're only having to have few Action potentials happening at each node you're not having to have a weighing of action potentials moving along every single little piece of the neuron membrane as you go the second is axon diameter so literally the diameter how wide is the axon of this neuron so large diameters action potentials travel faster because there's less resistance to the flow of ions so ions can reach parts of the membrane faster and depolarize them faster and cause a continuous wave of actual potentials if you've got a wider axon diameter which is great and very helpful so that's one thing that can affect the speed of transmission is how wide the axon is and then lastly temperature ions are moving in order for this signal to be transmitted we're relying on diffusion as well as active transport and those things are going to happen faster because the ions are going to be able to move faster at higher temperatures because they have more kinetic energy so that increases the speed however same with anything to do with temperature and proteins if we get to 40 degrees or above then the protein channels are going to start to denature and that's also going to decrease the speed of transmission so synapse is the term we use for the junction between two neurons or a neuron and an effector we have our axon and so that would be the pre-synaptic neuron it contains the vesicles of neurotransmitter so imagine our impulse is coming down the axon here and it's reaching the pre-synaptic neuron the synapse is the gap in the middle so our postsynaptic neuron has The receptors for the neurotransmitter on it those receptors are actually on sodium ion channels you can see there where the orange dots are attaching to the top of the sodium ion Channel and that's where the receptors are so The receptors aren't on the membrane and then the sodium ion channels are separate they are one and the same so the actual gap between the pre and postsynaptic neurons or the membrane edges is called the synaptic cleft on the pre-synaptic neuron we have calcium ion channels they are voltage-gative channels which means they respond to changes in membrane potential whereas the sodium ion channels are ligandicated the presynaptic bulb there'll be lots of mitochondria in there and because we're going to need to make these vesicles full of neurotransmitter we need a large smooth endoplasmic reticulum what's important here and it will come up in questions is they will ask you to explain how the structure of a synapse allows one-way transmission and it's to do with the fact that that only the pre-synaptic contains the neurotransmitter and only postsynaptic contains the receptors so this is going to be important in a question where it says how does the how does it ensure one-way transmission so how do we know that it'll always go in the direction we've said so this way and how old I wouldn't go back well that's because if you can only make neurotransmitter one side and you only have The receptors the other side if the neurotransmitter diffuses this way it doesn't matter there's no receptors there so nothing's going to happen so only if the diffusion of the neurotransmitter happens in this direction will it find a receptor and therefore cause an impulse and it will only cause an Impulse to be generated in this neuron the post active one not the presynaptic one first step is that an action potential must arrive at the pre-synaptic bulb and that causes depolarization of the membrane in this part of the neural the change the depolarization caused by that action potential arriving causes the voltage-gated calcium ion channels to open and therefore calcium iron Childs diffuse in to the pre-synaptic bulb so this influx of calcium ions we say influx that just means lots of them coming in at once causes the vesicles that are sat there ready to go containing the acetylcholine to move and fuse with the presynaptic membrane so they're going to move down to the edge of the membrane that is opposite the postsynaptic membrane they're going to fuse and release their neurotransmitter which is obviously a form of exocytosis and this requires ATP so the acetylcholine I've used ACH here as an abbreviation the acetylcholine is released into the synopsy clever by exocytosis as we said that will be one of the processes that requires ATP here the acetylcholine then diffuses across the cleft so up until this point we've had ions moving in this electrical signal when we get to the synapse we now have a chemical diffusing across a gap and that is a bit slower it can take a little bit longer so that diffusion the point where we have to wait for the chemical to diffuse across the Gap and to bind to The receptors is the only sort of part of this that causes a slight delay in the transmitting of the response between the two neurons okay so once that acetylcholine is diffused across the Gap it's going to bind to the receptor sites that are on the sodium ion channels on the post-synaptic membrane and it causes them to open so previously we have the change in voltage or potential difference because of the membrane potential changing that opened the calcium channels now we are having a receptor binding to that chemical binding to a receptor on the ion channels that's causing it to open once those channels are obviously open same thing as before we said there's an influx of ions so sodium ions can now enter the postsynaptic neuron and therefore cause depolarization just like it does and when we talk about an action potential being generated along the rest of the neuron body once we've got sodium ions moving in if that causes the threshold potential to be really reached if we dependerize the membrane enough then an action potential will then be triggered and it will move along the neuron keep being this influx of sodium ions until that neurotransmitter is removed from the synaptic clay there is an enzyme called acetylcholine esterase found on the membranes in and around the synaptic cleft and so what that does is it actually breaks down acetylcholine and then the two products are then reabsorbed by the pre-synaptic neuron and then they can be used to remake acetylcholine and stored in those vesicles again so it breaks it down into ethanoic acid and choline or acetic acid in choline and those two are then actively transported back in to the presynaptic neuron and what it'll do is it basically rejoins them back again to make acetylcholine and stores it in these so it gets recycled but most importantly it gets removed so there isn't this buildup of acetyl cone in the synaptic cleft spatial summation as it suggests is to do with physical space so in this case there are three different synapses because we've got three neurons junctioning onto one of the neuron so similar to what we were talking about with the rods so this allows weak stimuli signals to be detected so it's where two or more pre-synaptic neurons release a small amount of neurotransmitter at the same time onto the same cosynaptic neuron so we've got three presynaptic neurons they're all junctioning onto one postsynaptic neuron and so they will all release neurotransmitter a small amount if their signals are weak but there'll be enough neurotransmitter then in a synaptic flat to trigger an action potential in the postsynaptic neuron sort of temporal summation temporal meaning time so we have this idea that actually we've only got one presynaptic and one postsynaptic neuron but this is aware larger or intense stimuli can be detected so it's where two or more nerve impulses or action potentials arrive in quick succession from the same pre-synaptic neuron so it's about an increased frequency of action potentials coming down one pre-synaptic neuron so the larger or more in terms of the stimulus the greater the frequency of action potentials so that means more neurotransmitters will be released within a short time of each other so each impulse will release neurotransmitter and it builds up builds up builds up in the synaptic cleft and it makes it much more likely that then an action potential will be generated straight away in the postsynaptic neuron so we've got spatial more than one pre-synaptic neuron junctioning onto one cosynaptic neuron and then we have temporal which is about the frequency of those potentials coming down and therefore increasing the strength of the signal and increase the chances of an action potential so we're going to look at the neuromuscular Junction which is basically the synapse between a motor neuron and a muscle fiber so we're going to look at how we get that action potential coming from the motor neuron how it crosses that Junction the gap between the neuron and the muscle fiber and then how that starts to lead to a contraction so the synapse is actually between the end of a neuron so the synaptic end and the sarcolemma of the muscle fiber so that is here and you can see I've got sort of multiple acts on branches coming out with one muscle fiber and you can kind of see all of the structures we looked at in the last video so we've got the sarcoma around the outside we've got the sarcophasic reticulum in sort of blue green covering around the outside of the microl and then we have those tubules that we spoke about which is the infolding of this sarcolm and then we're going to make these tubes that go all the way down and around the myofibril so this time instead of initiating another action potential as if it would if it was a synapse with another neuron what actually happens is the signal passes across the synapse and it causes the muscle fiber to contract so that's the aim here we're not aiming to cause an interaction potential we're aiming to cause a contraction okay so you've got kind of closer up picture of an axon terminal kind of the actual neuromuscular Junction now which looks sort of similar to what we've seen when we looked at the synapse diagram previously and we're kind of comparing this to a codologenic synapse remember that's one that uses acetylcholine and initially they've had burst stages are exactly the same so an action potential arrives at the part of the axon just above the synapse and the pre-synaptic neuron and it causes the change in membrane potential and that causes the influx of the calcium ions to come into the presynaptic neuron which causes the release of the acetylcholine that's in those vesicles and they fuse with the edge of the membrane of the pre-synaptic neuron and release their contents by exocytosis into the synaptic cleft so all of that is exactly the same as how we described an action potential arriving at cholinogenic synapse it's just what happens afterwards so we're just mostly looking at the differences in the post-synaptic membrane and what happens there because we've not just got another neuron and it's a little bit more complicated so in the same ways before the acetylcholine is going to diffuse across the synaptic left and it's going to bind to receptors so this time you'll notice there are folds in the cycle level so it's not just like a smooth straight surface there's lots of folds and all of the receptors are within kind of the membrane on those Folds this opens sodium Channel sodium ion channels in the cycle so that part is also the same except obviously those sodium ion channels are in the sarcolemma this time not in the membrane and then the sodium ions n to the sarcolemma and depolarize it so it does depolarize the membrane in the same way but instead of sort of moving through and down kind of a narrow axon what actually happens is the wave of depolarization spreads along the cycle level goes along the supplement and then it goes down the T tubules to get to sort of the outside of that muscle fiber and you can see that the tea tubules then come into contact with the sarcoplasma reticulum and you can see the calcium ions there so that is where we're trying to take that change in membrane potential and that depolarization of the sarcoplasm then around the muscle fiber and around the sarcoplasmic reticulum is going to trigger the release of those calcium ions from the sarcophantic particular which are going to move down into the myofibril and that is what will trigger the muscle contraction so mostly it's the same as what we've looked at before with the synapse but we have to think about what where words were using the language so we're talking about the sarcolemma instead of talking headers out the postsynaptic membrane and we're talking about the weight of depolarization spreading along the cyclamma and then down the two tubules into the muscle fiber and then triggering the release of calcium ions from the sarcoplasmic reticulate all of that is new and different from one look to just the normal regular site Maps looking at muscle structure you've got your muscle which is your actual big skeletal muscle and then that is split up into muscle fibers and these muscle fibers are sort of long cells or bundles of long cells they've all been joined together and the cells are effectively very very specialized and they have all joined together end-to-end to create these really long muscle fibers and then within those they have organelles that are again very specialized called myofibrils so the idea of a smaller narrower fiber inside the bigger muscle fiber this is a section of a muscle fiber at the top here we have the synapse with the motor neuron which is sometimes also called the neuromuscular Junction this is one of the points where obviously the axon terminals so we've got the axon of the emotional and actually joins to the muscle fiber so it's how we get that kind of signal from the electrical impulse crossing over into the muscle fiber we have lots of mitochondria and they are inside the muscle fiber inside the cell just the same as they're called being a normal cell but obviously you need lots of them in this case because they're going to provide the ATP that we need for muscle contraction they are sat in and around the sarcoplasm which is basically the same as the cytoplasm the sarca Lemma again Sarco that prefix it's just the cell membrane goes around this specialized muscle cell the sarcoplasmic reticulum its role is very important with muscle contraction because it stores and releases the calcium ions that we need in order to do muscle contraction the t-tubule is the t-shirt for transverse so it's the transverse tubules they are in folds in the membrane that are tubes of membrane that come down into the cell and they bring or allow the transmission of that impulse down into the muscle fiber so they allow or allow the travel of the depolarization down into and close to the myofibril so they allow the passing through of that electrical impulse through the muscle cell and then lastly we have the Mario fabric so this is an organelle and it's right it is a type of sort of even smaller fiber but there's many of these within one muscle fiber they are cylindrical long organelles and they're highly specialized and they're made up or they contain the proteins actin and myosin which are going to allow the whole of this muscle fiber and therefore the whole muscle to contract they are the contractual units of the muscle so these myofibrils are split into repeating sections which are known as sarcomas and you can see there's one of these sections up here and the myofibril has repeating units of these cause alchemers and weeds and also know the structure of that as well we've got the Z discs they denote the ends of the sacrament so one sarcomere goes from Z disc to Z disc then we have this section called the eye band sometimes called the light band because it contains only actin so you have one of those either side obviously and so then in the Middle where you can see the myosin and the actin overlap this is known as the a band it's also known as the dark band so you've got the dark a band and you've got the light eye bands and also they repeat so it goes Light Dark Light Dark Light Dark that gives you that stripy or striated pattern that gives this muscle this kind of striped appearance So within the a band so although this band is dark there is a slightly lighter area in the middle called the H Zone that is where obviously you can see here there's no acting it's just myosin so that means it's although it's still darker than the eye band it's slightly lighter or a lighter patch in the middle of the a band because there's only myosin present there and then in the middle you can see these orange kind of sections here sort of generating where the middle of the uh the myosin filament is that is sort of a dark line in the middle of the age so which is known as the M line it just denotes the middle of the center of the sarcomere so they're actually two types of skeletal muscle fiber as well so there's a slow twitch and fast twitch muscle fibers different muscles will have different proportions of slow twitch and fast twitch fibers depending on what those muscles are used for slow twitch fibers are darker in color and they're darker red because they contain more myoglobin and myoglobin is a protein that enables the muscle to store or bind to oxygen Advanced twitch five they are lighter in color and they don't have as much mind maybe they have less myoglobin and instead they have more glycogen because they are going to have only predominantly doing anaerobic respiration the slow twitch fibers they contract slowly but they are slow to fatigue or get tired the fast which fibers do they say on the tin they are fast so they are for fast rapid quick contractions that they can get tired very quickly the slow twitch five is because they contract slowly but they don't get tired over a long period of time they're used for long distance running or things like the muscles in your back that are used to help you maintain posture for you to stand upright fast twitch fibers are for short bursts of speed or power so sprinting moving your eyes really quickly the pupil reactions for example sharp movements that's what we need the fast switch fibers for so we need the power quickly but we're not going to be doing this movement repeatedly over a long period of time or if you do it starts to hurt or get cramped because the muscle becomes fatigued the reason the slow twitch fibers are good and designed for their purpose is because they release energy slowly using aerobic respiration but as long as there's enough oxygen to maintain that obviously they can keep doing that over a long period of time the opposite is then tree for fast twitch they use anaerobic respiration because that releases energy faster think about respiration anaerobic respiration is just going through the process of glycolysis it's not going through the whole of the aerobic respiration equations so it's just quicker and faster to just do glycolysis and just release that small amount of ATP but fast but obviously over a period of time we're going to build up more of that lactic acid which is going to cause us to get fatigued so in order to do their job the slow twitch muscle fibers remember these are specialized cells they have lots of mitochondria to provide the ATP we need for doing the contractions over time and also lots of blood vessels to reduce the diffusion distance for gas exchange so making sure that we've got that good blood supply shortening that diffusion distance maintaining that concentration gradient to make sure we've got constants deprived oxygen to allow us to do the aerobic respiration in the fast twitch fibers they do not need as many mitochondria or blood vessels because they're doing anaerobic respiration which occurs in the cytoplasm or in this case the sarcoplasm and not in mitochondria and also there's therefore less oxygen needed as well we don't need as many mitochondria but they need some because they will need to carry out other energy requiring processes but they are not carrying out the majority of their respiration aerobically most of it is anaerobic we need to look at how the style command shortens and what we can tell from the structures how it looks once it's contracted the active elements slide over like this they get pulled towards a bit of a slider but both sides would move at the same time if we're looking at the real thing so we need to be able to once that has happened once that contractions happen and those acting filaments have slid over how can we tell that this is a contracted sacrament so the first thing is to look at the eye bands so the eye bands have become narrower remember that's the light band that's the region that just contains the actin and it would be either side of the Z disk and also the H Zone that has also become narrower so that zone in the middle that was just myosin only has now shrunk very very small because the actin has moved over it so we've got narrower eye bands and a narrower age Zone that have been caused by the acting sliding over them icing next we need to look at the Z discs so the Z discs have got closer together so as that acting has been pulled across the mice into the middle the Z discs which is the sort of The Binding point the joining point for the end of those actin molecules has been cooled as well so the Z distance together so the distance between them has got shorter the whole sarcomere has shortened and we can show that and then lastly we need to look at the a band so the a band is the thing that does not change it does not get smaller it doesn't get bigger it stays exactly the same and that's because the a band is where the myosin is it's made mostly of where the myosin and the actin overlap and although the acting have moved the myosin has not moved so where the actin and myosin are crossing over is staying the same so the a band does not change because the myosin does not move in this sliding filament theory only the actin slides over the myosin so as I said this happens in every Star come here the whole length of a myofibril every single cell command contracts at the same time acting as fold inwards and so the whole of the myofibril will contract because all of its sarcomeres are contracted and that happens in every myofibril and so that happens in every muscles fiber which then causes the whole muscle to contract and then the same thing happens when it relaxes so when they relax and they move back to their relaxed State then we're going to get the whole muscle relaxing as well because all the sarcomeres in all of the right Vehicles will also relax okay so this is the actual muscle contraction process and you might see it look very similar in diagrams in textbooks or you might see it as a diagram in a question and we just need to be able to talk through what's happening in these stages and then maybe we have to say what might happen if one of these stages was stopped or couldn't progress so the first things to think about is that the calcium ions are going to diffuse into the mind if you go from the sarcoplasmic reticulum as we just said and they will have been triggered by that depolarization of the supplement and the teachables and cause that release then the calcium ions are going to bind and cause the tropomyosin to move exposing The Binding sites on the actin so they're going to bind there they're going to move cause a sort of a shape change which is going to expose those binding sites that allows the myosin heads on the myosin filaments above and below attached to those binding sites and for what we call an actin myosin cross Bridge sometimes you can just refer to it as a cross Bridge energy that's been stored in the head will say how that's happened in a second so you could always start by saying there is energy stored in the head if you want to but that energy that's stored in the head you'll see we've got ADP and Pi there it's used to bend the head okay like we said it has that ability to move on that hidden shape and it pulls the acting filament along okay and that ADP and Pi are then released this movement is known as the power stroke and it pulls the actin filament along the top of the myosin a new ATP molecule comes because we've released our ADP and Pi that we've clearly are left over from ATP hydrolysis from before so now a new 80 the molecule is going to attach to the myosin head and causes it to detach for the actin binding site so the joining or The Binding of ATP the myosin head causes the head to detach from the actin so the crossbridge is broken the hydrolysis of that ATP to ADP and Pi by ATP Ace enzyme or however you refer to this enzyme in your spec but ntpase enzyme is is normally good enough provides the energy you need to re-cock the myosin head that means to kind of push it back down ready to go again it's already detached but it needs to lay back down and it's stored the energy then like a spring being pulled back okay it's ready to come back up and move back up and bind to The Binding site so it's gone back to its original position and it's got that stored energy in the form of ADP NPI kind of stored there ready to go again and this can go round and round and round in Cycles okay so speaking of energy and ATP each muscle fiber only contains about enough ATP to allow for about one to two seconds of contraction which obviously isn't very long especially if you're doing running long distance running or anything that requires you to move quite a long time so during the exercise the muscles must have a constant Supply which can come from a couple of different places obviously the main one aerobic respiration so most ATP in muscles is generated via oxidative phosphorylation in the mitochondria of the muscle cells and remember these are the muscle fibers when we're talking about the fast twitch in the slow twitch muscle fibers so specifically so for which muscle fibers are going to be doing a lot of aerobic respiration so that is where their ATP is going to come from fast twitch fibers so anaerobic respiration is going to be happening as well so ATP can be made readily by glycolysis in the sarcoplasm so remember that's not happening in the mitochondria that's why those fast twitch fibers don't really have as many mitochondria this is useful for the short periods of intense exercise so we'll get you enough ATP to give you enough of a power boost for a short period of time but the muscles are going to tie yeah after a while because the pyruvate is being fermented to lactate or lactic acid which builds up and that's going to cause your muscles to get tired and ache and that's going to be a problem so you're only able to do that for a short amount of time there is another store um of a chemical called phosphocreatine and it is stored in muscle cells because it can rapidly provide phosphate which helps to produce ATP so ADB plus the phosphocreatine it gives us ATP plus a chemical called creatine so it basically just separates the phosphate group from the creatine in this molecule the phosphoridine is going to run out after a few seconds so it's only used for short bursts of vigorous exercise if you really need it so that's why we get that idea of only having a few seconds of contraction because we have this phosphocreatine store it's anaerobic it doesn't require any Oxygen it doesn't form any lactate and creatine can be broken down into creatinine and removed from the blood by the kidneys okay so it's important for the body to control several factors to maintain homeostasis and these are all controlled by negative feedback mechanisms we're going to look at negative feedback in a minute but briefly we need to think about some examples of things that the body controls through homeostasis and why it's important that it is controlled so the main one or an easy one that you probably would have learned about potentially already at GCSE and will know the reasons why is your body temperature so too high enzymes into nature because obviously bonds can be broken in the tertiary structure that's holding the shape together so therefore the substrate will no longer fit into the active State and we can't have chemical reactions and that's obviously a problem because chemical reactions control a lot of our body processes things like respiration too low is also back bad as well though so reactions will slow down when the temperature is too low because there's just not enough kinetic energy for the particles moving around for us to actually have the energy to complete those reactions and that's also a bad thing as well so anything where our reactions will be too slow or the enzymes controlling the reactions are going to denature it's going to slow down processes in the body and prevent life cycles so your Optimum is about 37 degrees C obviously there is some leeway here can be a little bit higher a little bit lower depending on a age and all sorts of things whether you were ill but if it gets past a certain temperature it becomes dangerous either way you can either have a really high dangerous fever or be hyper so the next one is the PH of blood so mostly we're talking about blood blood plasma here tissue fluid that pH and the optimum is about 7.35 to 7.45 if it deviates too far from this this can be an issue because it can affect enzymes against but we've got um this idea of ionic bonding being disrupted by oh minus ions or h plus ions in solution which is obviously what pH is measured by and so they can be denatured those ionic bonds can be disrupted same thing as temperature tertiary structure is disrupted the shape no longer fits with the substrate there is no reaction occurring so it's for similar reasons to temperature but our blood phen also needs to be controlled so that's thinking of things like the carbonic acid that dissolves if um there's too much carbon dioxide present if we're not getting rid of it from the body properly that's the exact sort of one of the examples we talked about of um the pH kind of changing in blood so in other factors I'll hopefully again will be familiar with this from GCSE is your blood glucose levels we obviously it's important that we have enough glucose in the blood that we have it there to be transported for various processes specifically respiration but also the presence of glucose in the blood actually affects water potential if you think about it it's a dissolved substance it makes solution so if there's too high blood glucose levels you've got a lot of glucose dissolved in your blood plasma the water potential of your blood will be lower and if you've got too little blood glucose and other dissolved substances in the blood then that your blood water potential can be really high and that's something that needs to be controlled because the cells around it that's going to be so blood glucose level is important to control for the reasons that we need enough glucose to be circulating around in order to be able to carry out processes that require glucose such as respiration but also we need to think about how much there is in the blood because that's going to sort of be determined our water potential asthma and our tissue goes around our cells which can affect the cells which brings us on to the final one which is blood water content so the water content again of blood and the tissue fluid the water potential of those is very important you need to maintain it because if we don't have it within a sort of an isotonic range for our cells cytoplasm then it's going to cause osmotic effects of the cells can cause shrinking bursting obviously to the extremes so being able to make sure that the water potential stays within a certain range so that it is isotonic to our cells is very important we also need water for some reactions so it's important for metabolism of cells so that they can keep going and carrying out the reactions that require water thinking about condensation hydrolysis reactions if we don't have enough water present but then hydrolysis reactions are not going to be able to be carried out as efficiently and so all of this is important and so ultimate regulation the regulation of the water potential of the body is very important okay so we're going to look at temperature control briefly and then we're going to go into a lot more detail on the other factors we've talked about so the hypothalamus in the brain is the area that contains the thermoregulatory center and it contains receptors that are sensitive to temperature of the blood so that's where our receptors are it also receives nervous impulses from thermoreceptors that you have in your skin and then it sends impulses so the hypothalamus has The receptors but also acts as the coordinator here sends the impulses along motor neurons to various effectors so the this time we're using nerve signals when using the nervous system and control temperature we're not using hormones so one of the effectors of the pylor erector muscles in your skin which are responsible for raising and lowering your skin hairs so if you are too cold then and the hypothalamus detects this electrical impulses Action potentials are sent down motor neurons to these muscles and they are supposed to contract and as they contract they will pull up your hairs to stand up straight this is when you have Goosebumps and all your hair standalones that's what this is when you're cold and that raising of the head traps a load of air that is able to then insulate you around that layer of skin is obviously left over from when we had more hair on our bodies um because the hair we actually have doesn't actually make that much of a difference but um you see this in other mammals as well and they do it in order to kind of give themselves that insulating layer and obviously it works better if you have what in your body hair if you are too hot then the impulse is sent do the opposite they tell those muscles to relax and so therefore their hairs are lowered because we don't need to have that insulating layer of air anymore the sweat glands also in your skin so this is a gland that's an effect to this time so the muscle but they will be stimulated by the nervous system again to produce more sweat when you are hot so that you can lose heat energy by evaporating that sweat the liquid of sweat off your skin um and through a vibration so we lose heat energy that way and it just allows us to cool down skeletal muscles so mostly this is your arms and your legs but this is potentially also happened in other parts of your body if you've been really really cold um when you are really cold your hypo silence is going to stimulate your muscles to contract rapidly so again motor neuron signals will cause your muscles to contract rapidly contraction is going to generate heat energy because the contraction requires energy from respiration and so we release some heat through that process because we should hopefully know that respiration releases some heat energy and that helps us to warm up basically and so that kind of quick rapid Contraption is basically a way of generating heat energy through increased respiration your smooth muscle as well and we looked and briefly at smooth muscles and the fact that we have layers of smooth muscle in our blood vessels so these as we said are um can be under control of the nervous system and they can be caused to contract or relax and this is controlled called vasoconstriction when they contract and that happens when you are cold or vasodilation which means obviously to relax and dilate that which happens with you want to warm now the reason they do this is because if you vasoconstrict those blood vessels then less blood is able to flow through them the volume of the blood flowing through them is reduced so we tend to do that for blood vessels near the skin and at the extremities so fingers toes nose ears which is why they can become very very cold and some people have various syndromes where actually the the lack of blood flow to those areas in the cold makes their hands and things actually go blue and can be very very painful then the opposite is true whether you get really hot and really sweaty and if you do lots of exercise sometimes you'll find out you have a very red face that's because when basal donation happens we're widening those blood vessels so more blood is flowing through those capillaries that are close to the skin and also through the extremities to try and lose that heat energy same with the vasoconstriction we're doing the opposite by reducing the blood flow that nice warm blood stays closer inside of the body and we keep our blood like the warm blood flowing around the kind of internal organs don't want it flowing through the the parts of the skin that are going to get the most cold so we don't lose that precious heat energy negative feedback is a continuous cycle that goes on in the body in various places in various processes if a factor in the internal environment increases or decreases above or below the optimum level then changes will take place to restore the conditions to that Optimum so for example something a condition increases above the optimum level so it moves away from the option level as an increase that increase is going to be detected by receptors as we said it's going to be this same mechanism that we looked at with nerves where we've got a receptor a coordinator an effector and a response The receptors send signals to the effector or they will send signals to a coordinator which sends signals to an effector then the effector is going to bring about a change it's going to react in some way that brings about a change to decrease that condition back down towards the optimum and then the condition returns towards the optimum level and starts to decrease now there's exactly the same thing as I said it's a cycle so that factor is going to be decreasing towards the optimum it might then decrease past the optimum and carry on going or it could decrease for another reason at another time so it decreases below the optimum that the increase is detected by receptors again which sends signals to the effector or will send signals to a coordinator which sends signals to the effector and then the effectors are stimulated and they cause the change which hopefully will return start to return the factor back to the optimum level and again the condition increases and goes back towards the optimum and this can go up and down and up and down and up and down constantly it is a continuous cycle to make sure that whatever the condition is it is maintained within the limits are acceptable for the body okay so we're going to look at controlling blood glucose concentration so why is it important that we keep our blood glucose level within this range well if it drops to you though then cells might not have enough glucose respiration and they may not be able to function normally brain cells are particularly sensitive to this your brain actually needs quite a lot of glucose to function it requires a lot of energy so if your blood glucose levels drop similar to if your blood oxygen levels drop then your brain is very particularly affected if blood glucose levels are too high and can change the water potential and then have osmotic effects so cause water to start moving in and out of cells if the blood plasma and the tissue fluid aren't isotonic to your cell cytoplasm let's have a think about how we're going to control this then so the blood glucose concentration is going to be controlled by the parts of the endocrine system so it's to do with hormones and when using glands to be able to control this so the receptors that are going to be detecting the blood glucose levels are located in the regions called the islets of langerhans which is the the endocrine tissue inside the pancreas the signals that we're sending is hormones so hopefully from GCSE we should remember the hormones are insulin and glucagon and they are both secreted by the pancreas and they'll be traveling around in the bloodstream and then the effectors which are going to cause our blood glucose level to either increase or decrease are going to be in multiple organs and cells so the liver the muscle cells and fat cells are the target cells of these hormones so we need to know how blood glucose concentration changes so that we can understand the reactions and how interesting glucon actually cause these changes and there's some key terminology in here that we have to know that can trip to people so glycogenolysis basically means the splitting of glycogen glycogen o lysis lysis mean to split or burst break so it's basically the breakdown of glycogen into glucose it happens in the liver and then obviously that glucose can then be reduced into the blood so it can increase blood glucose levels the next one is gluconeogenesis glucone glucose Neo meaning new genesis mean to make so making new glucose the liver has this ability to be able to produce glucose molecules from other molecules so converting them into glucose namely it uses proteins from the muscles it could be examples are lactate and pyruvate and it also makes it use glycerol which comes from fat cell so they're both ways that blood glucose levels can be increased how about how do we decrease our blood glucose levels well the main one that blood glucose levels decreases is dry oxygen again and the liver but this time glucose is actually being converted into glycogen glucose molecules are being joined together to create glycogen and obviously that lowers the blood glucose levels next one is actually doing exercise your muscles are going to need more glucose in order to do more respiration so they start upticking or taking in more glucose from the blood the other two obvious ones that I've not really mentioned yet but hopefully this should make some sense so fasting obviously decreases blood glucose levels so not eating and then obviously the other side eating increases your blood glucose levels so if you eat carbohydrates and they also get broken down by enzyme in the digestive system and then reducing sugars including glucose are absorbed into the bloodstream every time you eat that's going to increase your blood glucose levels if you don't eat for a long time and you've been moving around so you've been using up the glucose that's in your blood then you are fasting and that will decrease your blood glucose levels until they get to a point where your body then kicks in and tries to return your blood glucose levels to the optimum and so we're going to look at how that does that next the endocrine tissue that's the eyelets of langerhans which are parts of the pancreas and they secrete hormones into the good kidneys enemies in response to blood glucose levels so when your blood glucose levels are too low it is the outer cells that are the cells that are in found in the eyelets of layer hands they secrete glucagon the hormone that is also then going to travel around in the bloodstream and it is going to bind to receptors on the target cells as we said so they have receptors for the hormones the hormone will bind and cause various effects so in order to increase our blood glucose levels because they're too low glucagon binds to liver cells mostly and causes it to start converting glycogen back into glucose so breaking down glycogen to glucose so it activates glycogenolysis it also activates gluconeogenesis so that production of glucose from other sources so namely proteins amino acids and proteins from the muscles and glycerol from fat cells so they will be being sent to the liver gluconeogenesis and both of those are triggered by system if the opposite happens and your blood glucose levels go too high for example after you've eaten a cake to make sure your blood glucose level doesn't go too high once you've absorbed all of that Sugar then we have this response so the beta cells this time they secrete insulin so they will detect that this blood glucose level is too high they will secrete insulin into the blood that will travel around the bloodstream and again bind two receptors on the tongue itself and the main thing that it does for them is that it causes these cells to undergo a change where they have more glucose Transporters in their membrane so it increases their permeability to glucose which means they start absorbing more glucose by facilitating diffusion and that increases glucose uptake which obviously removes it from the blood the other thing it does as well because obviously we talked about ways that we can decrease blood glucose is that it activates in the liver the process where we take glucose and we start binding it together to make glycogen so converting glucose into glycogen for storage but also this is good for the liver because it the process of it doing that keeps the concentration gradient quite steep between the liver and the blood in terms of glucose so because when glucose enters the liver it's being converted to glycogen straight away that means there's always or in this case for a short time there's more glucose in the blood than in the liver so it keeps that concentration gradient maintained so that glucose continues to enter the liver out of the blood and decreases that blood glucose level so that is in fact the negative feedback system that controls our blood glucose levels some hormones are what we call non-steroid hormones this means they have to bind to a receptor on the outside of the cell membrane I'm rely on what we call secondary messages to work inside the cells to amplify that original signal and cause the change to happen within the cell glucagon and adrenaline adrenaline is secreted by the adrenal glands which are found on top of your kidneys so you have one gland on the top of each kidney and they secrete the format adrenaline we're looking at both of these hormones because they trigger the activation of glycogenolysis in liver cells and it occurs through this secondary messenger model that we've mentioned so both adrenaline or glucagon can do this they bind to their receptors on the cell membrane of liver cells and these are classed as the first messages the adrenaline and glutenant have both been secreted as a response to low blood glucose levels in this case and their aim is also to try and cause a change in the liver cells that's going to release glucose into the blood so the first thing that happens when they bind to their receptors is that it triggers the activation of something called a g protein so we're going to take the G protein and activate it normally remember one photograph activation we tend to be adding a phosphate group um which is something one of those other uses of ATP is to be able to add a phosphate group to a molecule and it tends to activate it or increase its energy level that activated G protein then causes a shape change in an enzyme that's found inside the membrane called adenyl cyclase it's an enzyme and so this conformational shape change that happens when the gene protein binds to it makes it able to be activated so it changes the shape that you'll be foot to now accept its substrate and be able to catalyze a reaction the adenal cyclase enzyme when it's activated can catalyze the conversion of ATP into something called cyclic amp or Camp short and this is then the secondary messenger so this activation of ACP into Camp the cand is what then goes on to cause the changes in the cell that we want to happen so it's the secondary messenger it passes on this signal and causes the change in the cell so what CMP does is it activates the protein kinase enzyme Cascade so protein kinase enzymes are a group of enzymes and this idea of a Cascade is that one enzyme is activated which causes something to happen which triggers another enzyme Etc and ultimately this leads to the breakdown of glycogen into glucose or glycogenolysis and so therefore we're going to release glucose into the bloodstream so that binding of the adrenaline or the glucagon through this system has triggered a change in the cell which has resulted in the outcome that we wanted as the effector causes the response of increasing the blood glucose level so this is a very similar system used by a lot of hormones that have to bind to receptors it's similar and depending on obviously the target cell it will have different effects based on what this enzyme Cascade sets off but this is something that's quite common in cell symbology as a way of triggering an effect inside itself from the outside by being only being able to bind to a receptor diabetes is a group of conditions where blood glucose concentration can't be controlled properly and after eating blood glucose concentration doesn't reduce as it should as glucose is not being absorbed a regular blood glucose concentration of above 7.8 million miles is considered high enough to be diabetes we've got two blood glucose readings here after they've eaten some food you've got a really rapidly increasing blood glucose after eating the food and then it's quite slow to reduce so there are two types of diabetes we need to know both and we need to be able to explain the differences between them so the cause of type 1 diabetes is that the beta cells do not produce insulin anymore and this can be as a result of a genetic problem so you can be born with it or it can happen to you sometimes when you are quite young or even later in life the effect of this is that your pancreas will no longer secrete insulin at all the consequence of this is obviously your blood glucose levels can get extremely high especially after eating very high blood glucose levels are obviously quite dangerous and they can lead to a coma or even death if not shoot isn't just left to get higher and higher the main treatment for type 1 diabetes is insulin therapy so injecting insulin regularly after meals and throughout the day and normally they have to check their blood glucose levels with a test and then inject the correct amount of insulin to lower those to the correct level too much insulin could obviously cause them to go too low so we don't want that either and that can obviously have its own issue so managing that is quite important long term there are obviously the options of replacing those damaged cells in the pancreas with potentially a pancreas transplant but this would involve taking anti-rejection medication or stem cells again that can involve anti-rejection medication and again these are kind of really serious long-term treatments they're not regularly offered to people with type 1 diabetes when you have to know the differences and the cause is different in this case the practice makes insulin perfectly normally it's just that the receptors the insulin receptors on the target cells do not respond to an insulin and that doesn't mean all receptors on every Target cell doesn't respond to insulin it can be different it depends on the cause often this could be caused by a genetic issue but it could also be caused by things like fat around certain organs meaning that there are insulin receptors on those organs aren't responding so what the effect is is that obviously cells do not take up enough glucose so not as much glucose is being removed from the bloodstream as a result of instantly not binding and therefore not increasing those transport proteins for glucose on the outside of the cell membrane the consequences just are generally higher than normal blood glucose level all the time so it's not at the massive Spike scene with no incident introduced at all because again it's not every single insulin receptor in every single cell that doesn't respond here but we get to this point where your average blood glucose level is higher than normal most of the time so the treatment for type 2 diabetes is normally a healthy balanced diet which can be low carbohydrate or low sugar focused and regular exercise I think obviously the exercise really helps because that is going to be removing that glucose from the blood to use up in respiration and to help sort of use up that excess glucose that's in the bloodstream because even a slight increase but on a regular basis of blood glucose levels can have knock-on effects on the kidneys on the eyes on all other parts of the body there can also be the option to take glucose lowering medication if the balanced diet and regular exercise isn't working hard enough as well the other the last thing to note about type 2 diabetes is obviously type 2 diabetes cannot be treated with insulin therapy because it would make no difference because they do already have insulin in their bloodstream their pancreas is working it's the receptors that can't respond to it so adding insulin would not help okay so the causes and consequences of type 2 diabetes constitute like an actual health issue a global health issue but also in the UK so type 2 diabetes is increasing in the UK population because it's been linked to increasing levels of obesity so the increasing levels of obesity in the population have directly caused this increase in type 2 diabetes that has been demonstrated so the Obesity price is a direct link of unhealthy diets in the population and along with a reduction in reduced exercise and activity in the population type 2 diabetes is a serious health problem it can cause other risks such as heart disease stroke vision loss and kidney failure because all of these extra organs are having to work twice as hard all of this so Chaturbate is itself all of the associated health risks with taxi diabetes put strain on the NHS so Health advisors would like to try and get to the root cause and try and increase awareness about obesity and its impacts on things like increasing type 2 diabetes and increasing other health issues and so trying to reduce reduce obesity will help reduce all of these problems there is also another sort of branch of thought though that is as well as the health industry and the NHS trying to help promote healthier lifestyles in people the food industry also plays a role here if food and the kind of unhealthy diet is the source of the problem and food marketing especially around things like junk food it plays a role and so we Health advisors would like food industry Executives to be part of this conversation and trying to help reducing the poor diets that we see as a majority of the population educate people that healthy lifestyle is better and it can reduce some chances of non-communicable diseases including type 2 diabetes and also trying to help adults and other people make their labeling clearer so that people can make healthy choices when they choose foods those kind of red orange green triangle we also have to balance this with what the food companies are doing so they have responded by making some low sugar slow salt low fat products that you can get so zero percent fat but the way they've done that is to use artificial sweeteners to make the food tilt still taste appealing add two centimeters cubed of Benedicts to each sample before we put in the hot water once I put it on I'm going to give it a little mix for each one okay so those are all my known samples and then I have my patient one patient two and patient three unknown samples so I'm going to add two centimeters cubed to blend it to those as well the samples have gone into the water bath so I've used hot water from the kettle and just put those chewed in them giving them kind of a shake and a mix make sure they kind of evenly distributed through the hot water set the timer for about five minutes and we're just leaving them to sit in there waiting for the time to go off all the tubes have gone into the same temperature of water and have gone in for the same amount of time okay so now we're going to move on to filtering and then actually testing these samples so the main thing I'm going to do first is to filter these samples that we've done the Benedict test on to remove some of the precipitate if you have a lot of precipitate especially with the kind of very red orangey ones it can make the solution quite cloudy and that can affect the calorimeters okay so I have my color into here and I'm going to blanket or zero it or calibrate it using some Benedicts and distilled water and this is because we want our zero to be the blue Benedict's color that we've used to test all the all the samples with because we're looking for a color change from that blue as a starting point because that's the starting color of Benedicts so any color change from that it should then be detected by the color enter and give us an absorbance measurement so it's not using Clear Water this time because we need a blue reference point to start with because we're looking for many change in the blue color of beddox okay so now I've done my blank I can put my samples into the machine so I've just put one of my patient samples in this example and we get an absorbance reading okay so I'm going to do that for all of the samples including the unknown samples and then we can use those values to create our coloration curve so with all those readings that we took from the camera we have now plotted our graph of absorbance against the known concentration so my standards and created this calibration curve so now we need to use this graph to identify the glucose concentrations in the unknown patient samples so patient one the absorbance was 0.256 so go and find that on your y-axis draw line across remember always always use a ruler so that you do not mess up with this um it's really good to make sure you when you are asked to do this whether it's in exam or in your practical book to make sure you actually do this on the graph so they can see that you've done this work sometimes it can get you marks in the exam as well right so there's more results so what conclusions can we make from this because obviously the whole point of this practical is to practice doing the zero dilation practice using a Colorimeter but then also using a calibration curve to find concentrations of unknown samples so normal urine glucose is about naught to 0.8 minimola so what does this tell us it's probably the patient one and patient two are quite normal range of urine glucose whereas patient 3 is definitely outside of that range and definitely higher than 0.8 okay so that is this practical term so the kidneys are part of the urinary system they have two main roles the kidneys is part of this system osmo regulation which is maintaining the water's potential of blood so they help to either remove excess water or they help to retain water if we need to the other role of the kidneys is to remove protein so excess protein in the form of urea take it out of the blood and excrete it out of the body in urine they are fed in terms of blood and oxygenated blood by the renal artery and then the waste and other things from the kidney and the kidney tissues are removed through the renal vein the filtration process initially removes a lot of things including urea but we don't want all of that to leave the body because some of it is very useful so we need to reabsorb that and make sure that that doesn't get lost in our urine and that process is known as selective reabsorption and then the other process is obviously the ultimate regulation and to do with water is well so we need to be able to label these parts of the kidney you can see here is called the cortex so that's our the outermost layer of the inside of the kidney contains the tops of approximately about 1 million nephrons per kidney so this is one nephron here highlighted in green the top parts are in the cortex and that is how we carry out most of the filtration and the absorption and then the parts that extend down into the medulla are mostly used for osmoregulation and water control you can see one of the structures here sort of taken out of the section of kidney and we'll look at that in more detail as we go through figuring out the processes of reabsorption filtration now the bottom part is the medulla so these sort of inner layer of the kidney is the medulla and it contains the tubes that drain the filtered wastes into the renal pelvis so we can see here we've got some of those tubes of the Nephron coming down all the way down through the medulla and then on the larger diagram we can see the renal pelvis is kind of like the collection of tubes in the middle to join up to the ureter is where the urine travels down to the bladder so that's the overall structure we need to remember the cortex is on the outside the medullas on the inside top parts of the Nephron are and cortex the bottom parts of the nephrons are found in the medulla there's a so the first stage is ultra filtration and that is where we are at the glomeranus which is the first part and it involves the fact that there's a wider Lumen of the afferent arterial so blood coming into the glomerulus then at the efferent arterial so that gives us High hydrostatic pressure and forces small molecules out of the blood's plasma into the Boneless capsule which is the kind of cup that surrounds the Glamorous which is a lot of capillaries the capillary walls to the holes and the capillary walls the penetrations the basement membrane and the filtration slits from the podocytes all provide filter system that prevent large molecules from entering the filtrate that's going to go into the nephron stage is selective reabsorption where we're going to reabsorb all those useful molecules that we need to keep in the bloodstream so as the glomerular filtrate which is what we call it now it's come out and into the nephron is moving through the next part of the Nephron which is the proximal convoluted tubule 85 of it is reabsorbed including all the glucose or amino acids some ions and most of the Water by osmosis this happens in the PCT because the cells line in the PCT have got this special adaptations to maximize absorption similar to the adaptations of cells that line the movement of the small intestine so the next stage is kind of where most of the reabsorption of water happens so the function of the loop Headley is to create a low water potential in the medulla of the kidney so you'll see here the top part we're looking at the cortex now we've moved absolutely depending the link of Henley and the collecting duct are in the medulla part of the kidney so what happens is salts are moved from the ascending limb to the descending limb so that actively transported out of the ascending lymph and salts diffuse out as well and they then create a very low water potential in the tissue of the Madonna surrounding the lubricantly and that causes water to move out of the filtering in the loop of Henry by osmosis gets reabsorbed into the blood and you can see that network of capillaries around the loop of Henry we'll go into detail about how this happens a little bit more because you need a bit more specific about how this process actually works but this basically starts the process of concentrating the urine and removing some of the water the filter then passes up back to the cortex and into the distal convoluted tubule or the DCT this is where even warm water can be reabsorbed into the blood by osmosis nothing special happens here other than that as it passes through if there is more water in the filtrate than in the blood vessel surrounding it then they it will move out by osmosis and then finally we reach the collecting duct so the collecting duct is where the concentration of urine is controlled again it's in the mandala and you'll see here that it says that the first part of multiple nipples can actually drain into a single collecting duct so you'll see these branches off it and this is because more than one left we're going into this collecting duct and the permeability of the membrane of this connecting duct to water is regulated by the amount of antidiuretic hormone in the blood or ADH osmo receptors so receptors that detect the water potential of blood in the hypothalamus control the release of ADH from the pituitary gland in the brain and it controls how much water enters the urine so the lubrically is what we call a hairpin counter current multiply because what it does is it allows the concentration of the filtrate to be increased by reabsorbing water and it also increases the concentration of the tissue around the loop Pele in the medulla in order to help to remove the water which we'll explain in a second at the same time start with the ascending limbs remember that's where fluid is moving towards the cortex as fluid is moving up the ascending limb sodium and other ions are actively transplanted out of the filtrate into the tissue fluid they're normally moved out by diffusion at the base and then as they get fewer ions left in the filtrate as we move up the ascending them then we have to start using active transport what this does is when leaving the ions out is that it lowers the water potential of the surrounding tissue in the medulla so that's important because what we want that to do is we're going to need that in order to move water out of the filtering by osmosis but it doesn't follow the ions on the ascending limb because that is impermeable to water there's more ions leaving the base of the loop Henry because they're diffusing out as we go up they're sending them there's fewer ions which is why we're having to actively transport it so more being lost from the bottom of the loop depending water potential decreases as you go down further into the medulla the filtrate coming in at the top of the descending limb is going to have the most water so as it moves down it's going to lose water by osmosis and so we need to have this concentration gradient where we have high water potential at the top of the descending limb of the loop of family at a lower water potential towards the bottom the decent in the loop headache to make sure we maintain that concentration gradient of water so there's always more water in the filtrate than in the tissue fluid outside and that's going to guarantee that our water is going to leave the descending limb and go into the tissue food and then ultimately be absorbed into the capillaries that remember are surrounding this Loop of any so let's think about what's happening here and just sort of look at it overall because we've sort of done it backwards because it makes more sense that way but we started with a lot of water and a lot of ions at the start of the descending limb as we move down the descending limb water is lost to due to osmosis because the walls of the diesel are permeable to water so it moves out into the tissue fluids around and ultimately into the capillaries because it's following its concentration gradient because the tissue fluid of the medulla has a very very low water potential because of all the ions that are in it when we get to the bottom of the lubricantly then we start diffusing ions out so sodium potassium chloride so not only have we lost a lot of water by this point we're now also losing ions so although we've lost a lot of water we still have a lot of ions at this point at the very Apex so that's where we have our lowest water potential of the filtrate because we've lost the water but we've kept the ions once the ions also leave actually at this point we have a slightly higher water potential again because we will have some water still left and we've also lost ions so if we're removing ions that increases the water concentration and decreases the solute concentration so we've managed to absorb reabsorb quite a lot of water without needing to expend much energy most of it is through a diffusion of ions at the bottom of the lubricant we have used a bit of energy for active transport but because there's no water being able to leave the ascending limb it's just ions then we don't very quickly create an equilibrium with that water we it only moves out across the other side of the descending sounds in the wall of the collecting duct have receptors for ADH and they also contain vesicles which have aquaporins in them so aquaporins are just channels protein channels but specifically for water okay so here I have my cells so the cells are lining the collecting duct so obviously I've made them really big here but imagine that they're lining the collecting duct then I also have these vesicles they have the aquaporins attached to them and they are inside the cells and the acroporins will be found in the viscose but then also in the walls of the collecting ducts the kind of joining part that these Stars Branch onto and then I have my ADH receptors as well so if there's too little water in the blood there's not enough water in the blood ADH is going to bind to The receptors on the collecting duct cells so here's my ADH binding and then that causes in the same way that we've talked about all the other things happening using that secondary messenger Cascade it causes vesicles containing the aquaporins to move towards the membrane where it's joining the collecting duct what that does is that's going to increase the cell's permeability to water so it makes it more parallel to water this results in more water leaving the collecting duct through these aquaporin channels and then it won't move out of those cells and into the bloodstream so it's going to get reabsorbed into the blood but most importantly the water is leaving the filtrate and it's not going to be in the urine so we create a smaller volume of more concentrated urine it's more concentrated because there's less water to it because we've removed the water and reabsorbed it obviously if we think about the opposite then the opposite happens so if there's too much water in the blood less ADH binds to receptors so there's no ADH or very little ADH binator receptors at all the vesicles containing caproporins do not move and so they don't fuse with the membrane so this makes the membrane of the cells slightly less variable to water and so less water leaves the collecting duct and filtrate and goes into the blood and so we create a larger volume of more dilute urine because more water is going to stay in the collecting duct and more water will end up passing down through and into the urine and because we've got more water that dilutes the urea and the other salts that we create more dilute urine [Music] okay [Music] [Music] [Music] thank you foreign [Music] inheritance is something we will have looked at and done at GCSE it's just now got maybe a fancy name so remember that humans does our diploid which means they have two copies of each chromosome one from each parent One content comes from the sperm one comes from the egg they're a range of what we call homologous Pairs and that means that they'll have two versions of that Gene one on each chromosome these are called alleles so they are versions of a gene the location which is fixed so the fixed location of each allele on each chromosome is its Locus and so the alleles for each gene will be the same Locus on each chromosome remember obviously the reason we have this is that sperm and eggs gametes they are haploids so they only have one allele for each gene and they don't have pairs of chromosomes if you're thinking about alleles remember we give them letters often so either lowercase a or uppercase a is my pair of moleculars chromosomes bands all the stripes on these chromosomes they represent the genes so if we have two capital letter A's being a big a then that means we are homozygous dominant if we are two small A's two lowercase A's and that means your homozygous recessive so homicides just need the same so two both angles are the same either two dominant annuals or two recessive annuals if we have one of each so a dominant and a recessive animal attached away and little a then we are heterozygous hetero meaning different I remember dominant just means that you only need one of those allials for it to be expressed whereas we only see the recessive phenotype if we have both lowercase letters or both recessive alleles monohybrid intelligence then is the simplest version of inheritance because it involves kind of what we've been looking at here so one characteristics which controlled by one gene which has two alleles Okay so we've got a couple of monohybrid crosses that we can always rely on to give the similar predictable ratios the first one is that if you have both parents are homozygous so homozygous dominant and homozygous recessive all offspring are then going to be heterozygous all of the Austrian can have the same genotype and therefore they're going to have the same phenotype one of Mendel's examples of this was looking at specific traits in kind of peas so peas are seeds and whether they were round or whether so round and smooth or whether they were kind of wrinkly and bumpy so the round smooth phenotype is due to having homozygous dominant genotype and the wrinkled kind of bumpy theme type is from having homozygous recessive so if you put that into a single planet square with the same ratio that we just talked about so all of the Austrian heterozygous they all have one dominant allele and one recessive allele and so therefore the F1 generation have 100 Big R little r as their genotype so heterozygous genotype and so they're all going to be round and smooth so then if we take that generation the F1 and we're going to cross them two of those we'll see what happens in the F2 Generation because that gives us our second predictable ratio so if both parents again as heterozygous so they have Big R in Italy in this case there's always going to be a three to one ratio of phenotypes in The Offspring and that's because we're always going to get a one to one ratio of genotypes we're going to get one homozygous dominant we're going to get two heterozygous I'm going to get one homozygous possessive and again you can use the planet scale genetic diagram to kind of prove this and show that this always works so we have two round smooth seeds but they are both heterozygous in their genotype as parents that means each of them could have a dominant allele or a recessive allele in their gametes which means that depending on the mix of those we will get one chromosomes dominant two potential heterozygous and one potential homozygous recessive so we get that F2 generation three to one ratio three round to one wrinkled if we ask about probabilities we can also say obviously there's 25 chance of getting wrinkled fees there's a 75 chance of getting round smooth peas you can be asked in the same way and the idea that they are predictable so we know that it's going to happen every single time we have these similar crosses so I said that these ratios are expected and that is true and with some crosses you will expect to see exactly that ratio in the offering doesn't matter how many of they had a hundred Offspring 25 of them would be wrinkled and then 75 of them 75 out of 100 would be round and smooth but that's not always what we actually see in nature so we don't always see those perfect ratios and there's a couple of reasons for that one of them is obviously fertilization and the fusion of gametes Is Random so we're not always necessarily going to have gametes that can be both of those potential alleles potential that all of the gametes produced from one have the same alley there's another thing that's called codominant also affects these ratios sex linkage where some genes are specifically inherited on certain chromosomes the X and the Y chromosomes you could be taking samples from small populations so Mendel discovered these ratios because he was looking at really large populations so he was able to grow hundreds of plants and so he was able to get these ratios reliably the other thing is crossing over an independent assortment in meiosis the chromosomes lay on top of each other and where they land up to each other they form what we call chiasma and part of that chromosome breaks off it breaks at the charasma and one part that was attached to one chromosome swaps so then that means that whereas you would have potentially inherited a certain set of annuals now you might get different ones because those physical alleles have swapped chromosomes so they may end up in different and all of these are things we need to think about because you may get asked a question about why a ratio you've been given in an exam question isn't exact three to one ratio that we've looked at or some other predictive ratios we're going to look at okay so one of those examples I just gave was co-dominance so allials can be co-dominant if they're both expressed in the phenotype because neither one of them is recessive so we can still have obviously two chromosomes and in our homologous pair and we can still have two alleles but instead of having one dominant and one recessive allele both of these animals act as if they are dominant and so they can both appear in the phenotype so you can get the characteristics of both genes or you can produce what we call a blended phenotype which would make sense when you go through this example but there'll be somewhere you can get a patchwork effect of different colors for example or different traits mixed together or you can end up with what we call a blended effect so you pigments or whatever in this example it's going to be pigments come together and produce a blended sort of spectrum our example we're going to look at is flower color so the flower color in the petals so this is Gene c c for color it will either have white alleles or red alleles we've got two capitals here and they code for different colors in this case white or red if I have what we call true breeding cross to start with they are both obviously homozygous so they are having showing that they've got these both of these dominant aisles and that comes out as that color in the petals now we do exactly the same things we normally do with the Punnett Square the capital C's here and then we kind of do the same as we normally would with the letters on the top so I've got crcw crcw crcw crcw but we've got 100 pink Offspring because bows are dominant and by having both the red and the white alleles they mix together the pigments to form a pink phenotype it could be that you could have flowers that have blotches of red and white in this case we're going for a blended example so we get pink so although obviously this is an expected ratio it's not the phenotype ratio we'd expect because if it's different from their parents so let's do the second cross that we looked at so let's do a heterozygous cross with two pink flowers this time but this time they are heterozygous so they're both crcw so this time the gamut says they could either give an r or they can give a w so we're going to have this would be our three to one expected ratio of phenotypes but is it going to be that let's see so we're going to have crcr which is obviously going to be red we're going to have crcw which is going to be pink we're going to have crcw which is also going to be pink and then we're going to have cwcw which is going to be white so we have a one to two to one ratio of phenotypes not are expected three to one because of the codominance we have some red we have some white and we have some Blended Pink as well so this is where codominance can slightly change that expected phenotype but in the way we write it and the way we work this out is exactly the same as how we've done the previous cross you just have to have those letters as superscript on your capitals inheritance can affect the expected ratios and it could be that the alleles are co-dominant instead of big following the usual rule of being either recessive or dominant okay so multiple alleles occur when a gene has more than two alleles so they can have three or more within these three alleles there'll be more than one allele that's dominant or there could be more than one atom that's recessive for example so looking for a blood type then the immunoglobulin gene which we're going to have as I here codes for the antigens on the surface of red blood cells so it determines your blood type there's three alleles a A and B are both dominant and so they'll be co-dominant if they're present together and then o is recessive to both A and B so if it's there n Orbee will always be the antigen type that is present in the blood cells and if you get two o's and you basically don't have any antigens on your red blood cells they still can follow a certain expected three term ratio would occur if both parents have the same blood type so for this example we're looking at two parents that both have blood type B but they are carriers of the O allele so this would be when we have heterozygous parents in a normal ratio for example so we get two children with b o same phenotype as the parents one with double b and then one with double O so we get three to one ratio because three of those children will have B blood type and one will have O blood type because this is the double homozygous recessive it's rarer and so those O blood type people are rare in the population but they are the ones that obviously are the best people to donate blood the other predicted ratio we can get is if we have um two parents who have different blood types and again are carriers of the O allele so we have an a blood type and a b blood type so that means we'll get an A B combination and they're both dominant so that means that blood group is a b we will have an A and we will have a b type child and then we'll also get that at double recessive o as well so we literally have four different blood type outcomes from two parents so the ratio is one to one to one to one die obviously here meaning two so this is when we're looking at two characteristics that are inherited from two different genes which have different alleles so these can show the probability of inheriting certain combinations so two different genes and each of them has their own alleles so in this case P shape codes for either smooth peas or wrinkled piece and in this case my harmonica I've got both alleles for p color I can either have green peas or I can have yellow peas this is one of those sets of traits that Mendel use to be able to figure out how this type of inheritance worked so this individual that I've got here with my example their genotype is heterozygous for both so they have a dominant and recessive for both genes and because we're looking at two genes both the two alleles we have four letters that's our diploid genotype so this phenotype for this will be smooth green peas because dominant traits if I were to take two of these smooth green producing plants with this heterozygous genotype and cross them what gametes could this individual produce so normally we'd have two alleles for one Gene and then when we had our gametes we would have one allele of each so they could have either Big R or small r or either Big G or literally G but because we're looking at two genes the gametes are going to be two letters so because we have four possible combinations of gametes our Punnett Square will need to be double the size so there are expected ratios for this type of cross as well so in dihybrid crosses when the heterozygous parents across there's four possible gametes as we just saw so there's 16 possible Offspring genotypes and there is an expected ratio in this case of nine to three to three to one so often you'll be introduced to this idea by talking about how do we actually get the first generation homozygous dominant and homozygous recessive so the phenotypes that you get are from entirely and homozygous genotypes so we don't have any heterozygous mixing in there we just have all capital letters and all small letters to get F2 we're going to cross two Tetris Argus individuals and we're going to need this big slightly larger Punnett Square so let's have a look at what we're going to get so remember anything that has a capital R is going to be smooth and anything that has at least one capital G is going to be yellow so the easiest thing to do is to put the smooth yellow in first so everything with at least one capital r gets and one capital G gets a yellow Dot now everything that has a capital r at least a capital R but lowercase G is going to be smooth and green so do those next so I'm looking for lowercase G's but with at least one uppercase R will be smooth and green let's try three round and green and obviously this is starting to look like we figure out that it's going to be our expected three to nine to three to three to one ratio so anything with lowercase R's is going to be wrinkled but if they've got at least a capital G they'll be yellow so there's one two and three so they've all got lowercase R's at least one capital G so they are yellow but wrinkly and then last one we have are homozygous recessive for both genes is going to give us our wrinkled and green seed again this has given us our expected ratio nine to three to three to one but this ratio doesn't always actually occur in nature you're not always going to see this in breeding various plants together and this can be due to two things we had the list before but the other thing that can influence where you're looking at two characteristics inherited together are things like epistasis and linkage some genes can interact to control the same characteristics so it's not always one gene one characteristic but in this case the genes aren't coding for separate things separate characteristics they're coding for the same characteristic and when they actually interact with each other or they mask or suppress the other genes expression that's what we call epistasis so two genes are different locuses changing the expression of each other there's a couple of different examples often including pigments visible phenotypes so colors pigments something that can be changed by an enzyme as well so if there's kind of an enzyme substrate chain that can also be controlled by epistasis and in this case it's the genes are coding for enzymes that will change colors or pigments and that's how this interaction comes about so let's look at an example of flower color so we have two genes Gene one is codes for pigment so whether or not you can make a yellow pigment so if you have two copies of the recessive allele you will not make any pigment you'll be white if you're a flower or plant that has at least one dominant allele for Gene one then you will be able to make this yellow pigment then we have Gene two Gene 2 doesn't code for a pigment Gene 2 codes for an enzyme which will react with the yellow pigment and turn it orange so if you have two recessive alleles so little R's in this case for Gene two no enzyme is going to be made so it'll either stay yellow or white depending on what allials you have for June one if you have the dominant allele at least one dominant allele for Gene two then you can make the enzyme and that will react with the yellow pigment if it's there and create an orange flower now obviously Gene 2 is reliant on Gene one to a certain extent because if you are able to make the enzyme with Gene 2 but you don't have any yellow pigment because you can't make it because of the alleles you have for Gene one and there will be no substrate for that enzyme so no orange pigment will be made so there's no yellow pigment there can't be any orange pigment and so that is where we get kind of a masking of the expression of gene2 because depending on Gene one you wouldn't be able to tell whether a plant has Gene 2 what alleles the plant has for Gene too if you don't make any pigment with G1 so this is why you can have these different outcomes so if Gene one has a at least one dominant alien then the flower will be yellow if they then also have one at least one dominant allele for Gene two they'll be able to make the enzyme so they will be orange because they'll be able to turn that yellow pigment into an orange pigment however if Gene one is homozygous recessive so too little wise no pigment will be made so it doesn't matter what Gene 2 alleles a plant has there's no pigment to act as the enzyme substrate so then the flower will just be white or colors so these are kind of the options we have but the idea here is we're getting this idea of an interaction where Gene 2 doesn't matter what alleles you have it can be masked so you you wouldn't know what alleles they have because their phenotype would not exist if Gene one is homozygous recessive so we describe this as Gene one being epistatic to Gene 2 because it can mask the expression of gene 2. so these are our options for the genotypes and phenotypes two genes with different angles and we get three fingertips again this is an example of where you're going to get different phenotypic outcomes different ratios than those expected nine to three to three to one ratios that we'd expect if we were crossing two two genes so epistasis can be either recessive or dominant each is going to give us a different ratio other than that expected nine to three to three to one ratio for recessive epistasis it's very similar to the example we just looked at with the flower color so it's when two recessive alleles at the first Gene Mask the expression at the second Gene so for a heterozygous F1 cross we're going to get a 9 to 3 to 4 ratio so we're going to look at fur color in mice so in this case for Gene two we are going to be looking at the alleles a and a a and so if you have at least one dominant allele you will have brown fur if you have two recessive alleles for Gene two so two little A's you are going to be black can have black flat for Gene one we're going to use the letters b a little bit so for Gene one if you are homozygous recessive so two small bees you will have no pigment you will be albino so here we have again recessive epistasis so Gene one is epistatic to Gene two because if we don't have at least one dominant allele for Gene one so if we don't have a big b or um two big B's then we are going to not be able to make any pigment at all so it doesn't matter what is then at gene2 it doesn't matter whether we are going to have brown alleles or black alleles we will not have any pigment we will just be white okay so it works in a similar way so let's have a look at how we can get our gametes so we're gonna do a heterozygous cross and so remember this is recessive purpose stasis so Gene one is masking the expression of gene2 if there is no dominant allele for Gene one or if there's two homicideous alleles for Gene one anything that has a capital A at least one capital A and at least one capital B is going to be brown because if they have at least one capital B that means they can make pigment if they have at least one capsule a that means that pigment will be brown pigment and there's all our Browns for black fur we're going to be looking for anyone that has at least one capital B that doesn't have a capital A so then we will get black though which means they can make and may have at least one dominant for Gene one for B's but they are recessive gene2 so they are going to have black foot and then all of the others then that are left will be white because they will not have a dominant allele for Gene one so they won't have any Capital B's so therefore it doesn't matter what alleles they have for the gene a or Gene 2 they will be white because they cannot make any pigment so that shows us that we get that nine to three to four ratio so there's nine Brown there's four white and there's three black okay so let's have a look at dominant epistasis then so this is different because this is when you have at least one dominant allele at Gene one then we're going to mask the expression of Gene two so we're gonna get a 12 to 3 to 1 ratio this time if we do a heterozygous F1 cross so the example we're going to look at is fruit color in squash the color of the squash yellow or green is controlled by gene2 In This example so we're either going to have again if we have a dominant at least one dominant angle of the yellow if we have homozygous recessive for Gene T we will have green squash we will have white or no color if we have at least one dominant allele for Gene one so Gene one if we have at least one double an allele we will not be able to make any pigment we will have white or no color so in order to get yellow or green squash we need to have homozygous recessive for Gene one so we're only going to have color if we have a little bit little B for Gene one so Gene one masks Gene 2 if there is a dominant at least one dominant annual act Gene one so we're going to cross two white squash that are heterozygous so they are big a little a big b little B majority of these will be white because we're looking for anything that has two little B's and a dominant letter A will be yellow and the only way we can be green is if we can be homozygous recessive completely for both genes so homozygous of B will then give us a color and then we have to be homozygous at a in order to be green so there's only three yellow and one green and the rest of the 12 are all white and so this is how you can see the ratio is different so we get 12 to 3 to 1 ratio and this time we actually get sort of quite a majority of that kind of pale no color because of that masking being caused by dominant genes rather than recessive genes sex-linked genes are genes for specific characteristics that are found only on the sex chromosomes so that's going to throw up some specific patterns and these are kind of the common patterns to look out for that are normally are kind of explanations for why certain genes are going to be inherited in a certain way if they are settling so most sex linked genes are found on the X chromosome and so we refresh them as x-linked genes and this is because the Y chromosome is smaller it's about half the size so it carries fewer genes so why linked genes specific Wine ingredients that we know about are quite rare So males will only ever be able to have one allele of each sex linked gene because they only have one of each chromosome they don't have a pair and so they will always express the characteristics of that Gene even if it's recessive so it doesn't matter what alleles they have on the X and Y chromosomes they will Express them because that they aren't a pair so they won't carry the same genes they won't have two copies they won't have a dominant under recessive it will just have one recessive copy if they or one dominant copy if they have it so this means they're more likely to have recessive phenotypes because they can't be carriers of x-linked genes and so they're more likely to have any recessive phenotypes that are caused by recessive genes from the X chromosome females in the opposite side then so literally opposite to that they get two copies of every excellent Gene so they're less likely to have recessive phenotypes because they are able to have dominant genes and be heterozygous and so it's for them in order to have recessive disorders of genes that are on the X chromosome they would need to have the two recessive copies they or C can then also be carriers of x-linked recessive genes so they can be able to pass those on to their offspring but not have the disorder whereas males will be able to pass on those genes to offspring but they will always have the disorder it can't be a carrier in males all Y chromosomes are inherited from sperm obviously and all X chromosomes are inherited it from X X linked genes including disorders will be passed on from mother to son so that's why normally um we see these disorders being linked and sort of displaying in males but they come or have been donated to them from their mothers or to say it sounds like a fancy word but it basically just means non-sex chromosomes so the other 22 pairs of chromosomes in humans are all autosomes because they are not sex chromosomes so most genes that run separate or different chromosomes are assorted independently so the allele received for one gene doesn't affect whether you get the allele for the other gene or not this gives us the typical one to one to one to one or nine to three to three different to one ratios that we'd expect for dying hybrid crosses between different genotypes of parents I've got my chromosomes here I've got two different chromosomes and they're not a homologous pen and on this chromosome we have Gene one and it's not linked to the other genes so it's not going to determine if you get Gene one it's not going to have any effect on whether you get Gene to you Gene 3 or gene pool because they're one completely different chromosomes however Gene 2 Gene 3 and Gene 4 are all in the same chromosome so we say that these genes are linked because they are close together on the same chromosome so they are very likely to be inherited together so having Gene 2 means you'll have Gene 3 and Gene 4. like all of those genes are coming together as a package because they're very close to each other they're obviously and they're on the same current Zone they're going to stay too much together during independent assortment they will likely then enter the game together only crossing over would be able to separate them because that's the only way genes would be separated from the same chromosome and put onto another chromosome now this produces an unexpected ratio because there's more gametes which contain the linked genes and fewer where we get a random combination of them or recombinant where they've been swapped over now if we look at a similar example with leaked genes and I've just halved the number of chromosomes here to make it slightly easier to see so I've got two chromosomes but they have linked aisles and linked genes this time so I've got cancer away and caps will be on one chromosome little a little B on one chromosome it's more likely little a and little B travel together on on cattle B will travel only one chromosome to a gametes it's it's much less likely for crossing over to happen and to have split those two up so we get a different a combination where we would get a big a and a little B and a big b and a little a together it can happen and it can happen through crossing over but it's just much less likely so instead of the nice 25 chance of each of those being inherited because they're on different chromosomes because they're on the same chromosome we're more likely to inherit the same chromosome structure with the same genes as parents because they will stay on that same chromosome and just move into a gamete when they get separated Dan crossing over to happen and for us to get a different combination or what we call a recombinant chromosome so if we look at the actual percentages of what we actually get we've got 40 excite charts or nearly 48 chance of getting the A and B capital letters and the little a and the little B small letters because they're more likely to stay together and therefore more likely to end in the gamut together because they're on the same chromosome there's only two percent chance that we will get a recombinant chromosome in our gamete because it relies on crossing over to happen okay so we're going to look at the Hardy Weinberg equation which is sometimes um just under the category of population genetics so we're just basically going to use some algebra and some maths and some rules to be able to actually work out how many or the proportion of a gene or a phenotype or a genotype or an allele in the population so let's have a look at some key terms that we're going to need for this so when we say a population we mean a group of organisms that is of the same species and they occupy a particular space at a particular time so they're in a specific habitat and at that point in time they can interbreed with each other a gene pool you might have heard this time before but in this case what we're talking about is basically just the total number of alleles that are present in that population so the genes and alleles that can be chosen and passed on between organisms in this population and then the allelic frequency is the proportion or the percentage of a certain allele in the gene pool relative to the others okay so let's look at the presentation of those so I have a population in my population I have some red flowers and I have some white flowers they're the same species they can interbreed with each other in this field that we're in the red flowers are coded for by the dominant allele a and the white flowers are coded for by the recessive allele a little a the gene pool is all of the mixing that's going on so it's the total number of alleles that are present in that population at that time I've made some small so we can get our heads around it so I've got six red capital A alleles and I have four white lowercase a alleles in my gene pool the frequency of red allele a is 0.6 or 60 and then my frequency of little a or my white flower allele is 0.4 or 40 it has to add up to one because we've got these two areas here that we wouldn't this also gives us an indication of what the proportion is or the percentage chance or the probability of these alleles appearing in the gametes so for each gamete there'll be a 40 chance of there being a lowercase a letter in that gamete and a 60 chance if they're being a dominant letter A in that gamete and so that's when we do opponent's where and then we would probably find out that that was the chance of that happening so this is like a little example of a population where we've got breathing happening we've got these frequencies and in this population here we can see we've got a 60 chance of a dominant allele and 40 chance of the recessive annual being present in the genotype the hardy-weinberg principle states that this allele lip frequency so this 60 for red dominant 40 for white recessive will be maintained from one generation to the next it won't it won't be different so there's 60 in the 40 should stay like that generation on generation on generation this can be used to deter mine if change is occurring in a population so if we've got a kind of null hypothesis a sort of a blanket statement that it shouldn't be changing from one generation to the next then if it is changing from one generation to the 10 to the next then it's not fitting within those rules of the highly Weinberg principle which means something is causing frequency of alleles to change Evolution's definition is change in frequency of alleles over time and if you think about what we describe like natural selection what that does is it increases a certain allele frequency in a population and decreases a certain allium frequency in the population because the allele frequency that increases is the one that denotes an advantage to that species and allows it to survive and reproduce and therefore more of that allele is passed on so you can see how if we can see a change in frequencies of um alleles over time in a population that can demonstrate that Evolution or change is happening the reason this is like our Baseline our null hypothesis is because for Harley why I'm going to be true for there to be no change in annual frequency generation on generation some of these facts or some of these assumptions must be true so there must be no mutation occurring that means no new alleles are ever being created and we stick with the ones that we have and the same no migration of organisms into or out of the population so no new organisms come into this population and start breeding and they introduce new forms of alleles and no alleles leave with certain individuals and move away from the population and go and form a different population but the population we're looking at is sufficiently large so that the ratios and the percentages and the frequencies that we're looking at are representative that there's no selection occurring so all alleles have an equal chance of being inherited in every generation so like I just said if natural selection was occurring and uh organisms with certain alleles were not surviving and not reproducing because they were dying or they were being caught more easily by Predators or whatever then their alleles are less likely to be in hair parents by the Next Generation and the ones with the stronger alleles are more likely to be inherited so that can't be happening there must be no selection occurring every allele should be equally available to every breeding pair every single time mating Is Random so every genotype in the population can Bridge with everyone else and there isn't any sort of sexual selection and no one's going no females are specifically picking certain males or anything like that obviously this doesn't exist in real life because some or all of these forces act on living populations at various times and on some level evolution is occurring in all living organisms in all populations because natural selection is a fact of life the hardware formula allows us to detect changing allele frequencies between Generations see how much it's changing and there's for allow the simplified method of being able to show that allele frequencies are changing and therefore evolution is happening or changing over time and it might not be Evolution it might be other things that you were looking at so you might be that the reason that it doesn't fit highly well maybe you're looking at a really small population room so anything like this is a way of taking hardware and showing that change is happening in nearly all frequencies of a population and then you can use one of these reasons or there'll be background information that you can use to explain why that change is happening but in order to show that change has happened you need to calculate Hardy Rambo for some allele frequencies at a certain time and then hardy-weinberg for a certain allele frequency after a certain time has happened to compare them so something from the 1970s and now be able to show that there's a difference between those allele frequencies using the equations first equation we need to know is p plus Q equals one p is the frequency of the dominant allele in the population in this case capital A we're using our flowers Q is the frequency of the recessive allele in the population in this case little a so we looked at the frequencies on the last slide so red a capital A allele the dominant allele was 0.6 and little a was 0.4 this makes sense because that means p is 0.6 and Q is 0.4 P plus Q must equal one you can see how then if you're only given one of these either P or Q you can easily find the other one by doing one minus this also helps us to understand the second equation slightly longer slightly more complicated but similar in terms of what we're showing so this is now looking at not the alleles themselves but the genotypes so we've got p squared plus 2pq plus Q squared equals one so P was the dominant allele so P Squared is the homozygous dominant genotype in the population that's its frequency so capital a capital A gpq is the frequency of the heterozygous genotype so big a little and then Q squared is the frequency of the homozygous recessive genotype two small A's and they all also have to add up to one and this makes sense so if I do a little Punnett Square if we replace the letters big a little a with their letters here p and Q the algebra makes sense if you think what the letters are representing and then the maths make sense once you've got those numbers just representing those letters so that's genotypes or allele frequencies the last thing we have to think about is phenotypes so be careful here so red flower phenotypes would be coded for by both homozygous dominant Capital A's and the heterozygous genotype so we need to add together those proportions for those two genotypes in order to find out what percentage of the population would have the red flower phenotype and then obviously what's left over so the 16 the the homozygous recessive that would be the only one would give a white phenotype so we would get a the population would have been red flowers a few percent of the population will be expected to have one flowers natural selection is obviously in a process that will change our little frequencies and it is a process that obviously drives Evolution but it relies on there being variation in a population to start with so variation is the differences that exist between individuals in a population and most variation is due to individuals having different combinations of allials which produces the different phenotypes but variation can be caused by both environmental and genetic causes and most cycling it is always a combination of both so let's just remind ourselves what are the causes of both types of variation the humans lifestyle plays a big factor environmental variation so your food habits where you live the levels of pollution you're exposed to how much exercise you get for Animals it's things like our abiotic factors and biotic factors so availability of food or water for plants it's availability of light nutrients water as well and like light intensity other factors that can impact everything climatic changes so genetic factors then the main one is obviously mutation so a change to the DNA sequence so the sequence of bases and DNA all are changed to the number of chromosomes for example and all of these count as mutations and they can lead to genetic variation there's a link there obviously with the idea of environmental cause potentially exposure to a mutagen or a carcinogenic compound or UV radiation for example can then lead to mutation and then banking cause and genetic variation during meiosis we create genetic variation through independent assortment and crossing over and then finally fertilization of gametes Is Random so we do not know which sperm and which egg are going to meet and fuse so the new parental combinations of genes that are going to be made from the random Fusion of two gametes is completely induced a chance and so that new combination of Parental genes is random every single time okay so natural selection is one of the processes that drives Evolution the other is genetic drift in a interpolation not all organisms are able to survive before they will not be not be produced some individuals die or they fail to produce due to predation disease or competition for resources so food water space mates light whichever type of organism they are and these are all known as selection pressures so this idea of a change in environment or Predators disease competition these biotic factors or abiotic factors causing animals to struggle to survive and reproduce overall pressures which then drive natural selection to occur if selection pressures are different for different populations of the same species from each other in telligencies will become different over time especially if they cannot interbreed with each other and then we get Evolution occurring and eventually speciation the example is obviously the moths where we have dark moths and like moths in the population and women environmental facts have changed so the Industrial Revolution happened and made this kind of dark color on the outside of trees so we have this kind of soot layer on the outside of the trees that happen due to the amount of pollution and smog when all the factories sprung up so that was a change in the environment and That Was Then a selection pressure because the darker moths were better camouflaged against birds and so they were harder to see on the trees and so they were less likely to be predated upon this means that more black or darker patterned moths were able to survive and reproduce and pass on their alleles for that dark coloring what's interesting is that this actually then was able to be shown to be reversed so once the Clean Air Act came in the smoke and the smog prevented due to various techniques and we reduced that coloring so it moved back towards a more lighter color on the trees and so that was no longer a selection pressure being really dark was no longer favorable it actually shifted back to being more light colored being the advantage so the variation in the population can be shown as a bell curve as the frequency of phenotypes so obviously we have the mean which is the middle the hump in the Middle where there's the most of a certain phenotype because that is the average and then towards the edges of that we have slightly fewer of each finger detector and what we would call the extremes the actual selection is going to promote or eliminate certain genotypes and therefore phenotypes so the bell curve is going to shift or change depending on the type of natural selection that's happening so stabilizing selection where individuals with the phenotypes that's closest to the mean they're more likely to survive and reproduce and so the mean stays the same after selection has happened over time but the range of phenotypes or genotypes just reduced so it occurs when the environment isn't changing there's no kind of massive change to their surroundings but it's about something to do with survival normally so for example birth weight or mean number of eggs laid by Robins so we see that narrow bring of the bell curve into the middle and we get that kind of really tall Peak around the mean but I'm very less wide curve directional selection is when it moves this sort of a whole curve shifts to the left or to the right and the mean actually moves in a direction away from the original and this is normally when instead of favoring the mean the middle the middle ground one of the two extreme phenotypes on the ends of that Bell because favored was selected for so it's more likely to survive and reproduce occurs in response to an environmental change so the environment produced is belka and we've got this range of phenotypes and suddenly there is a change in the environment and one of those extremes is favored the moths and the trees you could also use antibiotic resistance as an example and then lastly we have disruptive which is slightly rarer but it's where individuals with alleles for the extreme phenotypes are more likely to reproduce but sometimes this is more than one so the mean in the middle the one that is kind of the average the one that was the highest in the frequency in the original environment is no longer what's favored and it occurs normally with a fluctuating environment which favors more than one phenotype so this is a hypothetical example but there could be it could have been a snowy landscape or a mountain and sort of white rabbits were more favored because they were better camouflaged a big melting of the ice caps and now there is no or it's more more of the year now is spent not in snow and so the kind of two other variations that exist in the population the black rabbits and the gray rabbits they're better camouflaged against the Rocks now and the white rabbits are more likely to be so by princes so then we get this splitting and a diversifying of the selection where we get two different phenotypes or genotypes increasing in frequency and we get one of them decreasing so there's two types of speciation and obviously both can create new species they both involve the processes of natural selection and then we've also got genetic drift which is another way that we can drive change in annual frequencies Evolution and ultimately speciation but without the idea of natural selection and the pushing or driving of a selection pressure to change populations allopatric speciation relies on geographical isolation So Physical separation of half of each population or a portion of the population for each other so they physically can't get to each other they've been separated split off of islands separated by a mountain range separated by a really large river that they can't cross so they physically can't get to each other in order to breed that's how they become reproductively isolated different environmental conditions can then occur in the two new areas where they are separated one of them may stay the same as it was before but the other environment that they've been isolated into could be an island and with a different environment and different abiotic conditions so because they have different environments they're going to be under pressure from different selection pressures the environment might be different the food source be different the temperature or climate might be different the Predators might be diff there might be a new disease so think about our bikes are going to about the factors that could be different in this new environment these will be the selection pressures that then mutations will occur so they'll be there'll be variation map operations anyway but we need to look her as well and then we'll have advantageous alleles that are different so but in the different environments different things different animals different characteristics are going to be more beneficial because the conditions are different these will different alleles will allow organisms to survive and reproduce and they'll pass those onto their offspring so over time we're going to change the little frequency in both populations and that means eventually that the phenotype frequencies will change and the populations will become so different from each other that they'll become reproductively isolated from each other so even if they mix back even if the barrier was disappeared or moved or they were able to mix back together as more population at some point they would be so different they wouldn't be able to breed with each other and so therefore they've become separate species and therefore we've got two new species so speciation has happened so our second type of speciation is sympatric space injection so this is where random mutations will change because from breeding with others that do not have the same mutational behavior within a population so there's no physical or geographical separation here that causes them to not be able to breathe with each other it's something to do with Behavior or a mutation or them not being able to recognize each other as the same species for example for some reason that means that they won't breed with each other so sort of two groups within a population separate somehow a small group goes off for some reason and then because they're no longer into breeding and you have this kind of isolated population within the whole group so actually they're not physically isolated in space they could breed with each other but for some reason they're not able to over time obviously the two groups will change in allele frequency just because you've got a small gene pool with this one group and you've got a separate gene pool there's one group and again different mutations will occur the small group that started this this new group they'll only be able to pass on the alleles they have and they'll pass on their behaviors and their courtship Behavior or whatever it is that they've got that's different and so over time the population has become separate from each other it's rarer for this to happen um because obviously it takes sort of random circumstance or a really specific thing to happen a mutation or something to occur that causes this kind of breakaway group within the same space as everybody else So eventually obviously the thing type frequencies will change and the populations become reproductively isolated from each other completely and therefore we've got speciation so the example we use is of this apple maggot fly and it's kind of one of the examples of sort of random chance but also differences in Behavior so the original population of Apple magnify lay their eggs on Hawthorne fruit this fly reproduces is once those eggs have hatched and they fly away when it's their time to mate and reproduce they will return to the fruit on trees that are the same as the fruit that they were hatched from so so it's kind of like a known place to make sure you go back to where you patch from everyone does it they find a mate on the fruit they mate and then they lay eggs in that fruit in the early 1900s the Apple was introduced to America and the apple is a very close kind of evolutionary relative of the Hawthorne and obviously that fruit that's kind of similar some small group of flies in this population started laying their eggs in apple trees because of the way it works where I've seen you only go back to mate and lay your eggs in the same fruit as whatever you hatched the ones that started laying their eggs in apple trees at this new precedent so they will only go back to those apples and they will only be able to make with flies that are also going back to those apples and they'll lay their eggs in apples and then the cycle continues so at no point with the flies that laid their eggs in apples or the flies that hatch from apples ever go back to mating with the flies that hatched out of the Hawthorne so nothing has actually stopped these flies from mating with each other and they're still in the same environment they're still kind of flying around and they can still technically go over it and meet each other and mate and reproduce the gene pools aren't they're not physically separated in any way it's just that behaviorally they have isolated themselves as two separate groups because they're not going to mix they're not going to mate with each other because a fly that hatched from an Apple would never go back to a Hawthorn to try and find a mate the main thing is to recognize be able to recognize which one's which and be able to describe what happens in each so genetic drift is another way that allele frequencies can be changed and this is where we can change the frequency of alleles and ultimately lead to Evolution and speciation but it's not influenced by environmental factors so we don't have selection pressures which determine the survival and reproduction of organisms and they it doesn't determine which alleles get passed on based on natural selection the alleles that get passed on are due to random chance okay so it's often due to only some of the generation some of each generation in a population reproducing it's due again it's due to kind of a chance Factor as opposed to this allele is more successful in this environment so therefore these will survive and reproduce where the others will die and so that's why more of that allele gets passed on it's not about that it's just about the fact that the chance then causes a certain more of a certain allele to be passed on than others so the mechanism is that we have variation in the population same as always same as the start of natural selection than anything else and then by chance an allele for one genotype is passed on to more offspring than the others so the number of individuals with that unreal increases in frequency in the population now this is most likely due to it there are bottleneck or a Founder Effect which we'll look at in a second which is very similar to what we've said about so far with speciation so obviously speciation can be caused by natural selection and different selection pressures if we're talking about geographical isolation for example if by chance the same annual is passed a more often over repeated generation so it doesn't just happen once normally it's about repeated generations of this happening then it can lead to Evolution because we're going to change the allele groups you can see this more in small populations because if you have a small population to start with if you split that population some up up somehow or you some chance event happens it's more likely to have an influence on the gene pool because you've probably not got very many genes to start with so in this example this is the idea of a bottleneck effect that we call it so we have a big population in this case there's more blue alleles than there are purple alleles random charts causes a massive decrease in the population or a small amount of that population to be isolated then we have a really small population left of surviving individuals and so the gene pool is massively decreased if they're left to reproduce over time it's likely that because there's a smaller number of alleles to choose from in that gene pool the allele frequencies would have changed so you can see in our next couple of generations after a few Generations we now have way more of the purple allele than the blue just because by chance there were more purple alleles in the gene pool for the new smaller population a niche is the role of a species within its ecosystem all within its Community they can be biotic so water eats or what it is praying for that could be its rollerbiotic role it could be an abiotic role so it could be the temperature range that an organism lives in or the time of day it's active in that's its niche in the ecosystem or community that it lives in niches can be separated by time so different organisms can have different niches based on the time location or behavior so two organisms for example may live in the same tree but they might eat different food so that's Behavior or or they have different hunting styles again Behavior it may be that although they live and occupy the same physical space they could be separate about when they eat even if they eat the same food if you don't separate your Niche from other organisms you will overlap and if you overlap your Niche you're going to share resources with other organisms in that same environment in that same Nation you're going to have to compete with them for those resources if two species occupy the same Niche it's a more successful species so the one that's able to survive and reproduce more and therefore produce more offspring is going to eventually out compete for other species unless the other species can adapt somehow so changes Behavior change its location change the tummy to whatever in order to change their name if two organisms are occupying the same Niche and they're directly competing for resources one will eventually out to complete the other one so adaptations can be for biotic or abiotic conditions the abiotic embryotic lists of conditions or factors don't change really so you just have to think about an adaptation for all the factors that we already know are abiotic so water obviously web feet being able to swim hold breath go underwater temperature so anything that's going to insulate and keep the warm reduce heat loss enable them to hibernate that's a physiological adaptation because they can hibernate by shutting down body systems over winter light intensity so mostly plants um this but also some organisms are able to produce kind of UV protectant kind of sunscreen hippos is an example of that um to protect them from UV damage and therefore radiation could which could obviously cause mutation or if you're in a plant it can obviously mess with your photosynthesis soil conditions so anything that could adapt them to low nutrient soils like carnivorous plants adapted to Salt price salt soils or alkaline or acidic soils anything like that is going to be an adaptation to kind of your nutrient availability and also your soil conditions by biotic adaptations then anything that increases your food sources so access to a food source that others can't get so I'm thinking about pieces of tools or behavior specific behavior that allows you to maybe learn to smash a shell on a rock that then other animals can't do that so then you get the nutritious food and eating with anyone for that food source finding and attracting mate sounds like a sort of difficult one but again remember that biotic conditions also mean being able to interact with other animals around you and specifically competing for things like mates that is a competition factor between members of the same species so anything that allows you to make sure that you're going to succeed or more likely to succeed um or you're making sure that you're definitely going to mate with the right and correct species so that means that you'll have successful mating actively stopping competition with other always invite part of some way um so bacteria can produce antibiotics that will kill other bacteria around them but not themselves that helps to reduce competition plants and the creative bush is an example of this it can secrete toxins from their roots and that can damage the soil around them but other plants to grow so they're not going to be able to grow nearby population size is the total number of organisms of one species in one habitat we need to know some new term which is carrying capacity sometimes represented by the letter k a lowercase letter K which is the maximum stable population size of a species that an ecosystem can support So for each species or for connectively the species in the community within this ecosystem what is the maximum that that can get to that that connected by that ecosystem because they think about that's all of the ideas about the linking between how much food there is what the conditions are like how much competition there is between organisms what that sort of stable food web so when conditions available more organisms are going to be able to survive and reproduce so the population increases because we're going to have more food we're going to have good weather we're going to have less chance of dying from disease or we're going to have less chance of being predated upon or even if there are predators there's enough a large size of the population so then we get that increase so that's what's represented here and obviously we know that these changes could be seasonal and happen within a season because we've got the winter where it's cold and it's gray and there's very few babies being born and there's not much food and then obviously as Spring Farms we get all of the animals being born because there's a surplus of food there so we get this increase in population the weather's warmer they're not going to die of cold all of that stuff and then as conditions become less favorable more organisms going to start design and few are going to survive to reproduce this is the population size decreases again this happens and at that point as well there will be other things that are going and so there's biotic and abiotic factors that can affect the population size throughout a year but also over longer periods of time and then obviously we have starvation and that ties in with this idea of competition with your other organisms so it's about the availability of food and competition so the main thing is if we get too many individuals if the population size grows too large you're ultimately going to not have enough food to support population and they're going to be competing for food we get to that Peak and then that's going to start causing that decrease so then the overall number of organisms that are in the population that is the species sort of group that is supported by that ecosystem that doesn't really change too much is the carrying capacity so that's the stable amount that it can support on a regular basis and it normally fluctuates slightly above and slightly below that carrying capacity as we've seen through the seasons so you get this kind of a carrying capacity amount and we get fluctuations up and down that tend to stay around that carrying Trust and if we go too far from the carrying capacity it decreases as we've seen for all these reasons and then again if it goes too far below that then conditions will improve because there's less competition and there's less Predators because they would have also lost their population size as well and so then we go back up and it sort of oscillates around this carrying capacity or k and that's on a seasonal basis if you look at this long term you shouldn't get too much fluctuation if your ecosystem is stable so if you've looked at a really really long term graph you wouldn't see the Titanic fluctuations you'd just be able to see long term what was happening and they should stay relatively stable around apparent plastic unless there is large environmental change and large environmental change is what triggers say mass extinction events or cause is an organism to go extinct there are two types of competition intra specific competition is the one we're going to look at first intra meaning between within the same species so if you are competing with an organism that is the same species as you then is intra-specific competition it occurs when individuals in the same population compete for the same resources it can cause cyclical change in the population size around the population's carrying capacity which is where the population grows and shrinks and then grows again unless there are large changes in the carrying capacity to bring it down and so then that would maybe change the number of the average number of the population but otherwise it will just go in this kind of pattern okay so now we're looking at into a specific competition so in trust specific meant within the same speed machine so organisms of the same species competed with each other this is when we look at the competition between organisms from different species so inter meaning between two different species it occurs when different populations compete for the same resources for example food if they're having to share a food resource they'll be less available food for both of the population so the sizes will be limited and they will not be getting enough energy to grow or reproduce so that will limit their population size but if one species becomes better adapted to their surroundings so they're more able to find food or catch food or they're bigger or they're heavier for example they can out-compete the other one and that population will Decline and then can be wiped out from that habitat this is exactly the example we looked at in a previous video about red and gray squirrels so the gray squirrels are larger they're able to get more nutrition out of their food they're able to put on more weight and therefore survive the winter better a debit more adaptive to certain habitats than Red Squirrel so where they used to overlap now the gray swirl has out competed them and the red scroll is basically not found at all in those habitats anymore Predator prayer relationships are slightly different because is obviously in this case one of the organisms is food for the other organism so predation in this sense just means an organism killing and eating another organism the sizes of predators and prey in an ecosystem in a community in a food chain or interlinked with each other because as one changes it causes the change in the other population because obviously they're interdependent as we see the prey population in future competition in their own species can fluctuate anyway and then any predation factors has an impact on top of those changes so examples like the one we're going to look at and the one that's often used is hair and the links so like a rabbit and then like a cat type creature they're normally used because they come from a very specific habitat where the food web is very small so there's not many other food sources for the links for example and so therefore we they're literally tied to very closely to each other in reality the relationships that we're looking at are a lot more is not only one product it doesn't geostreline and normally there's more than one predator for each species there's other factors also involved like we've talked about like the ability of food for the prey which could be due to an abiotic factor change it could be due to competition whether their own species so that fluctuation is going to be happening as well within the hair as a species without the impact of the links and so that can then affect the link separately okay principle diagrams normally look like this you'll have the troughs of of predator and prey and normally the Predator diagrams there's some rules that they follow so the Predator Peaks are always on delay so after the prey Peak there will be a predator Peak so that always normally shifted to the right and there's always going to be more prey than there are predators so be careful some graphs in the exam might use two axes so you could have like hundreds of a predator and then thousands or tens of thousands of a prey and so because the units might be different they might put them on different axes so just be aware make sure when you are in touch with these graphs you're really sure which one is prey and which one is present so in this case obviously our hair is the prey there's more of them and our links is preparator there's fewer of them and their graph is down and shifted to the right so there is a delay in the effect on the population size of the Predator after the changes to the population size of the pro so we need to be able to explain what's Happening Here Again you may have done this at GCSE and it's very similar so at one my Lynx population is increasing and it's increasing after the hair population as those curly women an increase in the hair population so there's a lot more of them to eat they've got more food available which means they've got more energy so they're going to be surviving and reproducing more and so more babies links are being born then are dying and therefore we get an increase in the population the hair population starts to form and it could be due to starvation because they've reached their carrying past or they've exceeded their carrying capacity they've run out of food the hair preparation starts to fall down it also could be as well that predation is getting easier there's more links and so there's more premises around they're finding it easier because there's more hair and because the hair are weaker because they're running out of food they're having to compete with each other so they're easier to catch these two things into play here and we get a decrease in the hair population because more of them are being eaten then ultimately we get that delay in sort of response from the links but ultimately the links suffers the same match as the hair so the hair is the food so remember they've eaten too much of the hair the hair has disappeared we've decreased the number so much that now there's lack of food for the links the links is now obviously potentially competing within their own species within their population so less food means less survive and reproduced so the population numbers four we've got more links dying than are being born and then this is going to go up and down and up and down repeat the time scale is quite long we're talking decades here so kind of one cycle every 10 years or plus years or so it's not something that happens every season it's going to happen over sort of large periods of time okay so how do we measure population size well we can't count the exact number of every organism in a large area we can't count and necessarily be able to find catch and identify every individual of a species in a population in a certain habitat it just would take too long and in some cases there's too many to count you're not going to assuming how to stop them they could be camouflaged it's just not possible so in order to kind of estimate population size or do as we sample so we take a sample from a specific area and we use that to multiply our and estimate the entire population in that area in order for this to work your sample must be reliable so it needs to be a large sample it needs to be a decent proportion of the real population attention so that when we're scaling up we're not taking a tiny tiny tiny Bush and trying to apply that to a really large area so the larger the area is the more small samples need to be taken from that area in order to make sure that our sample is reliable in order to make sure again that the proportion we're taking is representative of the whole population we need to make sure that the whole of the area that the population is present in could be sampled equally so it should be randomly and without bias where the samples are chosen and so every time a sample is chosen it could have equally have been the chance that we need to sample any of the area that we're looking at and so we've got techniques now to do that and hopefully remember this from GCSE with like doing the quadrats so as long as your sample is reliable and representative and you do it in certain ways that allow it to happen that's all that needs to do so the sampling method in the way you're going to sample is going to depend on what organisms you're sampling um for plants anything that means very very small for example here in my picture I've got some rocks and on these rocks will most likely be Olympics amongst this series so there will be seaweed here and that's obviously not going to move or go anywhere and potentially inside my area inside my quadrat sample there's going to be limpets if you're not 100 sure what if it is it's kind of like a little shelled organism and it lives on rocks and it clamps down it it clamps down and sucks and attaches itself to the Rock and so they very rarely move they will move very very slowly and they tend to really move around when they're grazing which is normally when they're carved in water so when the tide is down at this and you can see all of these exposed rocks and this area there will probably be little bits there and they're not going to move so although they're an animal they're not an animal that moves or it's an animal that moves very slowly you can also use a Quadra if you're going to be looking at animals that can move around you need to catch them then you're going to need a different sampling method but for the first couple of examples we're going to look at we're going to look at non-motile and non-living organisms and plants so we're going to use a quadrat again we'll have seen quadrants before so it's just a wireframe typically with internal grid and we use it to Mark our small area there'll be different sizes and depending on how many squares you've got there'll be different ways that you can use this so we're going to have a look at how we place the quadrats which again is similar to GCSE to sample and area and then we're going to look at different ways we can measure and count the organisms within that corporate track okay so we have two ways of sampling our non-motile organisms with quadrax we can do random sampling so that's where we eliminate personal choice or bias and we select the sample using random coordinates and we use a grid sample probably with two tape measures we make sure that we've got this area that we need sort of grid it up and so we have some coordinates and then we select the coordinates at random because throwing a quadrat is not truly random because you don't have an equal chance of sampling the whole area it's based on the direction you're throwing it's based on how far you can throw how strong you are so that is technically bias so you need to randomly choose coordinates using either a random number generator dice or just picking numbers out of a hat and that makes your sample more reliable because it's not due to personal choice you've not chosen where to put the quadrant the more quadrats you can use to the sample to make the sample the more representative it'll be of the whole population so as it's the larger the area the more quadrants you should be doing to get it to be more representative so I've got my X and Y axis that I've made with some tape measures just laid out on my field and then I'm picking coordinates out of a hat so say eight and then 20 I go along eight and then up 20 and that's where I lay my quadrant and then I've looked at that quadrant and in that I have just counted the number of yellow flowers and that is six because I'm not counting those two bottom ones because they are over the edge of the quadrant so I could just do that and I could repeat that for every quarter and then I could calculate the mean number of yellow flowers in total because I could add them all up and divide them by the number of quadrats but there are other ways I can also count or estimate the abundance of that organism and we'll look at that in a minute because that can be done in either of these methods so systematic or non-random sampling with transients allows scientists to see how the distribution of a species changes as the habitat changes so we can't necessarily see that with the random sampling unless for example you are randomly something in two different areas so a field that has been known and a field that has not been known for example or a field that has lots of shade and a field that doesn't have lots of shade you could do that and compare your answers but with this one what we're doing is we have a changing habitat or a changing abiotic or biotic factor that goes across a gradient and so we are taking a transect across that area so we know that the environment is changing and we're just going to look at how the distribution of the species changes as we go towards all the way from something so my two examples are either from directly underneath the tree which will be very very shady away from the tree there's other things you could look at there obviously there's competition potentially with the tree or we can just simply measure the light intensity or you can go right from the edge of a riverbank away or the sea for example away and then obviously you've got Warsaw water warm water closer you get to the Sea then you have further away so you should see what we call zonation which is a change in the distribution of species based on the abiotic factors there's two methods with the transects either you've done what I've done in the images so you have separated them out at regular intervals so every five meters or every two meters along your tape measure and that is an interrupted transect where they're placed at regular intervals or you have a belt transect where the quadracks are placed directly next to each other there's benefits to both and we'll see the interval or the interrupted one where there's intervals between them is faster because you're covering more kind of length but you're doing fewer quadrants the belt transaction probably gives you more information you can see more of a change you have to do and as you can see in both pictures you have to repeat the transect so at the same kind of angle or the same start point and end point but to make sure those quadrats don't overlap with each other at any point so you're not something same area but you should repeat them and then you have a repeat for each of your distances so when we're using a quadrant we can obviously count every individual that's in that quadrupt sometimes that's harder to do than others um there's still too many you can't really see or separate individuals especially if you're looking at something like grass you can't separate the blades of grass aren't always going to be from separate organisms for example or if you're trying to do it quickly and it can take too long to count all of them there's sort of different ways that you can use a quadratically estimate population size so the first one is percentage frequency so the probability that species will be found in a single quadrant so we work that out by doing the number of quadrats that a species was found in divided by the total number of quadrats times 100 so for example 30 quadrats are randomly placed in two different fields maybe one shadier than the other maybe one is the grass is cut in one and it's not on the other maybe they've got two different sort of crops growing in the fields and in one field days were found in 18 hours 30 quadrats so it's just whether they're present or absent that's all it is is it it's usually have at least one individual in that quadrant and in the other field days is already found in sit out of the 34 so then we can obviously do the number of quadrats this which was found in divided by the total number which was 30 for each one and then that gives us a percentage so 18 out of 30 times 100 gives us 60 the percentage cover until 2 6 out of 30 times 100 gives us twenty percent so the other way we can estimate of how how much space a species is taking up in a certain area is using percentage cover so percentage cover is faster but it's more subjective because you are not actually really counting or measuring you're using a visual estimate of an area of a quadrant that's covered by a species so it tends to be overestimated for flowering plants where they think about they've got sort of broader flowers and leaves covering a certain area and then also underestimating plants that grow very close to the ground and ones that you can't see so easily so it's often easy to do this if you can use quite a large quadrant a quadrat that will be 10 by 10 squares because then you've got 100 squares and then that means that you can just see how many squares are covered in total in area by the species how many sort of rough squares you can find that species in and then out of 100 that will give us a nice easy percentage so here's an example I've got three different switches of plant they're all different different colored flowers and then I also have graphs as well in my quadrant that's obviously the grass is just the green so how much is Just containing the grass and then you've got red pink and white flowers of the different species so I've roughly counted sort of if it's a whole Square it's obviously covered it definitely counts and then I've actually used my kind of subjective judgment as to whether something's covering the majority of square or not and sort of a rough estimate of how it is and obviously this makes up roughly just under 100 so it's not perfect and obviously technically there's grass you every Square it's just about where the grass is the majority and where it's the minority so percentage coverage you can see is a way of doing it quite quickly and get general idea of how much area a species is covering but it's not going to be as accurate as actually counting them individually or even doing percentage frequency okay so let's look at how we sample motile organisms so in order to catch organisms that are moving you can need the right equipment and it depends on what you're catching and where you're catching depends on what current you'll need to use and in order to when we're capturing them obviously we're just capturing them to identify them and count them so we're not catching them for a really long time and we should be just obviously identifying what species we've got and Counting them and then they go on their way so the best method is going to depend on where you're doing it and what you're capturing so the equipment that we might need to mention here is something potentially like computer which is something that can connect small insects and you suck into a little mouthpiece and it creates a little vacuum and there's a little suction tube that then can suck insects into the canister it's perfectly safe in there there's a little filter to stop you sucking off any insects and then you can observe them in the little house and then you can remove that and then tip them Pitfall traps for larger animals and literally when you dig a little hole you cover it all up so you can't see it and they will fall in obviously they can't fall too too far but it should be deep enough that they can't get out straight away and then you would have to check them count them identify them then you could help them back out sometimes you might need to put food or some kind of bait in there in order to get them to come towards the track sweetness so really big long Nets can be used for catching insects like things like butterflies and things in the air sweeping it along Tall Grass which would disturb the grass and then things will fly out of the grass and trap them in the net large Nets as well for a classic organisms so you wouldn't need as much dense fine mesh necessarily but you need to let water move through it and then you could use that to sweep areas of a moving river or lake for example so once you've picked your equipment you have to think about how you're going to sample and there are some ethical considerations with this some people think that capturing organism is unethical completely because it causes the animal oil there's some stress and so it shouldn't be done but if that is the only way that you're going to be able to sample a certain area then you should be making sure that your handling with it should be kept on minimum like I said you really don't need to keep them for a very long time and you don't need to hold them or handle them for long and all organisms should be treated carefully and with respect the main reason as well for the stress is obviously because that's not nice for to put an animal through that but if they get really stressful if they get really affected by being captured it could reduce their chances of survival after you release them so it's not just only the impact you have while you have them but also how that could end their life once you let them go okay so the method we're going to use to take a sample of moving organisms and use that to estimate population size is the mark release recapture method so when you take a small sample of the population using whichever appropriate equipment and Method we've decided on depending on what organisms they are and how it's live in and we should take sample and then count them you'd probably take more than one sample you'd take it in different areas do repeats Etc but you do that when you count them after you've counted them you'll have to handle them to do this but you'll mark them in some way a spot of paint and identification tag some of it's harmless and there should be some considerations about what you're marking where you're marking what you're using to Mark with and then you let them go so then you release them back and then you need to wait long enough for those individuals that you caught in the first sample to have mixed randomly back in with the population because the point is that we're going to look at when you recycle the proportion of the marked individuals to the unmarked individuals and that should give us an idea of the proportion that our sample is to the giant population so you need to leave at least at least 24 hours if not longer for them to mix back in and then you'll take a second sample in exactly the same way so that's important there because it needs to be the same time same place ideally the same type of sample so the same equipment used same time of year same time of day same place everything should be the same and then you're going to record the total number of animals that you get in the second sample and the number of marks animals that were in the second sample that you got and so then now you estimate the population size we're using this formula so we take the number that we caught in the first sample we times it by the number call in second sample and then we divide that over by the number of marked individuals that we've had in our second sample and that will give us an estimate of how many of that individual there are in the total population in that area now obviously if you've done repeats you could do the mean number call in Sample one the mean number core example two of the mean number of marks on the two or you can just do the total of all your repeats as well so there are some problems with using this technique to estimate population size because it relies on assumptions which are obviously some are realistic assumptions or assumptions that we can be confident that can happen and some that can't so it relies on the idea that you're that Yorkshire is closed so without the youth sampled your population the population itself the number of total number of audiences of the population stays the same that would mean no migration out or into the population so no more reasons leave no reasons come in and there's no births or deaths that occur and this just has to be in the time between the first time you take your sample and the second time you take your sample this is something that obviously can't be controlled the sooner your sample is taken from between first and second then less time there is then you can kind of be a bit more confident that this is less likely to have happened but you can't control it at all and also there's things like actual death so or the chance of all this is actually dying then there's also things to think about like oh what if that all doesn't got trapped somewhere or what if that organism has flown away or what if that organism can't be captured for other reasons because it's a caterpillar that's now gone into a cocoon so it's not moving anymore so therefore it can't be captured there's sort of other things that can limit how the chances of you getting the same number of organisms to sample each time it also assumes similar to what we've just been saying that all members of the population mix randomly so when you've got them back they're completely randomly mixed up they haven't stayed in the area near to where the Trap is they've sort of gone back talking to the population next and so that each member of the population has an equal chance of being captured every time so when you won't go into your sample obviously you've collected a certain number of organisms you put them back you need them to go and completely mix randomly so that when you go and do your second sample you're not just recycling the same ones that you've already done again it relies on the fact that all the animals will behave exactly the same that they will disperse that you've left enough time for them to disperse and it also relies on certain animals behaving in a certain way so for example males and females are often going to behave differently especially if it's around Springtime and the females are caring for young so they're not going to go exploring they're not going to leave nests they're not going to leave their children or they might not be able to move as far because if they've got Offspring they're not going to be able to take risks they won't be demonstrating risky Behavior so they're not going to sort of go into somewhere they're unfamiliar with so they're less likely to be caught so in reality if you're only really sampling males at a certain time you're not sampling all the population or you're not able to equally chance of sampling all the population again this is something you can't necessarily control that you assume that the marks that you've put on or the tags that you put on have not been rubbed off or lost or removed between captures so that you definitely know that if you marked them before they will still be marked when you go back this is something easier and something maybe you can try and control a bit more but you shouldn't try in order to do this use anything that is really sort of sticky or really toxic or anything that could be sort of super waterproof and therefore is a danger to the animals and really think about what you're using in order to tag them ethically as well as trying to make sure it doesn't rub off also you're assuming that your tired will affect its survival in any other event it shouldn't likely change its Behavior it shouldn't make it be I don't know shunned by the other organisms and like left out and then not shared food or whatever or get not given access to certain places it shouldn't make them more likely to be predated so for example if you put bright paint on a prey species that is normally going to be camouflage you've sort of ruined that in some way and so then predicism will not need to be able to see it and therefore they're more likely to catch it and eat it which means you've increased the chances of your marked organisms being killed uh predicted upon before you do your second sampling and so therefore then you've got an unfair test there because your marked ones were more likely to die so there's gonna be fewer of them in the population when you sample the second time so it's one of those things again you can try and do the best you can to control this but you're not always going to be able to account for Animals Behavior okay so let's go through this then so primary succession is our first example it happens on land that is newly formed or exposed where there is no soil so often this is from something like Iglesia Retreat so when the ice melts or a glacier is moving slowly over time because they do move and sort of slide what they leave behind is what's often called a scree slope so it's bare exposed rock that hasn't been exposed this has been trapped under the ice and then obviously once the ice Retreats it is then exposed to all of the different elements and then also obviously plant species can start to colonize it so seeds and spores blow on the wind and they're going to land on this bare rock surface and they're going to begin to colonize it the conditions are very hostile so it's going to potentially be very exposed there's going to be high light intensity there's going to be little water because it's like dry bare rock and there's nowhere for the water to sit and be whole and like contained so it could be when we say exposed it can be very windy for example so you've got all of these kind of harsh hostile antibiotic conditions that mean only certain species could actually grow here so even if some other seeds were blown over at the time only some species like lichens for example would actually be able to colonize and start to grow on this bare rock face then we get our pioneer species proper so lichens are a pioneer species they're one example and then we're going to get some of our other lycos as well but also some small plants annual plants so that means they live for a year they don't come back each year they just kind of live for one season grow and then die so that means their life cycle is quite short and so they're gonna die and they'll be decomposed by my organisms through the process of Decay that we know because microorganisms would be able to survive here especially if they have cereal to break down which is what they're going to have when these plants die and so that starts to create a layer a layer soil on top of the bare rock so the breakdown means it's going to release some nutrients and we get this called a hummus um which is basically the soil that's on Top of the Rock but it's a very thin layer at the moment the new organisms are then able to come in so the pioneer species have started to create this even better kind of thicker layer of soil and so what they're able to do is they're made the conditions less hostile less harsh because there's more soil which means there's nutrients also there's soil for roots to grow into which plants need to be stable there's going to be water that's going to be able to be trapped in between those soil particles so that means that they've got access to more water and therefore more of them can grow so we get this more of them growing and therefore more of them dying and if more of them die and Decay then we get an even deeper layer of soil with even more nutrients in it so we're making the conditions even better for other plants to come along and colonize so now we get to a point where there's enough soil that we can actually have some shrubs and some small trees appear and they are sometimes shade intolerant so they're used to having a lot of likes there's still a lot of light if they're quite small and they're all on the same kind of height level they will become what we call the dominant species so the dominant species is always the species that's having the most change and the most effects on the environment but biodiversity has increased so we're increasing our biodiversity as we go along because we're increasing the amount of different plant species that can live there and remember that's also having an effect on the number of different animal species that can live there as well and then lastly we get to our climax community so the climax community is the greatest and most biodiverse community that this habitat can now support so we will have a mixture of sugar cheese but mostly we're talking about large trees and then some small shrubs that can cope living underneath them in the shade that they're creating and we've got this kind of normally we've got Oak for example Oak Forest Ash Forest that we're going to have in the UK is what our normal climax community would look like so if all land was just left to go through this process of succession we'd have forests of some kind covering most of the UK and that's what it would have looked like sort of back in the early times before humans have really colonized a lot of the land and sort of starting to chop down trees and things like so then trees and Big Trees become the dominant species because they are now the ones that having the most effect on the environment but it stops there so it doesn't change anymore it becomes a stable community a stable environment so we don't get much change it would be like that for hundreds and hundreds of years after that point it has taken hundreds of years to get to this point this does not happen overnight this takes a very long time to occur and then when we get to that climax community then that would be very stable and it wouldn't change so we talked about which species become the dominant species as we move through that process of succession and it's because they're changing their Baltic conditions the most and the main thing is they're making it more suitable or less hostile for the next species to grow so we need to have a think about some examples don't necessarily need to know all these examples off the top of your head although realistically for pioneer species you really we should know lichens but it's also thinking about how are they actually change how are they improving the antibiotic conditions how are they making it less hostile and more suitable for the next species that's the point you would have to get into your long answer if you're talking about succession so we'd be going through the stages talking about primary switches maybe give an example explain how it makes it more hospitable for the next species than saying what the next species would be say about the increasing in the soil and then moving on to oh what the next species potentially be and how would that make it better for the next species after okay now how come trees can come and that's the kind of answer you would need to give so here's system kind of walkthrough of each stage and sort of talk about how they actually change that abiotic conditions so the pioneer species we said lichens the reason lichens are good at being a pioneer species is because they secrete acids so they erode the Rocks the bare rock face and start to release some of those minerals and also break up the surface of that rock which increases little cracks and crevices that the seeds that are then going to potentially come and be able to sit mosses also is sort of the next stage of pioneer species they have very very small roots and they're very good at retaining moisture so that they are able to grow very very little amounts of soil then we have marigraphs so this is a specific example of sanding so sand genes are an example of where succession can happen because obviously their sand is the same as bare rock there are no plant species there so Maron grass is normally one of the first pioneer species to colonize sand dunes and they can do that because they have very long roots they reach right down things they can get some water but they can also get through the sand hold on in the sliding kind of sand environment they've got how do these Pioneer switches change well as we said they release minosterone rocks they create soil so most of those main things to say is that they decompose when they die and they form this first layer of very thin basic soil which starts tripping water and so therefore increases water availability and increases some nutrients for the next species so the next kind of intermediate stage what could we have or we can have grasses we can have funds we can have small flowering plants then we've got things like sand sedge which is the next stage in a sand dune example how are they going to change the abiotic conditions well they create a deeper richer soil when they die adding more even more nutrients in their full tracking and also even more water and moisture they also some of these species can then start associating with nitrogen fixing bacteria or mycorrhizer fungi as well and that increases the concentration of available nitrates and phosphates if we're talking about Microsoft fungi these are mostly talking about how we're making conditions most plants that were associated with nitrogen fixing bacteria are even to survive in low nitrogen soil conditions so then as I was saying before if then the soil becomes quite rich in nitrogen they're not going to be as adapted and when other species come once the nitrogen is there they will out-compete them it can also do the opposite and sand says for example can actually make the conditions more hostile for the species before so the baron grass will die out or not be able to be as successful in the sand scent is therefore out competing it because it actually stabilizes the soil and stabilizes the sand and Marin grass needs the sand shift and move in order to grow effectively so there's kind of two Computing sort of ideas here one is that obviously these plants are making the conditions better and so we're practically be able to come and grow here but they're also potentially out competing with the plants before or preventing them from staying and so if you see this disappearing as the Marine grass or the sand dunes if sounds they're just present because those conditions are no longer how the baron grass likes to be able to grow and the last thing we have the climax community so normally like I said these are bigger organisms Big Trees big shrubs in the UK things like Oak Birch Ash are kind of on normal trees for a climax community in a deciduous forest in coniferous forest the tree species will be different if we were in a colder climate so this is the other thing you have to think about is that obviously the climax community is going to look very different depending on what the actual climate is like in all of your different examples so like I said if we have like a more Northern Scottish Highland kind of snowy cold General temperature then that climax community is living more coniferous forest so kind of trees with pine trees and needles and Spruce and all of that rather than big broadly trees like Oak Birch which will be more used to be seeing in sort by the Southern England same as if you're looking at the climax community and Antarctica or if you're looking at conference community in the desert like on the sand dunes they're not going to get giant oak trees on the sand dunes their climax community will be small shrubs of some kind okay so that's something to think about when you're if you're given any examples any data or a description or pictures or something like that in the exam you'll need to kind of adapt this succession story to what they've given you in terms of the species they're present how do they change the antibiotic conditions well this is sort of moving from the late intermediate stage into the climax community they're going to do things like create shade which can stabilize temperature because it means that it'll be cooler for some of the plants underneath they can also decrease light intensity but that makes it a prime environment for things like shade tolerant plants they can trap air underneath campy layers and that increases humidity which obviously is good for some plants because if they're like a humid environment they can reduce the wind exposure so get less exposure they're starting to blow over all of it also increasing biodiversity because they act as shelter and food sources there are some organisms animals that only live in trees or up in trees they wouldn't move around on the ground so you need a big canopy of trees that they can jump from tree to tree without going on the floor and then also increases the leaf litter so the more trees and shrubs you have Falling Leaves especially if they're losing them in sort of Autumn and stuff like that they're going to then collect on the ground which creates Leaf litter which some organs live in also some orders was feed off of so think about all the fungus and the microorganisms that feed off of all of this detritus it also increases the depth and the nutrient content in soil and again increases the water content and things like that so that's how we get from sort of just no soil and how these antibiotic conditions being changed every single time with these new communities that are coming up how is it improving it for the next one allowing those species to compromise so secondary succession is the other example of succession you need to know and it happens with a plants are removed but the soil remains kind of intact so really just above ground all of those plants and everything else that's removed and so we go back to Bare soil but it's not bare rock so the examples are like a forest fire or deforestation where they can come down and Shop down a hot forest and clear the land but there is still soil there there's soil there's nutrients there's kind of water retention so the conditions aren't as hostile to start with as they were the primary succession remember is bare rock and there's no soil or anything so it can occur at any stage after the pioneer species stage of primary succession and it happens in the same way so the same stages the same steps you're just starting at a later stage so instead of starting with bare rock and lichens and mosses we're starting with the kind of small grasses flowering plants Etc so sometimes humans do not want full succession to occur and so sometimes secondary succession can be forced by Human Action in order to try and regenerate land or to try and prevent a climax community from forming most of the times because we're trying to conserve a pioneer species or a species in the intermediate range and we don't want the climax community deformed because that would out-compete that species and it would be lost so most of the time this is a conservation method and we're going to look at conservation next but this is one of the ways that conservation can be maintained so example of methods that are used to prevent it some of these are conservation and some of these are just through human actions so controlled burning which happens over Heather's Heather Moors in Scotland for example where you you don't set fire to a whole load of land and let it run right and run sort of wild because that would be dangerous obviously but you can burn and control where you burn and sort of fit the fire out and make sure that it doesn't run away as this sort of end points and barriers to make sure it stops at a certain point grazing herbivores so letting animals graze deliberately sometimes we do the succession controlling in order to continue there to be land for herbivores to graze or to feed but sometimes it's that just the act of grazing animals eating the grass keeping the seeds and the plants down so they eating to get Too Tall that can actually maintain a sort of meta-like structure mowing does the same things so cutting the grass actually mowing down the grass and keeping it at a certain height also prevents succession from happening and then copsing trees so preventing those kind of early tree species from getting too large and growing into major trees and then creating lots of shade what we do is we chop them at a certain age to a certain height down to a stump and then they regrow back from that stump but they regrow in quite a fine way so the twigs and branches are sort of finer and they grow kind of slower and so then it doesn't always create this really big dense canopy that makes a lot of shade and that can change Stop Those abiotic conditions from changing that way and then prevent succession from carrying on so cultivation in protection and management of a species and habitats in order to maintain biodiversity remember biodiversity is just the variety of the number of different species present in a habitat so biodiversity is decreasing we've got a little infographic there's so biodiversity loss has been caused by so many things or being caused by humans including climate change habitat loss over exploitation like overfishing habitat loss at deforestation pollution our effect of climate change and invasive species and this is becoming more and more and more common and happening in more and more places around the globe because the population is growing exponentially and because there's more people they need more space to live to build homes they need more space to grow food because we need more food because there's more people to feed and so the impact of just us taking up land and us the way we're using the land and using the natural resources and the farming and agricultural practices that are increasing to try and increase the food demand all of that is having an impact on biodiversity it's unsustainable the way we use resources and the way agriculture is currently being done and that's having an impact impact on biodiversity of all species in pretty much all habitats people especially places where they are very reliant on the land and very reliant on the natural resources or reliant on farming are often quite reluctant to embrace conservation efforts to try and prevent the impact of their current practices on the species around them the wild environments around them because it can directly affect their livelihood their income and also obviously can reduce their access to something natural resources which they are relying on for food and shelter and Fuel and money income as well so conservation efforts are always constantly trying to find a balance between maintaining the sustainability the natural resources maintaining protecting areas to allow species to live in the world peacefully and to reduce biodiversity loss but still allowing countries that need to develop and people their places that need to expand and need more homes and more land to that to happen as well so thinking about sustainability practices like management of forests fisheries and farmlands and then conservation practices like wildlife parks preventing overfishing preventing hunting preventing poaching and just generally kind of more different species and preventing them from being damaged by human impact so as we said there are conflicts and it's becoming more and more necessary to find careful management processes to try and get a balance between the conflicting pressures that are affecting actual efforts to try and conserve biodiversity of various places and we need to kind of be aware of these conflicts so that we can kind of kind of talk about the designs so obviously obviously the main side always is trying to make sure that species are protected that biodiversity is not being lost but we have to balance that with the costs that it might take in order to try and pay subsidies or to try and encourage people to follow these rules and also it's quite tricky to sometimes having to employ people to enforce the rules as well it can obviously affect local economies so we've said that it can affect people's livelihood people's income if practices that are now sort of limited are the ways they get their income or they have to take up other alternative jobs or practices that are part of the conservation effort rather than what they were doing before and they could have made more money previously trying to allow the development of society to continue whilst trying to reduce the impact from species so that's trying to still conserve species and conserve their way of life but still allow people to build homes and spread out and take up space so thinking about ways of limiting that and not stopping people from developing where they need to balancing the conserving of species with the need to protect food security for growing population there is no doubt that obviously with more people comes a greater food demand we need to feed everybody I mean to make sure there's a supply of food everywhere and that everyone's getting enough in order to survive but in order to do that we can't overfish or overwork the land in order to a point where to try and increase yields but at the expense of other species that is obviously not acceptable so there's this constant touring and throwing between maybe local populations or farmers and the people who are trying to conserve the species and you may get questions where they present case studies or data where they might sort of ask you to see both sides or evaluate what's happening or just to kind of discuss the issues that can happen around conservation and why some people might not be as open to it as others okay so how does agriculture impact from biodiversity reduces biodiversity because they're growing monocultures which is obviously just one species often even one variety of one species so a very narrow range of allele frequencies in that population and that obviously a large area of that just one species has a really low biodiversity and if you're using a really large area to support just that one species if most of that air is taken up by biomass then there's little area and resources left for anything else to grow nearby anyway and they also use herbicides and pesticides to prevent other plants from growing weed species growing nearby and also insect species or anything that they think will be a pest that could spread disease or damage the crop in some way so killing those organisms of the farmer doesn't want reduces fiberglass even further there's fewer food sources so if there's just this one species for a really large area that's it there's Emily killing everything that feeds on it that there's not going to be plenty of habitats or food sources to support other organisms also from Pedros so you can see my two Fields here this sort of on the left it used to look like or would be the idea would be all Fields would be bordered with a hedge and so there would be this kind of separation between the fields and make them smaller potentially and have these different species and plant species forming kentros in between so although we do have large areas of one species there's a mixture in between to help kind of increase those habitats and food sources but obviously Farmers have removed them and farmland's getting larger and nicer with sort of fewer and fewer Hedges between them and just ditches instead or tracks with no plant life on them so as we said hairdos have this narrow belt of small plants shrubs maybe some small trees and they don't intend to surround fields and then go along roads they used to be marking the boundaries between the land of the different owners of the different fields and also to prevent animals from moving from walking field to another when you do want your cows escaping if you put a decent hedge around it they couldn't they couldn't escape but there's loads of other benefits to hedgerows as well they help prevent soil erosion from flooding if you think about obviously potentially spraying nutrients and other things onto the fields and liquid but also if there's really heavy rain soil can get washed away and get washed into rivers and things but having the hedgerows there with all their Roots really helps prevent that soil erosion from occurring they provide food sources and nesting sites for Birds they support a diverse and plant animal species range because they provide lots of different niches there'll be lots of different food sources in them there'll be lots of different habitats in them underneath the Hedge in the Hedge brushes sort of perched on the top maybe in a small tree they can also attract insects away from crops so they could technically insectically be attracted to maybe some of the flowers some of the natural sort of plants on the hedgerows but equally they can also be kind to other insects but these could be useful because they could be predators of the pest species that would normally kill or damage the crops in some way for example aphids aphids can spread diseases and damaged crops ladybirds are predators of aphids so if you've got species that support ladybirds in your hedgerators then they are likely to go off and eat the aphids that might be needing your crop plants they also act as Wildlife or migration corridors so being able to move between fields or across this landscape by going in the hedges and in the trees around the edges of all the fields is much safer than trying to run across the field if you're a rabbit or a hedgehog or a field mouse because then you're more likely to be exposed more likely to be caught by a predator also there's herbicides and pesticides and chemicals there that you don't want to go near if you're certain species so being able to run around the safety of the edges if they're covered up and include with these Hedges then that's much safer for you so that increases biodiversity increases their safety why might Farmers want to get rid of the hedgerows then so what's their argument counter argument it's because they act as a refuge from pesticides and herbicides so weeds grow there and obviously they can seed Dead Flowers spread their seed their seed can be drawn the wind back into the field and also pests and insects can live there and if they're not spraying the hedges because they're not supposed to then they won't be killed by the pesticides so they can then go back out into the field and start eating them again they also reduce the crop yields slightly because obviously the hedges and all the roots of all the plants around the edges will be going down and underneath the soil and then you can also use up some water and nutrients including some of the fertilizers that goes on the fields and so if that's going to the hedges it's not going to the crops and that will could reduce the growth of the crops because they're having to share and compete with the Hedge species for nutrients and then we've got smaller field sizes so by having that edge to your land you then have to start planting further in away from the Hedge it means that there's slightly less area that you can plant your crop in and also you need space to be able to move Machinery around the edge of the field and if the hedges are there then you can get your Machinery caught in those Hedges so you need to move your Machinery in so you just end up having less yield because you're unable to plant in an as wide in an area whereas if you just didn't have the hairs and it went all the way up to the edge of the road then you'd have plenty of space for your tractor or whatever to move around so these are the arguments against it for Farmers there are as I said doing schemes where they're trying to promote Farmers from still keeping these hedgerows and keeping these wild orders on their land and actually paying them to try and support them to do that [Music] oh [Music] [Music] [Music] foreign [Music] cell cycle so we've got obviously G1 growth phase G2 growth phase two in between there's S phase otherwise known as synthesis phase it's where the DNA is replicated and special proteins proofread this DNA to try and stop mistakes being made when replication happens so mutations happen when DNA replicates and so it's normally checked before the cell carries on through the stages of the cell cycle if at this point a mutation was found and there was something wrong and they realized the protein is proofread it went along we'll see because we've realized there was something wrong the cell cycle would stop at this point and the cell would go into program cell death or apoptosis but sometimes it does not work and a change happens so mutation happens a change to the base sequence happens and we carry on through the cell cycle so mutations happen randomly and they're happening constantly all the time they're natural and they continuously happen and obviously sometimes they have an effect and sometimes they don't what makes mutations more likely to happen or the likelihood of one occurring is increased is if you are exposed to some physical or chemical factors that can actually damage the DNA and cause this mutation so UV exposure to UV light something like sun beds or obviously exposure to lots of UV light Sunshine sunburn without Sun cream x-rays radiation gamma radiation or some kind of nuclear radiation carcinogenic chemicals from cigarettes or other carcinogenic chemicals such as materials like asbestos so all of these are something that we call mutagenic agents they are chemicals that are able to damage DNA and cause that damage often tends to cause mutation but they because if you're exposing yourself to it you're increasing the likelihood of a mutation and really it's about how much explosion you've had how regularly you have it so there are obviously people like radiographers who work with x-rays they wear a little bash to measure how much x-ray exposure they have they wear lead vests or aprons they normally stand behind a lead screen so in reality their exposure to the level of radiation should be minimal and if it was if they didn't have all of that protection and they had that long-term exposure to x-rays then that would increase their likelihood of having more mutations so as we said mutations are random and they happen continuously all the time and most of them have very little or no effect on the phenotype so they don't have any effect that we can physically see or or have evidence of but not all mutations are negative obviously some end up being quite positive because a random mutation can end up giving a benefit to an organism if they are then more adapted to their environment it can lead to Evolution and negative effects occur when there's a change to a codon which changes the amino acid and that tends to result in 40 proteins proteins that don't do their jobs or proteins that are different from what is needed and so a lack of protein can result in something with disease most obvious ones would be changes to enzymes so if we change the base sequence we change the primary structure of the protein otherwise known as the amino acid sequence this has a knock-on effect because the primary structure changes there'll be different R groups that will be present or the r groups that were there before could be in different positions if they've moved around this changes the secondary and tertiary structure because it affects the ionic and disulfide bonds between the amino acids because a lot of those bonds that hold the tertiary structure in place occur between R groups so the r groups in a different place the bonds between the r groups are in a different place and that dictates the tertiary structure and therefore is different if the protein is an enzyme so if it's got tertiary structure or if it could be an antibody or something else but if it's got tertiary structure it could be an enzyme so that means that the active site could change shape which means it can't form enzyme substrate complexes anymore because the active site will be no longer complementary to the substrate and so therefore it can't bind and so therefore whatever reaction that enzyme was responsible for cannot take place anymore this could be the same for if it was another tertiary structure protein where shapes are relied on fitting together so a receptor for example or an antibody that binds to an antigen or an antigen that's got a 3D shape so if that changed it wouldn't be recognized anymore all of these if you think about it any mutation that codes for a structural protein so a 3D protein that has tertiary structure or quaternary structure can be affected so another example is hemoglobin in sickle cell disease the quaternary structure is affected because the tertiary structure of the subunits isn't right because of the change in the minimal acid sequence and that means it can't actually hold on to as much oxygen as it should and that is what causes the majority of symptoms in Sickle cells not being able to carry as much oxygen per hemoglobin molecule as normal and it results in that different shaped red blood cell which then can also trigger a lot of the other symptoms because it can't move through the circulatory system as a normal shaped red blood cell would okay so this is one of those questions that would be a long answer question potentially where you'd be given an example or given some context and asked how a mutation can affect enzymes activity or could affect how could a disease be affected by this it might not always be an enzyme as I said it could be something else that requires on shapes fitting together but the answer would still be the same because you'd still be changing the primary structure which would affect the secondary and tertiary structure because of the bonding you need to make sure you say that because of the different R groups being in different positions changes the bonds between them and that is what changes the tertiary structure and they'll no longer be a complementary shape that could be the active site of an enzyme it could be the variable region of an antibody it could be an antigen it could be a receptor or it could be something that fits into a receptor whatever it is if it's no longer the shape it should be then it won't have the effect it has to have in the body anymore and that could be the cause of many different types of disease Sickle Cell is just one example so we need to know the different types of mutations and be able to explain what happens for each type of mutation and also what caused that house so first we'll look at the mutations that cause a frame shift so deletion is where one or more basis have been removed and that can cause a frame shift so here I've removed the base a insertion or addition is where one or more bases are added we've added a base T and duplication where one or more bases are repeated that can also result in increasing repeating subunits and because this repetition gets kind of stuck and it just repeats and repeats and repeats and repeats and repeats so here we've got a g a g but you can have really long repeats where it's say 40 bases of just the same two or three or four letters repeating and that is known to be a sign of some genetic diseases so Huntington's disease for example either just a few bases being repeated can cause duplication so here I've added an A and A G after the other AG so all of these are what we call frame shift mutations and these can have a huge effect of the basic machine because they change the number of bases in the DNA codes you'll notice in the first one with deletion I'm one base short in insertion I've added a base and then in duplication I've added two bases so I've changed the number of bases in my secrets and what that does is it causes a shift so either left or right all of the bases shift up or all of the bases shift along and that means that all the triplet codes after where that mutation happens are going to be different so we call that Downstream so where from where the mutation happens past that point Downstream of it all the codons after that mutation have been changed which means we're going to get a very different sequence of amino acids so if we think about what our codons were before and obviously remember each codon codes for an amino acid so these are my codons before that first one and that second codon are the same so those two amino acids will be the same but after that if you look at what the codons are they're all different if AGA becomes G EAC ctg becomes TGC CAC becomes act they will code for three new different amino acids which means we will get a different protein and that's the same for all of these that's what a frame shift means so that's why these mutations can cause big changes the other kinds of mutations don't often cause as much of a change so substitution is where one or bases are swapped for another so here I've swapped it a for a c and the inversion where a c x base is reversed so again there is no change to the number of bases we're just swapping the letters around that are in that space so instead of c a g I have a g a c so you can just see it's been flipped around and reversed so because there's no change to the number of bases these mutations could be what we call silent mutations and that's because the codons are mostly the same except this codon is the only codon to have changed and it's only Changed by one letter c instead of a CGA May code for the same amino acid as AGA in which case there has been no effect or no change caused by this mutation we get the same sequence amino acids and it wouldn't be a problem and if it was a problem we're only changing one amino acid in the sequence that might not cause as much of a structural change or physical change to the protein as a whole change to a load of different amino acids in the sequence so these can be silent but they generally tend to have less of effect and as the frameshift mutations do okay so stem cells are cells that retain the ability to divide repeatedly and differentiate or become specialized into a range of different cell types this is sometimes called potency or plasticity so how potent or how plastic a cell is describes how much can differentiate what differentiating power it has stem cells become specialized because they only transcribe and translate parts of their DNA so as we said every cell every new case of every cell has the genome in it has the entire DNA but not all of those genes are switched on or expressed in every cell and the different combination of genes that are expressed whilst the rest are being what we call switched off or not expressed they will determine what proteins the cell makes and what features the cell has so which genes are expressed determined by the conditions the cell is in now this could be hormones external cell secretions other proteins being secreted by normally the cells around them so in order to encourage cells to become a certain type of cell they'll have to be in the right conditions the kind of conditions that may trigger the proteins to be transcribed and they modify the cell causing it to become specialized for a particular function we're going to look at transcription factors and how gene expression is altered through various factors and so that's how these stem cells are ultimately going to become specialized cells okay so we need to look at the four different types of stem cells we need to be able to name them we need to be able to talk about how much they can differentiate and talk about where we can find them and give examples and sort of explain sort of why they have this differentiation ability so the first one is toast ecosystem stem cells or omnipotence of stem cells so totally coming from that word total gives us an idea of what we're talking about here so there's cells that can differentiate into any tissue because they are the cells of the very early embryos of eight cells of the moral stage of the embryo which is round day three to four of embryo development so because these cells any of these cells need to be able to become any cell in the body and it will become a whole organism a whole human then they need to be able to have full range of differentiation ability so all of the genes in the nucleus can be activated and transcribed in these cells at this stage the next one is pluripotent so plurry coming from the same word as plural so these are cells that can differentiate into any of the three germ layers so you have Exodus endoderm mesoderm so these are kind of like your outside layers your inside layers and your muscle and skeletal layers so they're the kind of different categories that we give to the tissue layers in the body so they occur in early embryos so the blastocyst which is day five to seven which looks kind of like this and in the cambium tissue of plants so we have the phloem we have the xylem and then in the middle in this kind of strip in here we have the cambium and that is the stem cells where we can produce new plant cells now obviously in animals we've talked about there being in the blastocyst so only at this stage between sort of five to seven days can we get these pluripotent stem cells from embryos after that point there are no more pluripotent stem cells in an older organism of an animal whereas these plural process stem cells are found for the whole lifetime of the plant in this cadmium layer so that's how plants can be cloned you can chop parts of the plant a little grow into and differentiate into stem Roots leaves whatever is needed and that's because they have this constant supply of pluriposis stem cells in the cambium tissue between the enzyme and the phloem in the vascular bundle multi-potent stem cells so these can divide to form different cell types but in a limited range so the example we have in animals is stem cells from bone marrow that can produce most of the immune system cells red blood cells platelets but also and there's yellow bone marrow which is pictured here which can produce fat cells kind of cartilage as well so some genes have been switched off but they have genes for some different cells still able to be expressed so they can't just make one type of cell they can make a few kinds of cells and then lastly we have unipocent stem cells so obviously thinking about these two words we have multi as in multiple and then we have uni meaning one so these are cells that can only form one other type of subtle tissue so the example is cardiac stem cells they can divide from other heart muscle cells called cardiomyosines so they are just an example that there are some stem cells in the heart that if there was damage to the heart in some form then they could renew those cells and replace those cells with new heart cells and but they can only make heart cells so they have Union potent stem cells so lots of genes have been switched off here and that's through regulation of transcription factors and so they can only divide and renew and produce one type of cell so as we go down this table so we're decreasing our potency or plasticity so we're decreasing of differentiation ability as we go along so the most potent or the most plastic is the totally coated stem cells down to the union process stem cells which is at least potent or plastic so they have the least differentiation ability but because they're all able to divide multiple times and they're all able to differentiate into some type of new cells they are all still stem cells okay so like in GCSE we still need to be able to talk about the differences between adult and embryonic stem cells so the source for most embryonic stem cells is unused IVF embryos because these will be donated for research if they're not going to be used by couples who have gone through the IVF process and put some members in the Deep Freeze and if they've had maybe one or two children or it's not worked or they don't want any more children they don't want to use any more of those embryos they can be donated for stem cell research instead of being destroyed whereas with adult stem cells as we've seen bone marrow is one of the easiest places to get these stem cells from it can be removed with a simple operation that carries little risk because you don't have to be completely unconscious or anesthetized but it can be quite uncomfortable and painful afterwards for the person that is having the operation so what are the uses of embryonic stem cells well they've been used to grow new organs or tissues for treatment for a variety of conditions for example anything to do with the nervous system so Parkinson's disease or spinal cord injuries being able to develop new nerve tissue and new nerve cells and put them back into patients suffering with this where those cells have been damaged or being degenerated and then they can help them improve their function they could obviously improve the quality of life for many people and also reduce the need for organ donation if we could grow new organs from them then we don't need to find donors in order to get them primer is already being used and has been used for a long time so bone marrow transplant being able to donate your bone marrow so your stem cells to someone else in normally used to treat blood conditions where abnormal blood cells are the issue so things like Leukemia Lymphoma sickle cell disease and skid they have also been used to treat paralysis because spinal cord injuries can be used to replace nerve tissues so they can be used as well as embryonic stem cells the best thing about the adult stem cells part is that you remove the issue of projection so if you get donated embryos from somebody else they will not be genetically the same as you but if you have your own bone marrow cell samples then they are going to be genetically the same as you and so it's less chance of your body is going to obviously reject it issues with embryonic stem cells again this is very similar to what we looked at GCSE some people are objecting to the use of embryonic stem cells because they see that it could be a potential fetus if it was implanted into a womb it would grow into a new fetus and it could become a new human some people believe that because fertilization has happened is that the embryo has arrived along and isn't going to be used but obviously these embryos would have been destroyed if the people no longer want them or need them and are no longer willing to pay for them to be stored in a freezer they would just be destroyed they're not likely to be implanted into a win but this is some people's issue with ambulance themselves obviously also as well the kind of storage is expensive and can be expensive to store those over a long period of time some people babies now being born if there is a potential for genetic disease or a high risk of disease in the family they're suggesting that storing the umbilical cord blood or placental tissue could be stored because it could be a source of stem cells that are genetically identical to that baby that's been born and stole them in case they need stem cell treatment later on in life and obviously that can be quite expensive and that is really only available to people who can afford to do that which is somewhat controversial the issues with the adult stem cells is that they're only multipotent they are not totification or pluripotent so they count different changes any cell types as embryonic stem cells can which means they can't help as many diseases or be used to create as many tissue types as end unit stem cells that counts so there's a limit there there is a potential way we can solve that problem of the adult stem cells not being able to be plastic or potent enough as the embryonic stem cells there is new ways of creating what we call induced pluripotent stem cells so these stem cells are Crest in a lab they're taken from specialized cells so the easiest one normally to take is skin cells um because they're easily accessible and it's not very harmful to take them from a patient and then these cells are reprogrammed to become pluripotent so these are not stem cells they're just normal skin cells that would not have the ability to do anything or become any other type of cell they differentiated they are specialized but we can reprogram them using maybe a viral Vector which can introduce transcription factors again we're going to look at transcription factors in more detail in the next video these are just proteins that can control the expression of genes so if you can insert these proteins or insert DNA that's going to change or trigger this change in the cells it will cause them to turn back on or switch on all of those genes that are normally expressed in a pluripotent stem cell so that's like an embryonic stem cell and so we can take those noun induced stem cells and then we can use them as we would embryonic stem cells but we've got these from a patient and so it is genetically the same as them so we have the benefit of Both Worlds we have the pluripotency of an embryonic stem cell so the ability to turn it into many different cell types and we have the genetic makeup that makes it identical to the patient so it removes that chance of rejection and that's why these stem cells are so like useful and interesting and very important in terms of the way we can move forward with stem cell research so clinical trials are already undergoing to look into the use of these induced pure protein stem cells to do things like replace disease or damaged organs or to replace damaged tissue so we can use these new cells to treat loads of different things so neural cells neurons nervous tissue all of that we can use to treat neurodegenerative disorders so things where the nervous tissue is being attacked or like we said paralysis so spinal injuries Parkinson's even potentially Alzheimer's things like that skin cells can be grown so instead of having to get a skin graft instead of having to take skin from Elsewhere on the body or getting skin cells through a donor you could create a skin graft to replace burnt tissue so if you suffered really bad Burns then you could grow new skin to replace and cover that burnt skin cells pancreatic cells literally growing a new pancreas or growing new islets of langerhans that will be able to produce insulin to help treat type 1 diabetes there are lots of potentials here for this treatment okay so before transcription can begin a Gene needs to be stimulated or activated by a latery protein which is called a transcription Factor so our definition for transcription factors are that they are proteins which travel into the nucleus and control the rate of transcription so either by activating or repressing RNA polymerase or the action of RNA polymerase so each transcription Factor will bind to a promoter region on the DNA so it's a section of the DNA at the start of the gene that's going to be transcribed and it's called the promoter region and in here you can see it's got this kind of green box around it it'll be a specific sequence at the start of pretty much every Gene that is where RNA polymerase and goes combined and also the transcription factors know where to bind in order to start the process of transcribing this DNA transcription factors then bind to this section of the DNA in the promoter region and then that binding is either going to block or promote the action of RNA polymerase so we'll see here we've then made this complex where we've got our transcription Factor we've got our RNA polymerase LC the RNA clearase is doing its work and we're producing that mRNA transcription factors can either activate or block the action of RNA polymerase so we call transcription factors that act as repressors they are repressors they prevent the RNA polymerase from binding and therefore they stop transcription of the gene or we have activators or promoters which bind and then allow The Binding around a polymerase and therefore trigger the transcription of the gene so transcription factors can also be regulated which is adding another layer of complexity but basically transcription factors can be stopped by inhibitor molecules so they can be stopped from binding to the promoter region these sort of in terms of molecules combine to the transcriptional factor and prevent it from attaching so without the transcriptional factor the gene may not be transcribed if the transcription factor is an activator or the gene May then be expressed or switched on if the transcription Factor was a repressor so let's look at example because that sounds a bit counter-intuitive but in our transcription factor is a repressor transcription Factor normally transcription wouldn't happen it would be stopped so no transcription of this Gene is happening so RNA polymerase can't bind it's blocked by that transcription Factor being there so we're not going to get any expression of this Gene we're not going to make a protein from this Gene however if a transcription Factor inhibitor comes along that inhibits that transcription Factor prevents it from binding to the DNA then now RNA polymerase isn't blocked and so the transcription occurs so a transcription Factor inhibitor in this case if the transcription factor is a repressor causes the transcription of the Gene and we will get mRNA and therefore hopefully we should get a protein as well opposite case to this is if your transcription factor is a promoter so The Binding of the transcription Factor normally promotes the transcription or activates the transcription of the gene then you'll get a gene product you'll get mRNA produced and we'll have hopefully a protein translated from the MRNA that's been transcribed from this Gene but in this case if we have a transcription Factor inhibitor then we're inhibiting a promoter transcription Factor so that means that we won't get transcription this time so without the transcription Factor there RNA polymerase won't be known to bind or won't be activated to bind and so no transcription will happen so if we inhibit a promoted transcription Factor then we don't get any transcription of the Gene and the gene is turned off or Switched Off if we inhibit a repressor transcription Factor then the gene is turned on or expressed so you will be given context in an exam you'll be given either a diagram or an explanation of an action of a transcription factor or its inhibitor and so you will be just applying this knowledge that you know and you've heard about transcription factors you know they can promote or they can and repress and then you'll be kind of given the context around it and sort of asked to figure this out using your knowledge okay so an example of a transcription factor that we should know is that hormones can act as transcription factors so a hormone response element or hre is a short sequence of DNA within the promoter region of the gene So within that promoting perception it's able to bind a specific hormone receptor complex and therefore regulate transcription so if we've got that hormone response on it then our transcription Factor can be a hormone so The Binding of that hormone can either activate or repress transcription it basically just acts as a transcription Factor so if you see anything in the exam where it says that something binding whether it's a hormone or a molecule or it names a molecule and if that binds it will cause a protein to be made or not cause a protein to be made it's acting as a transcription factor that is what it is doing so an example that we have to know is estrogen so to affect transcription estrogen can't move through the membrane and move into the nucleus and do it itself it has to bind to a transcription Factor called an estrogen receptor so that's on our cell so all cells that are affected by estrogen or can be affected by estrogen will have these estrogen receptors if they don't have the receptor then obviously if estrogen is Flowing around the bloodstream they won't be affected by it so an estrogen estrogen receptor complex is formed and obviously only in cells that have the estrogen receptor will this happen the estrogen estrogen receptor complex can then move from the cytoplasm and go into the nucleus where it can bind to that promoter region that hormone response element in the promoter region of the gene that it's going to affect the complex will bind to it and then it activates or it's going to repress transcription so if it's going to activate transcription in this case then obviously we get The Binding of the RNA polymerase and then we go through the process of transcription which will produce our mRNA our Mna will leave the nuclear through the nuclear pool and then it will be transcribed in the normal way so in this case estrogen will have acted as an activator transcription factor and it will have activated the transcription of this DNA and therefore produce mRNA which will then produce a protein and therefore it's caused the change within this cell by turning on or switching on or expressing that Gene it could have the opposite effect and obviously it could also be a repressor and it could prevent transcription it could prevent the RNA polymerase from binding and then we wouldn't get an outcome we wouldn't get protein it will depend on the cell whether the estrogen causes the transcription or represses it again this is an example you need to know you need to be aware that hormones like estrogen can act as transcription factors and be able to explain how they as transcription factors using this method and then you'll be given contacts and examples about what in a certain particular cell it's causing to happen and change and you'll be asked to comment on whether you think that's obviously activation or repression okay so another way we can change gene expression is to instead of affecting transcription effect translation so interfering rnas is a way that we can do that they're sometimes called rnais so we have short interfering rnas and micro rnas and both of these work in plants so they start off as double-stranded short interfering RNA and so it's different from normal RNA because we're used to RNA being a single stranded but in this case it starts off as a double strand and then what happens is it Associates to the protein complex in this last part of the cell and it starts to unwind and then one of those strands is degraded so it breaks down so we are left with a single strand of RNA attached to this protein complex the single strand of short integrating RNA binds to the Target mRNA because it's complementary to the base sequence in a section so this short interfering RNA has been made to be a complementary match to the MRNA we're trying to stop being translated so my frna is leaving my nucleus and then it's going to end up binding to this protein complex and short interfering RNA and then what happens is that protein complex and that binding triggers the breakdown of that mRNA so it degrades it it breaks into small pieces so it can no longer be translated so ultimately the level of the protein that this mRNA codes for is going to decrease in the cell and we've stopped that expression of that Gene because the protein that that Gene encodes for never get made another example is my rnas in animals so short interfering or S I rnas only found in plants micro rnas are found in both plants and animals but in Plants they work in a similar way to short interfering rnas in animals something slightly different has to happen they have to go through a processing stage to get to be single stranded they don't start off single stranded so initially we start off with what we call a hairpin structure where the actual s-a-rna is folded on itself so it's held together with hydrogen bonds and it's fold into this like hair grip shape then we get a protein complex which binds to it and breaks it into these short double stranded sections and then those short double transactions go through the same processing as before so one of these strands will degrade it will break down leaving us with a single strand bound to the protein complex now you'll notice that these mrnas are slightly shorter than the acid rnas and that's true so they tend to be quite short sequences and so they tend to be maybe less specific because there are only a few base pairs long so they can bind to more than one type of mRNA which is sometimes useful but sometimes we don't want that because it just means it's not as specific so we can't necessarily control always what it's going to affect same thing happens so we get to this stage where my micro RNA is going to bind to my mRNA wherever it is complementary and the protein complex that's associated with it is going to either cause it to degrade or it'll block The Binding of the ribosome so it can either prevent it by breaking it down to short pieces in the same way that short interfering rnas do but it could also block the ribosome from binding and therefore prevent translation that way it works in two ways and it depends on the protein complex it depends on the MRNA but either way that's what will happen and in both instances it's what we're doing is we're stopping translation so we're preventing gene expression preventing proteins from being made from these genes okay so epigenetics is the study of heritable changes in gene function that have not been caused by changes to the base sequence of DNA so we've changed Gene function gene expression but we've not changed the basic as a DNA but that change can still be passed on so let's have a look at what we mean to understand the differences when we're talking about the genome versus the epigenome so in the genome the sequence of bases in the entire DNA molecule of an organism so the DNA sequence is fixed so you inherit that and that is your DNA sequence and it doesn't change throughout your lifetime unless there are some factors that we're going to talk about in a second the tags on the histone proteins which are associated with DNA can be changed quite easily so it's quite easy to change the epigenome during a lifetime DNA sequence can be changed but only by mutation so physical change to the base sequence happened because of mutation which we do understand happens randomly and can happen quite frequently or all the continuously during replication but whether those changes stick or stay is dependent on whether they pass obviously that check at the S phase of cell division and also whether they actually make any changes so they can change this DNA base Secrets but again they might be in an intron and so therefore they might have no effect the tags on the epigenome can respond to external factors and change gene expression without affecting the DNA sequence so quite rarely does mutation actually change a Gene's expression whereas these tags and the epigenome being changed can actually cause change in gene expression quite easily without affecting the DNA sequence at all mutations in DNA can then be inherited from parents to offspring so if there is a mutation in a certain Gene you can pass that on to your children because you've changed the main sequence and so that will be in your comics epigenetic tags are often removed embryos to be charity potent so we've talked about stem cells and how embryonic stem cells are Titan and in order for that to be the case you have to start from scratch with every Gene in the genome being able to be expressed so normally all academic tags are removed and the whole DNA sequence is therefore able to be transcribed to start with but sometimes the epigenetic tags do remain and so those changes to gene expression and how the expression happens due to the epigenetic tags and how the DNA whether it's transcribed or not certain genes can be inherited environmental practice can influence the genome by causing mutations but these are very specific so a mutation is likely to only change a few bases and so it will have a specific effect in that specific section of DNA that it changed and that could affect one gene it depends on what type of mutation we're talking about again we looked at mutation and we saw that obviously sometimes that DNA based Secrets change could have no effect at all so it's very specific what will happen at the environmental factors can influence it are going to be things like what we talked about with UV radiation and chemical mutation those mutagens cancerous chemicals for things in like cigarettes or asbestos exposure to UV or x-ray or gamma radiation is going to be those environmental factors that are going to potentially increase the damage to DNA and potentially cause a mutation with the epigenome there's a lot of environmental factors that can influence the epigenome and they give you wide ranging so something one event in your life or lifestyle or diet or exposure to certain chemicals or drugs or the amount of social interaction you have or pollution that you're exposed to as a child or the amount of stress that you're under all of that any of those and we'll look at another big list of them in a minute but they can influence the epigenome and they can have more than one effect to more than one Gene and cause wide-ranging outcomes not just one specific base in one specific spot and one specific Gene which is what a mutation would do so there are two ways that epigenetics can control gene expression DNA methylation and histone acetylation so either adding actual groups onto the DNA model yourself or looking at those tags that are on the histone proteins that we looked at so if we go look at DNA methylation first so this is where we are adding a methyl group to the DNA itself and by methyl group we just mean literally a ch3 molecule and you'll see it's here so I take my ch3 and it literally is bound to the DNA molecule it actually attaches to the cytosine bases on the DNA so where there's a c base we can attach a methyl group and this is often done by enzymes known as DNA methyl transferase enzymes nice and easy it transfers methyl groups and it's an enzyme so it ends in A's methyl transferase what does that actually do well it Alters the DNA structure making it bind more tightly to those histones And So It causes the DNA to stay wrapped around the histones as chromatin prevents transcription factors and enzymes like DNA polymerase and other things RNA polymerase from binding to it so it prevents expression and therefore switches off or stops the expression of the gene so by adding this methyl group we're just making sure the DNA stays bound tightly to these histones more like to have a stronger interaction with them preventing our RNA polymerase ends up and getting in and actually being able to carry out transcription so therefore we don't transcribe the gene we don't get a protein from that Gene that Gene is effectively turned off or not expressed so hysterocutilation is when we are acetylating or de-acetylating histone so we add or remove a CO ch3 group or an acetal group when histones are acetylated so and acetyl group is added the DNA loosens through histones making it less condensed this means the transcription factors and enzymes can bind to the DNA and transcribe it so here is my acetyl group so it is then attached to remember these histone Tails so it's attached to all those tails and therefore I've got loose DNA that is therefore able to be accessible by the RNA polymerase for example and therefore we can transcribe the gene if we remove those acetyl groups then we de-acetylate the histones we remove these These are groups the chromium contenses back into the nucleosome and the transcription factors and enzymes can't bind it to the DNA so it's not transcribed so if you notice here on my tails on my histone in my kind of condensed nucleus so we don't have any acetyl groups so adding acetyl groups loosens the DNA allows transcription removing acetyl groups does the same thing as methylation it condenses the DNA prevents transcription from happening the enzymes that do this again they do what they say on the tin so they transfer the acetyl groups so they are acetyl transferase enzymes to add the acetyl groups and then they are D acetylase enzymes histone D acetylase enzymes in order to remove the acetyl groups and you probably don't need to learn those two enzymes really well at the top of your head because you won't be expected to go into this much detail you'll need to be expected to know what methylation is and what it does you'll need to be expected to know what acetylation is and what it does that's pretty much it in terms of your factual recall knowledge but what you will need to be able to do is to be able to understand how there could be things like enzymes that are adding and removing these groups and if anything can interfere with those enzymes or if any drugs can do methylation or stop it or do acetylation or stop it then they're going to be able to alter the gene expression in the same way so like coming to look to the transcription factors and we said the transcription factors can change whether a gene is expressed or not expressed but you add that other layer of complexity by saying well we could inhibit a transcription Factor so that that will change whether the gene is expressed or not expressed this is the same thing so we know that advocacytal group does one thing and we know that adding methyl groups does another thing but if we interrupt the process of that so we interrupt the enzyme that can do that or reverse what they've done with another enzyme so either adding acetyl group or removing it then we can change the gene expression as well if we inhibit those enzymes that's going to affect the gene expression it's about being able to look at the kind of larger picture I'd be able to think about patterns of what might happen if a process that we understand I know acetylation will cause a gene to be switched on or a gene to be loosened and therefore transcribed if I get told that something blocks the enzyme that carries out the acetylation what will happen oh well that Gene will no longer be transcribed we need to have that logical pattern of thought to be able to work through some of the problems in questions that you might get about epigenetics so we said that the epigenome can be affected by environmental influences so there's actually loads of different examples of what we mean by that that have actually shown that they can influence the epigenome in the ways we've talked about so through acetylation or methylation so things like Diet exercise and your microbiome to the bacteria in your small intestine and large intestine the kind of range of species you have in there which we know have now seen through research that can affect mental health and things like that as well your social interactions how you were brought up how you were raised your kind of people skills and who you've been raised by and how you've been raised whether you have a lot of you know nurture love and care and various things like that your psychological states of stress any stressful environment any trauma anything like that that can cause changes in your gene expression as well things like drug abuse toxic chemicals you've been exposed to that can include things like pollution so depending on where you live living in cities and being experience the various creatives in the air or things in the water toxic chemicals that you may have not even been aware you've been sort of exposed to what diseases you've had so any virus any illnesses that you've had especially childhood ones and then just kind of General other lifestyle stuff to your diet and how much you exercise and things like that as well as medicines that you take whether you take alternative medicines whether you take therapeutic actual drug medicine it could be any of those so this is how we can start to explain how the environment can play a role in affecting your behavior your health your personality and other kind of physical symptoms that you might have and how these changes could be passed on to your Offspring and there's been lots of studies now looking into kind of long-term effects and changes of environments so things like Diet low nutrients starvation or deficiencies have been shown to show up in sort of large populations that have experienced this and then they've tracked that through the next generation and next generation and seeing the actual physical impact that that has had so epigenetic changes in gene expression have been shown as I just said to cause my response to environmental changes so pollution availability of food or for example in Plants as well this isn't just in animals so drought implants can show that if it's experienced by an organism the effects it has have shown to be inherited and then are present in the children and sometimes even the grandchildren of that organism so it's thought that this makes sense because it's an evolutionary response to prepare your Offspring to be able to survive the conditions that they will be being born into so if you're a plant and you are living through a drought or you're an animal that's living through starvation and you give birth to babies or you produce seed that you know is going to be spread and will germinate in the same conditions that you're currently in it makes sense that any Gene changes or gene expression changes that can happen or have been brought on about the conditions you're in to help you survive in those conditions you'd want your Offspring to have those Gene changes as well so that they are able to survive in those conditions and this is how we think epigenetic kind of control and this epigenetic these changes becoming inherited came about as like a sensible thing to help prepare Offspring to survive in certain conditions so if we understand that epigenetics can affect gene expression then it makes sense that in the same way that we've looked at other ways that we can change gene expression so transcription factors Etc then we can use epigenetics to treat diseases that are caused by genetic causes so epigenetics can be used to treat disease because these changes are reversible unlike genetic modifications so there's actually kind of quite a positive hope that epigenetics could be a Way Forward rather than focusing and relying on Gene therapies and changing of actual base sequences or genes or using recombinant DNA technology but any drugs that we are going to use for epigenetic changes must be very specific to their target genes because some epigenetic changes are necessary and important to normal functions in all cells of the body so we don't want returning off or turning on or acetylating or methylating anything that could then impact everyday function of cells because a lot of this is going on just to produce normal gene expression so think about some examples this is basically one of those patterns where you can link together your knowledge of say enzyme inhibition and what we've said about DNA methylation so DNA methyl transfers Inhibitors so they prevent the enzyme that methylates DNA which means they stop genes from being switched off so the gene remains uncondensed and we can produce proteins that are potentially missing which is what's causing a disease so if we've got a mutated gene or a gene that is not producing the protein and we need it to produce a functional protein we could use this method to potentially counteract those disease symptoms so that's a methylation example let's look at an acetylation example and this can go both ways so my uncondensed Gene my transcribed Gene has acetyl groups attached to the histone Tails so therefore it's uncondense and it can be expressed my condensed Gene doesn't have any acetyl groups attached to the histone cells so that's why it stays tightly bound to my histone proteins and therefore it is not able to be transcribed so let's have a think about what could turn one from the other and then we'll think about what the inhibitor action will do to those so in order to switch off a gene so take it from being transcribed to not transcribed so stop the protein being made from that Gene histone do you see today's enzymes can be used and so they would remove the acetyl groups from the histones and therefore we'd get a tightening condensing of that DNA and so the expression would be stopped to go the other way so to take my condensed DNA my Gene that is turned off inactive not being transcribed and to make it transcribable we need to loosen up that DNA and unwind it a bit so that the access can therefore the RNA polymerase enzyme so to do that and acetylase enzyme would add acetyl group to those histones and it would unwind and that DNA would become accessible again so let's now think about the action of Inhibitors so if I have a histone de-acetamase enzyme inhibitor so for example myromidepsin that's going to stop that process block it so that means there will not be a change from uncondensed to condensed so the drug inhibitor will cause that protein to still be made and that Gene to remain expressed if I have glaze enzyme inhibitor then the drug is going to block the action of the acetylase enzyme we're not going to get any acetyl groups added to my condensed Gene my DNA so we're going to have no access to the RNA polymerase so therefore the gene remains turned off or not expressed last thing to think about then is epigenetics and cancer because we've tied this whole little set of lessons together so abnormal methylation too much or too little methylation of the DNA specifically of protoncogenes and tumor suppressor genes can cause abnormal cell growth and Cancers to develop so if we think about that we know that proto-oncogenes if they are overexpressed can cause cancer and if tumor suppressor genes are turned off that can cause cancer so we need to just think about those linking those things together so we know that methylation can cause changes to whether a gene is expressed or not and we know how the expression of those two genes can result in cancer so again this could be cause for treatment if we know that a cancer is caused by a faulty tumor suppression being turned off the Taps we could turn it back on if we know that the cancer is being caused by an oncogene maybe we could turn that oncogene off using DNA methylation and this is one of those avenues that they're looking at for cancer treatment as well so hypermethylation adding methyl groups to tumor suppressor genes prevents them from being transcribed the proteins they normally produce which slow down cell division will not be made and this can cause the cells to divide uncontrollably by mitosis and form tumors so we've got this idea of adding methyl groups to the promoter regions of a tumor suppressor Gene is going to stop that Gene from being able to be transparent it's going to wind it up tight prevent that RNA polymerase from coming and transcribing that Gene into proteins those proteins that we looked at like tp53 will not be transcribed will not be translated will not be made and therefore they won't do those checks in the cell cycle and then we could get that uncontrollable division occurring because of that equally we could reverse this so if we know hyper methylation adding methodox we could demethylate those genes in order to try and reverse some of that change hypomethylation so removing methyl groups of protoncogenes causes them to act as oncogenes and produce proteins that encourage cell division this can stimulate cells to divide up controllably by mitosis and form tumors so in this case we're de-methylating or we're removing these cell groups from our promoter region of our protoncogenes acting as oncogenes then because they're going to start producing proteins that actually encourage cell division to occur so again if we know that this removing of methyl groups is having so that demethylation is happening and that's what's stimulating the proteins to be made to cause this cancerous cells form maybe we could do the opposite and methylate those genes using some sort of drug and we looked at how methylation can be done and how we've got enzymes that can do the transfer of methyl groups so maybe there could be an answer there for a drug for cancer as well if it's caused by an epigenetic cause okay this is a lot this is probably some of the highest level knowledge that you will get at the a level it is sort of the Forefront of Science and where it's going at the moment and our understanding of the epigenome and using it to our advantage with things like drugs and treatments is very much a very high level scientific process at the moment so there's a lot to unpack here but as I said most of this won't be stuff you will need to wrote learn or be able to say you need to understand what methylation is what acetylation is understand that methylation happens to DNA acetylation happens to the histones be able to explain that structure of DNA be able to explain what happens when the DNA is condensed being able to explain what happens in the DNA is uncondensed link that to methylation and acetylation and then just be aware of all of this other stuff that you can link and bring in like how it could affect cancer like how it could be used as a treatment for drugs to look at enzyme inhibition of those enzymes that do that methylation and acetylation all of this is part of that application process that you need to go through sometimes with exam questions and this is definitely one of those topics where they can bring it in in the exam so what do cancer cells look like what are their features they're very different to normal cells and their structure and their function they're either going to die through apoptosis because they'll not make it through the cell cycle eventually or they can be destroyed by the immune system because it will recognize them as foreign or different to normal body cells hopefully if you remember that when we looked at the immune system that one type of cell that can be triggered and recognized by the immune system will be a cancer cell because it will have different antigens on the surface membrane than your normal body cells they have some other key features as well some of which are really useful because we can use them for diagnosis using a biopsy using microscope pictures like this we take a sample tissue and look for these classic features some things you're not going to see with a microscope but the body will recognize or just is a feature of the cell itself so they have large dark nuclei so you can see how kind of big and how much of the cell these nutrients take up in these cells these are melanoma cells so these are the skin cancer cells and they're particularly quite large in this case they have a regular shape or variation in size and shape so you can obviously see they have these kind of this kind of weird bumpy outside structure or an irregular shape they're not these perfect spheres and that's sometimes a normal feature and they can have irregular shaped nuclei as well although most of these are quite round they can have multiple nuclei which I didn't say mentioned so this one obviously has two this one has sort of this multi-lobed potentially three nuclei here that are ready to splits off so they don't look normal sometimes they can have multiple nucleoli as well so more than one nucleolus they're not going to be arranged in neat layers so if you have cells for example that should be like polymer cells that form kind of nice neat layers the cancer cells will not form that they'll be kind of all over the place they won't be able to form that structure remember they grow in kind of layers and layers and layers on top of each other then to format tumor they're not able to kind of arrange themselves neatly then some of the other things that they'll have proteins there's one's the usual growth regulation processes so there'll be growth factors coming from outside hormones some cells are and they can stop themselves from overgrowing by making realizing that cells and then that kind of stops them from growing too much and growing in layers they won't listen or pay attention to those they will just keep going anyway they also need their own blood supply but often if they become very dense or they're growing quite thick layers far away from the blood vessels nearby they won't be able to provide provide enough oxygen and so the rate of self vision is very high and is using up more oxygen than normal anyway but what they can do is they can release growth factors that actually encourage and cause capillaries to grow towards them and that's called angiogenesis or angiogenesis just as a way of kind of having this ability to kind of adapt and sort of make the body kind of Feed and Fuel this cancer growth rather than starving themselves an option because they get too dense and there's not enough it's too dense for oxygen diffuse into the middle of the tumor if it gets too large proto-unku jeans are an example of one of these types of genes that can end up causing cancer in the cell so Proto oncogenes are actually genes that cause cancer when they're over stimulating is not activated so normally they're activated and they can help cells grow but they're turned on and off as the cell needs in order to be able to promote growth and control cell division but normally they respond to signals and turn back off again when they mutate or there is a mutation they can become permanently activated so instead of turning off and turning back onto coals controlled cell division we get uncontrolled cell division and obviously that causes cancer a mutated proto-oncogene becomes what we call an oncogene and you may have heard the term oncology which is the study of cancer or the region of medicine that looks into cancer when this happens the cell preserve control and obviously we get cancer there's an example that we can look at called Raz Razz is a sort of protein that is also a transcription factor that has a control over one of these proto-onco genes so Raz GDP is the inactive form and then when it's activated it forms whereas GTP so you can kind of see where that's going DP to TP suggests a phosphorylation has happened in order to activate the protein when we have that activated protein that GTP then that's going to stimulate transcription of a protonper gene and cause controlled cell growth it if we look at what happens if a mutated form of Raz GDP is made though this is permanently activated there is no response to conditions where it will inactivate and go back to its inactive form it just is permanently on and in the active form so it's permanently stimulating the transcription of a proton Gene which is now become an oncogene and we get uncontrolled cell growth and obviously this could eventually leads to a tumor for me okay so let's have a look at tumor suppressor genes then so these genes do what they say sound like their name sounds they can cause cancer when they're inactivated or turned off because what they do is suppress tumors from falling or stop tumors from Fall so normally they help cells slow down or stop cell division repair DNA mistakes or tell cells when to die so the process known as apoptosis or program cell death so if the DNA as we said can't pass that checkpoint in the S phase of the cell cycle because it's too damaged it can't be repaired it will start off the process of going into program cell death so when tune with superpressor genes don't work those checkpoints are not made the cell cycle is not paused or stopped and the cell doesn't die instead it keeps continuing and division occurs and then that can cause the sounds to become cancerous so an example is tp53 which is a gene which codes for the p53 protein the abnormalities or mutations in tp53 have been found in more than half of human answers so there's a good evidential link here for this Gene being one of those ones that if mutated can lead to cancer being caused so p53 protein Acts as a tumor suppressor so remember when we're talking about tumor suppressive genes or proto-ancogenes like in the example we looked at for the proto-oncogenes the gene being mutated causes a faulty protein from that Gene to be produced and that protein's job is either to suppress tumors or stop the cell cycle or it's to activate or not activate transcription of a certain Gene so remember when we talk about mutation in genes that always means a mutated protein and that means proteins role is then changed or stopped or altered in some way which then leads to the problems that cause cancer so if we look at what normal p53 protein does it can detect the abnormalities in the cell cycle it will then use that motion and stop the cell cycle and when the cell cycle is stopped then it can trigger or stimulate the DNA to be repaired if the DNA is repaired successfully then it can restart that cell cycle again and then off it goes back into its normal routine if the damage cannot be repaired so it's too great it can't be fixed then it will trigger the program cell death or apoptosis so in this way it's protecting the cell from continuing to divide with damaged DNA so either it repairs it and fixes that damage to make sure that the cell doesn't then divide out of control become cancerous or have severe abnormalities or if it really can't fix it rather than let the cell continue to divide and potentially to become cancerous it stops that DNA repair it stops that cell from dividing any further and causes it to die so looking at the action of a mutated p53 protein DNA damage occurs still and but this time it's not detected so the cell cycle continues to progress and because of that we're causing that damage DNA to be replicated further we're continuing to replicate the cell and that means that that cell can continue to divide with damaged DNA means it can become cancerous and as we said that mutation or change to that p53 protein has been seen in more than half of human cancers so clearly this inability to stop the cell cycle when damage occurs and allowing that damaged DNA to continue dividing and continuing your replication of the cell is incredibly likely to then lead to that cell becoming cancerous there are other mutations that are known to be linked to things like certain terms of so breast cancer is an example where about five to ten percent of breast cancers are also caused by a mutation or found in gene brca1 or brca2 and they are known to suppressor genes so once we figured out where some of these mutations are it means that these can be a target for certain therapies so another example of a tumor suppressor mutation is a cause of breast cancer so the brca1 and brca2 genes have been identified as tumor suppressor genes where if there's a mutation in these genes it sort of massively increases your risk of developing breast cancer and so knowing these mutations and sort of where they are like tp53 and the brca1gs gives us this opportunity to run screen people so that they can make decisions about whether or not they want to take measures to lower their risk of getting a cancer or potential should be a target for certain therapies that we can use to Target these changes and try and prevent them from causing the cancer concept so as well as mutation there has been some other links shown between estrogen and breast cancer so increased exposure to estrogen over an extended period of time is thought to increase the woman's risk of developing breast cancer now we have already looked at estrogen as a transcription Factor so although the exact cause isn't fully understood there's some theories about how high estrogen could increase risk of breast cancer so acting is a transcription Factor it can increase the chance of mutations by increasing the division of cells in the breast tissue or it can act as a transcription factor to promote faster cell division if a cell is already cancerous or is going through that stage so there's reasons why you might have extra high estrogen could be that you are taking estrogen containing medication for either periods or for the menopause starting your periods in Life or Staffing menopause lazy life so basically just having your periods for longer because obviously that's when we get high peaks of estrogen so again it's not really fully clearly understood and we're not really sure of the links behind it but the there is obviously evidence that estrogen access a transcription factor and it can specifically act in cells where there are receptors for estrogen so the ovaries and breast tissue are two of those places so it's likely that that's where estrogen is going to be able to enter the cells and act the transcription factor and could be one of these triggers for increased risk of cancer in those areas so we need to have anything about treating cancer because most of the questions that we're going to get given in the exam could involve us talking about cancer treatment and then if you think about it trying to link the idea of cancer treatments and the way they treat cancer to the causes of cancer and also thinking about kind of genetics of the causes of cancer as well so Cancer Treatments can control their own cell division in cancer cells by targeting the cell cycle so that's normally where the target is going to be is to try and prevent the cell cycle from moving forward prevent that uncontrollable cell division stopping them from dividing further eventually will kill them or it could Target them for when you get cell death anyway the treatments are not able to distinguish between cancer cells and other normal body cells that divide fast so the point of these treatments is that by targeting the cell cycle they're targeting cells that divide rapidly which cancer cells but there are other cells that divide rapidly in your body as well so hair cells stem cells in bone marrow they're obviously making your blood cells cells that line the small intestine as well tend to remain quite quickly because they're being shared a lot this explains a lot of the side effects of cancer treatment so we may have heard about obviously the kind of typical side effects of chemotherapy for example so hair loss reduced immunity which is why anyone who's going through chemotherapy was obviously one of those high risk people during the pandemic and nausea as well so kind of aggravating the learning of useful intestines and the stomach is going to be causing nausea reducing immunity because we've lost those white blood cells because we're damaging our stem cells in bone marrow that are responsible for making the white blood cells and then hair loss because those cells are rapidly dividing that produce our hair are being killed so they're not able to produce the hair so this is why we have trying to develop more targeted cancer treatments and more targeted cancer therapies that don't just kill off other cells healthy cells in the body as well as the cancer cells but that try and make sure the drugs get to the cancer cells without damaging the rest of the cells in the body so one of the first treatments is likely to be surgery where possible removing the tumor itself is kind of the main hope and the main aim if it hasn't spread and if it is considered likely that the tumor can be removed without Parts breaking off because then if Parts break up during the surgery then obviously we know they can travel in the bloodstream and maybe cause cancer elsewhere and so that's obviously metastasized the the cancer through that surgery which we don't want to do radiotherapy and some chemotherapy drugs as well they damage the DNA so they stop the cell passing those checkpoints in S phase so mutations might get through but actual physical damage to the DNA won't be able to then replicate it and so it won't get past that checkpoint and there will be no cell division so it should force the style to kill itself to go through the apoptosis stage where the cell dies but the main thing is that it won't divide it could be obviously targeted by the immune system as well if it doesn't go through the apoptosis stage so this is an example of one of the drugs you can see here there's actually the drug is bound to the DNA so what one of these drugs does is it actually starts linking together the bases to try and kind of join the DNA at places where it shouldn't be joined so putting extra linkages in between various bases in the DNA and so that means that when the process of trying to replicate that happens it won't be able to there'll be blockages there'll be damaged to it and therefore we will stop that cell division and so that's one way these drugs can prevent cells from continuously dividing immunotherapy and cognitive therapy can help direct treatments to cancerous cells this is the kind of a large area that's been looked into at the moment so reducing the side effects reducing damage to other cells in the body drugs cancer therapy drugs can be attached to antibodies which have been made to bind to antigens on the cancer cells so really targeted therapy getting those cancer drugs right to where they go because the antibodies will only bind to cells which have the antigens and those cells should only be cancer cells so that drug isn't affecting anything else any other cells that don't have those antigens in the body chemotherapy obviously some chemotherapy drugs work in the same Rose radiotherapy but chemotherapy inhibits enzymes needed for DNA replication so again stops the cell cycle before the S phase can't take place DNA can't be replicated so cells won't be able to divide and again they'll go through that cell death stage so you've got either damage to DNA to stop replication you've got preventing and enzymes that will be needed for DNA replication so things like helicase and then also this idea of targeting drugs to the cells so it could be the chemotherapy drugs or the radiotherapy drugs are those that are bound to the antibodies to Target them or it could be that the drugs are very specific so they will be targeted because they disrupt a specific process but either way the way of cancer treatment at the moment is just to try and prevent those cells from dividing anymore so we need to talk about genome projects and how we Secrets genomes or sequence sections of DNA so we've looked at the genome before and we should know that that's all of the genetic information in an organism or in a Cell so genome projects are just technology and projects that use Technologies to determine the complete sequence of bases that make up the DNA of an organism so it's about sequencing the entire Genome of an organism so we know all of the bases in the order that they exist in the main example for this and we will have probably talked about this at qcsc as well it's the Human Genome Project so it was a collaborative effort for scientists all over the world they sequenced 3.2 billion bases which is obviously a lot previously up until this point the most that we manage to secrets in one row or in a chain was about 10 000. as a result We Now understand and know the sequence of the human genome we can diagnose and treat diseases and we would never have been able to do that without understanding and knowing these sequences we can now try and Trace causes of inherited diseases and they can be found in dates so we can look for mutations in games instead of trying to understand it and figure out what mutations were causing an apple which could have taken years beforehand so this is a timeline it took from 1990 all the way to 2003 to actually achieve this but now genomes are secrets in a couple of days so genomes of other organisms because of the technology advancements that happened during this time and the collaborative effort that everyone working on this technology the technology has come forward so quickly and so fast a sort of exponential increase in the abilities of the technology that we were using throughout this time that now we can secret things even faster what is the use of this why do we try and sequence genomes well apart from the medical uses that we've said so being able to diagnose and treat diseases identify mutations that cause disease if that's really important but also we can start comparing sequences between species or within species and you can highlight where you might see mutations and then they cause disease so kind of predicting or looking for mutations but also comparing genomes that be used to explain the evolutionary relationships between species so that building of those phylogenetic trees that we've looked at and an idea of how we identify who's related to whom and that change in DNA over time that led to these new species well we needed to be able to know what the DNA and sequences are to be able to compare them and this is the only way we can do it is by sequencing genomes so developing on from genome sequencing we are able to once we have sequenced the genome we look at proteome sequencing so we talked about the protein before the proteome is the sequence of proteins that's coded for by the DNA based sequence so it's all of the proteins that can be coded for by genome this is only simple so working out the proteome is only simple in organisms with small genomes such as bacteria and viruses because they do not have the non-coding sections of DNA so the base sequence can be exactly translated into the amino acid sequences so they don't have in neutrons and electrons they just have exons or they just have DNA that codes for things all of their DNA code for something so it's helped identify antigens or viruses and then they can be used to produce vaccines much faster monitor mutations and variations as the path that it involves we've all been exposed to that and tracking of mutations and variants over the last few years and they also enable us to identify antibiotic resistance mechanisms in bacteria so being able to track the genomes of bacteria and look the differences in their genes that could code for resistance to certain antibiotics so obviously this is much harder in complex organisms like humans because we have large sections of the genome that's made up of non-cone DNA or introns in humans it's actually 98.5 so there's very little of our genome that is actually coded football codes for proteins the rest of it is often referred to as junk DNA although it does have some functions so there's genes in there that code the TRNA and ribosomal RNA so it's how we code for ribosomes and obviously they are functional proteins and they have specific roles and so that's why it sort of suggested that that is coding for functional things rather than other proteins some is left over from thousands of years to repeat infections with retroviruses so every time we've been infected with a virus then their DNA gets integrated into our DNA and then that obviously stays and gets passed on to offspring so over millions of years of this happening to all organisms being infected with viruses there's a lot of viral DNA in there it's kind of leftover it's not really doing anything it's just dormant it might just be left over from a viral infection this means that the protein will is hard to determine from The genome as it's unknown which sections are exons and which ones are introns so we don't know which bits code and which bits don't work still being done on the human protea so far we've got more than 30 000 human proteins and we've identified them but we obviously haven't got in there close to knowing understanding what all of that sequence codes for and what it produces so we need to know that DNA secrecy methods have improved they improve during the Human Genome Project and after on sort of an exponential level in terms of the technology and its capabilities so the armed methods that were used during the Human Genome Project were labor intensive they were expensive you could only do a few short lengths of DNA at a time and then have to stitch them together whereas now it's all automated we have big machines and computers that can control the process it's much cheaper for that reason so it takes a lot less time and so now human genome sequencing is only around a thousand pounds it may even be less than that now and it's more cost effective to do it on a large scale so sending large amounts away per sequencing all at once is actually cheaper than sequencing small sections so in order to be able to manipulate genomes or to clone or copy pieces of DNA or even Secrets pieces of DNA we need to be able to isolate genes that we want to know or want to understand so separate them from the genome itself that they're in and then we want to be able to take those sections and then we can work with them because we can't work with whole genomes so there are three ways that we can make DNA fragments or isolate DNA fragments or genes from genomes first one is using reverse transcriptase enzymes to make DNA from mRNA so there's reasons why you might want to do this so you might want to get RNA so mRNA because then you know that the gene is being expressed in the Cell It's also because there's going to be a lot more mRNA in the cell than DNA the reverse transcriptase enzyme is added and we've taken that reverse transcriptase enzyme from viruses and it uses free DNA nucleotides to make DNA from the MRNA template we call this cdna or complementary DNA because it matches the MRNA and so then to make it a double strap and piece of DNA or cdna then we get our DNA polymerase to come in and to make it double-stranded and then we have a fragment we can use so method two is to use restriction enzymes so restriction enzymes or restriction endonuclease enzymes are a group of enzymes that can recognize and cut or hydrolyze bonds at a specific recognition sequence in the DNA and that recognition sequence is complementary to the operative site we call those restriction sites so it'll be a sequence that each restriction enzyme will cut a specific base sequence and that'll be the restriction site so you need to find a restriction enzyme that is complementary to a sequence before and after your Gene mix those in with your DNA and it will cut and form these Frets of DNA that have sticky ends so that means they've got an overhead of a few free nucleotide bases that will then be in theory if you cut your restriction site wherever you want your Gene to go if you cut the DNA open with the same enzymes then the sticky ends will be complementary so then you'll be very easy for them to join together and then finally you can you can machine to literally nodes DNA apartments from scratch so it doesn't require a template so we're not taking it from somewhere that already exists like with the other two or making a copy of DNA from RNA what we're doing is we can literally build it from scratch or you just need to know the DNA sequence that you want and you can feed that sequence into a computer and it will build sequences of nucleotides that are initially attached to a solid bead or something as a support and then they'll be broken off and you can create these sections of DNA with the secrets that you know and it's the sequence that you want it literally means in the living in Vivo so using living cell to amplify or replicate DNA fragments and this is for example they can also produce proteins like insulin so it could be that you're using this method to replicate aging it could be that you're using this to replicate a chicken because you want the organism to also create the protein and then you want to harvest that like we do with insulin hopefully genetic one education at GCSE or it could be just that you want to genetically modify an organism to have it to have that Gene inside it so this is another way that we can do that in Vivo cloning relies on recombinant DNA technology or genetic modification because we're adding a gene to another organism this method works because the DNA code and protein synthesis Machinery is universal so it's the same in all organisms bacteria have ribosomes they have the ability to do all of the processes we would want them to do so they the genome can sustain the letters and all of the systems about how DNA works how it's translated how it's transcribe it is all the same in every organism and so putting the DNA code into another organism just means it'll be read transcribed translated like anything else so the genes need to be isolated from one organism in one of the ways we've just talked about and then insert internal moralism and will use a suitable practices for this and that creates a new combination of genes you're taking a gene from somewhere else and we've put it into a new organs the vector is usually a plasmid but it could also be a special type of virus so if we're trying to get a gene into a bacterial DNA we could use a bacteriophage which is a virus that's specifically infects bacteria remember viruses are good at doing this and that's why they have the reverse transcriptase they're able to inject their RNA into organisms and then turn it back into DNA and then that DNA goes into the Genome of that organism where it gets transcribed that's how viruses work so by modifying a virus to inject the DNA that we would like that that is another way of getting that DNA into that organism the disadvantages of this method because we are going to look at the in retro version in the next video is that it takes longer because you're relying on the growth of organisms and making sure that they've actually taken up the plasmid and not all bacteria will take up the gene initially so you have to then use various techniques so Mark genes growth conditions to be able to find and select the bacteria that you know definitely have the plasmid with the genome that you want and then once you found them then you can grow them up but that takes a while and it takes steps in order to do that and you're relying on organisms that are alive and living and they don't always do exactly what you want and so they can be quite difficult to work with sometimes it's very easy to contaminate your samples so it's one of those ones that's a little bit more time intensive so let's look at the method of how we carry out in the back learning or how we carry out recombinant DNA technology and use it to transform bacteria so first of all we need to get our desired Gene isolated using restriction endonuclease enzymes which we just looked at and then the gene fragment that we've taken now we need to make sure that it's got a promoted region and a Terminator region it means that the gene can be correctly transcribed so it needs to have a promoter region because that's where RNA polymerase binds and then it needs to have a terminate region to tell RNA Polaris to stop once it's gone through the whole Gene sequence okay so then we get our Gene that we've now cut out and isolated and we insert it into a vector this is usually a plasmid the plasmid's cut with the same restriction enzymes used to isolate the genes so the sticky ends are complementary and the gene is able to easily rise with the Placid we need to add ligase enzymes into the mix in order for the backbone the phosphate backbone of the two bits of DNA to be joined together to make one half plasmid so you mix your fragment together with your carp plasmid and then you add large enzyme and then we should get hopefully some recombinant DNA plasmids we will also have put or there will also slightly be marker genes in the plasmids so these are going to help us to identify which Theory I have taken up our plasmid at the end so now we need to get our plasmids into our bacteria so actually do the recombination so we transfer it to host cells by mixing them together so we have our DNA and we have our plasmids and we mix them together in a solution and normally obviously there'll be nutrients there for the bacteria to be able to grow and respire and we normally have to do something to encourage the bacteria to take up the plasmid or to make their cell walls more permeable so we can use sodium fluoride heat or electricity so heat shock or what we call electroporation which literally means using electricity to make holes in that cell wall in order to get the plasmids in and then that's how we'll get the outtake of the plasma to happen obviously as do the little things all of our classmates may not always contain the gene that we want them to all of our bacteria may not take up the plasmid that we want them to so this is why we have to do the last step which is using those marker genes and growing the bacteria up and trying to identify which bacteria we have actually successfully transformed okay so as we said we allow the host cells to multiply and we now hopefully will be able to successfully identify the ones that taken up the gene using the marker genes as we said the marker genes are inserted into the vectors at the same time the genus or they were already in the plasmid that we were using because we bought the plasmid with particular marker genes in they can be used to quickly identify bacteria that are taken up classes that contain the gene so this is where our aseptic technique comes in because we're going to be growing these bacteria on agar plates now the market Gene could have many different functions and depending on what marketing you have depends on maybe what type of nutrient you'll need to grow that nutrient angle you'll need to grow these bacteria on so for example it could be that the packaging you've given them is for antibiotic resistance so that means you're going to think about putting antibiotic in your anger the other thing that you could have given them is you could have given them specifically the ability to break down or use a substrate like a certain sugar that otherwise the bacteria wouldn't be able to break down so then you'll need to only put that nutrient sugar source you've done if you issue the bacteria the ability to produce a fluorescence protein so the ability to flow under UV light these are all different options and in the exam you could be given different examples of marker genes and as long as you understand what advantage or what that marketing allows those bacteria to do the way we use the plates is to make a situation where only bacteria that have that Gene will be able to function survive or will be able to Glow for example so you're just trying to make it so you're making it in an environment where only the bacteria that have your plasmid in with your marketing will be able to grow and be upset or that you can identify them using UV light or that they fluoresce some certain color so here's my plate and here's my colonies so I have used my my marketing antibiotic resistance Gene then I would have put antibiotic into this angle so that means only the transformed bacteria with the resistance Gene this antibiotic will be able to survive so only the colonies that grow will be ones that contain my plasmid and therefore I'll be able to know that they container plasmid because they're able to survive in this antibiotic environment that I've created and so therefore they're the ones I would like to try and grow and continue to grow in order to get more copies of my Jeep if I've added in my marker genes to code for UV fluorescence so growing on a UV light they might look normal and then that all of them will be able to grow but when put a UV light over only those few that are glowing green will be the ones that contain my passage so that they can be isolated and then they can be grown up so in the antibiotics this is one not all the colonies will grow not all the bacteria will grow only the ones of the plasmid in the UV fluorescence one more colonies will grow because there's nothing there to kill them but only the ones that will glow want to give you like are the ones that we want they're the ones that have been transformed you can combine so they're carry more than one market Gene in a plasmid you could put antibiotic resistance and fluorescence protein in geoplasmid so then you can use both so only the ones that survive the antibiotic and glow are the ones that definitely have the plasmids or only the ones that survive on the specific sugar substrate you've given them and glow are the ones that have been transformed you can use a combination of different Market used to try and really make sure you've definitely only got bacteria that contain your plasmid so alongside understanding how confident DNA technology would work so you'll seem to think about the advantages and the disadvantages so be able to evaluate the uses of this technology and think about what are the benefits but also what are the disadvantages and what should we be concerned about now we have this technology and this ability to modify the genomes of organisms and outer new genes what are the issues with it so we need to think about industry Agriculture and medicine and look at the different impacts and the look at the different advantages and disadvantages that might be present within those kind of sectors so when we talk about industry what we're really talking about is microorganisms so bacteria yeasts doing things like producing insulin and other drugs or potentially proteins or other chemicals that we could or molecules that we could get these to produce or doing things like we've seen them be able to break down Plastics or be able to absorb poisons toxins from the soil heavy metals and things like that so the advantages are is that they can be used as little machines so they're not part of an ecosystem if they're being used and contained in a lab so we're not worrying about their interactions with other organisms bacterias swap their DNA amongst themselves all the time via plasmids they can actually join with a little Bridge or a little tube called a pilus and they can actually pass plasma to each other all the time it's called horizontal Gene transfer so us putting new plasmids into different bacteria isn't really any different from that many life-saving drugs insulin being one of the main examples but even more than that can be produced specifically modified bacteria let's not think about the disadvantages then bacteria could leave the lab and genes could be past the wild populations so this could be concerning if those genes were for bacterial resistance for example contamination from other products of the bacteria so any drugs or proteins that are being produced by these microorganisms could be concerned dominated so it depends what they're being used for but insulin for example gets directly injected into the body so if there was any contamination with toxins or other products and from the bacteria then that obviously as an issue and we use antibiotic resistance genes as marker genes in the plasmids so this could create an untruthful pathogen especially if it was to get into a wild population if it was to leave the lab then obviously this could be a big issue because antibiotic is a big issue anyway agriculture so this is looking at kind of genetic Technologies on animals and plants so genetic manipulation is an advantage because it reduces costs and it increases production of crops and yields of animal products so if we can reduce costs increase profit but also increase the amount of food that is my people then that's a good thing because we need to do that with our growing population genetic manipulation isn't really any different from selective breeding it just has sped up the process the risk of famine from pathogens killing non-resistant crops is too great so it's too great to ignore it's too much of an issue that we need to think about because famine being left without places in the world being left without any food for a year or any way of supporting themselves or their families because of a pathogen coming and wiping out a whole crop for one season is sort of too much of a problem to actually just ignore and not do anything about so think about the disadvantages then any genetic manipulation reduces the variation with the population normally because we're using clients so if we've genetically modified a plant we will use clones of that plant so we're not going to genetically modify loads of different organisms we'll just genetically modify one and then clone it so that's obviously a problem because then we're reducing the genetic variation in a population we're reducing the right diversity there could be Health implications for the animals involved so anything where we're genetically modifying or altering genes it comes with risks like viral infection or if we're using a viral vector or cancer potentially we don't always guarantee where the genes are going when we're implanting them and so obviously then there is also a risk to the humans eating the organisms for food there is has always been a small element of risk there even though that currently up until now have been no evidence of any risk to people eating genetically modified organisms the plants mostly plants in this case are going to potentially cross breed with wild varieties and release their genes into the environment same as the bacteria we're all worried about potentially those antibiotic resistance genes getting loose same thing could be for something like a herbicide resistance so we could create plants that we can't control we can't kill with chemical sprays or pesticide resistance it could lead to changes in food chains impacts on insects and other populations you don't know what it's going to do and there can also be excessive corporate dominance control over GMC you see this at the moment so there are companies who produce genetically modified seed for crops and they inbuilt into them that that seed is not able to develop and fertilize so it can't produce offspring of the Next Generation that means that every year if you want this seed you have to re-buy it and so that means there's a constant cost and if that company is the only company that makes seed they've got a patent for making that particular seed with that particular genetic modification then they can charge what they like for it and so that might Edge out other companies from being able to do if they've got a pattern it also might damage some places who can't necessarily afford to pay for that genetically modified sieve that might have disease resistance so then they have to have normal seed and then they're more likely to suffer from famine if that crop fails so it's about who controls this technology who has the patents over it if they you know use it and want to make corporate gain from it and profit then they're potentially going to be disadvantaged other people in humans the big advantages are to do with gene therapy so being able to add functional alleles to body cells so that there's a working copy of that Gene present and if the inserted allele is expressed then the individual can produce a functioning protein and we no longer have the symptoms associated with the genetic disorder that's kind of current gene therapy working at the moment so we're adding genes using this recombinant DNA technology there's also obviously other Gene therapies and we've looked at things like the short interfering rnas and thinking about epigenetic technology but this is about adding actual genes into cells and the alterations can be made to the patient's genome in body cells which means it's not passed onto The Offspring but wherever that faulty Gene is causing symptoms or issues we can transform those cells in the body in those areas for example in the lungs for cystic fibrosis and then they will not suffer as many symptoms which is obviously amazing the disadvantages are that currently it's not completely successful but everything we've tried and every disease it's also short term because we're not changing every cellular body we're only sort of targeting some cells with this gene therapy and adding say a plasmid or using a viral Vector to introduce some genes separately into cells then we can't always it won't last forever and it needs to be repeatedly done the treatment over and over again and it's not in every single cell in that person's body so they can't pass it on they are not cured of the genetic disease it's just a form of treatment the use of viral vectors could cause an immune or inflammatory response this was very early on something that was a big problem with early Gene therapies is that actually the risks of causing a sort of a toxic response or an immune response from injecting this DNA using a viral Vector actually caused some deaths early on in the process of developing this treatment so it's always a risk there concern any Gene alteration can cause cancer if we don't know if 100 if the DNA is going to be integrated into the DNA in those cells or where the genes going there's obviously always a risk that potentially we could trigger some uncontrolled cell division which could lead to cancer concern that this technology could be used to edit gametes or zygotes so now we have this technology and this ability to edit genes and genomes we have got laws and rules and regulations that the scientific Community have decided that there is unacceptable to change or genetically modify gametes or zygotes so that these recipe modifications can be passed onto Offspring or are present in every cell this is partly to do with consent because obviously Offspring from these gametes or a zygote cannot consent to be modified in this way and there is a chance that we do not know what the editing would have done to those gametes or zygotes until those organisms grow up and we will not know whether we potentially damaged DNA in the process and their lives could be at stake so it's a very much considered that this is not an acceptable thing to do but the technology obviously is there and it exists and you may have seen in the news recently that there was a scientist in China and he did edit the genomes of two embryos Twins and he genetically engineered them and changed DNA in their genome and then they were then those embryos were then re-implanted into a woman and those genetically modified children now exist and although the intentions behind what they were trying to do with genetic modification were good there it was seen as obviously a gross breach of the scientific rules and what is accepted and what is not accepted and that sign this has been struck off from being able to practice medicine and was put in jail and the safety of those children is now obviously being looked at very closely by people who obviously want to make sure that they leave happy and healthy lives and that they haven't been affected by this in any way but that is one of the concerns that should this get technology get in the wrong hands or be used illegally it could have some serious implications so in vitro cloning otherwise known as the polymerase Chain Reaction it is literally meaning in the glass in Victoria vitamining grass so replicating or amplifying DNA fragments in a test tube or lab not in a living organism like in Vivo we don't tend to use test tubes anymore in these little tubes we're going to be doing the polymerase Chain Reaction which replicates or amplifies short sequences so up to about 10 000 base pairs so still pretty long and it uses artificial DNA primers say artificial here is that normally these primers have not been extracted from other DNA they've normally been made using a gene machine so in the way we talked about being able to make a custom sequence that you know and that you want specifically that's normally how primers get made so that you are very specific about what the complementary sequences that these primers are going to bind the fragments of DNA undergo a series of heating and cooling steps like we said in what we call thermal Cyclone or thermocycle machine it replicates them many times in a similar way to DNA replication in the nucleus so although we're not using as many enzymes as happens in the nucleus we're still going through the process it's unzipping the DNA and then using DNA polymerase to attach to it so it's still in a very very similar way we're still doing semi-conservative replication we're just doing it in a machine not using as many enzymes and using temperature instead it makes millions of copies of fragments of DNA in an hour so you can go from having a really tiny sample of blood type of a crime scene and you need to get more of that DNA in order to test it sequence it analyze it you don't want to ruin that small sample so you take a small bit of that which contains only one or two fragments of DNA and you can have millions of copies of that made in hours which then you can use for testing and analyzing you must sequence at the end to determine what genes you've actually Amplified so until you know for sure that your primers have worked and they've found to the beginning and end of the secrets that you wanted because it's very unlikely you want to replicate a whole sample you put in you just want to amplify a gene or a section of it you'll have to sequence it at the end of your PCR product to find out what you've actually Amplified and checked they've worked so there is still although it's a lot faster than in Vivo there is still some checking and processing that has to be done so let's have a look at the polymerase Chain Reaction itself so what do we need in our reaction mixture to start with well we need our DNA that is containing the gene that we would like to isolate and amplify we need our DNA primers and we need our free DNA nucleotides we need our DNA polymerase and remember this is Tac polymerase so this polymerase is from the thermos aquaticus bacteria so it has a higher Optimum temperature than normal human DNA polymerase and then we have a buffer solution which just keeps everything from being denatured controls the pH of all the normal things that above the solution is you useful for the DNA primers just to make sure we know what they are they're complementary to the start and end of the secrets that you want to amplify so you could put in a whole DNA sample from a person so take your whole genome here but you only want actually a small section so your primers are designed to binder just before and just after in order to allow DNA polymerase to bind so it only binds there and it only amplifies the section that it would like so it replicates section that you would like this is all done in one of these little eppendorf tubes and all the mixture goes in there and then that gets put into a thermocyclone and this is where the reaction is going to take place because that's what does the heating and cooling steps so let's look at the first part of the reaction are sometimes known as denaturation the mixture is heated to around 94 to 96 degrees to break the hydrogen bonds between the complementary nucleotide base pairs and separate or unzip the double stranded DNA into two single strands and we need this to expose those nucleoside bases that's what we're doing we're just saying that we're breaking hydrogen bonds we are not saying hydrolyte because it is not a covalent bond so we can't hydrolyze it we're just saying we're breaking the hydrogen bonds here so we use high temperature or heat to break the DNA stranded to single strands and expose those bases the next stage is the annealing phase where what we want to happen is we want our primers to bind or anneal to our sequences point where they're supposed to so we have to cool the mixture down to around 55 to 60 degrees and then our primers will bind where we want them and that identifies where the DNA polymerase is going to bind to start reading it so we have a forward and a reverse primer one for each of the strands that we have so do you know polymerase is going to move in this direction on this Strand and DNA Primrose is going to move in this direction on this Strand and so that is how we're going to fill in the gaps and replicate from those template strands and build two new double strands of DNA lastly we have the elongation phase so we need to get the temperature back up to about 72 degrees which is the optimum temperature for the Tactical polymerase and that catalyzes the addition of the DNA nucleotides by complementary base pairing to create two complete double strands of DNA so we've taken one strand of DNA and we've Amplified it because we've made it into two so we have doubled it so our products for the first cycle is two strands of DNA of the section of DNA that we wanted from the template and as we said this is just going to go around around and round repeatedly now so we're going to go back up to 95 degrees and then back down to about 55 degrees and then back up to 72 degrees again and again and again and again and this process will just repeat so the whole process repeats for many cycles usually about 20 to 40. 20 kind of being sort of the standard you could go up to 30. it's quite rare that you would need to go to 40 but you can the amount of DNA increases exponentially as we do this because obviously we started with one strand we made it two and then it will double full 8 16 32 and so on if you get told the number of Cycles so how many times division has occurred because that's it happens every cycle then you can calculate how many copies of DNA you will have by using the formula one times two to the power of the number of times doubled or in this case the number of Cycles so we can see how with a few Cycles we can quickly get into millions of copies of DNA and we can also show this using a graph so a PCR graph can show you this as well it shows the exponential increase of fragments and usually this is because we detect it using the fluorescence of nucleotax so in the same way that c sequencing work so we looked at how the sequencing machines read fluorescent nucleotides this is done in the same way so you get DNA polarized some of the nucleotides you put into your start of the reaction some of them will have a fluorescent tag on them so when they're added to the DNA the fluorescence can be measured so how bright it is the increase of grasses is obviously proportional to the amount of fragments that you have and so it becomes this massive exponential increase so the reason it starts off quite slow we have this kind of low bass line is remember there's quite a few fragments at this point although yes it's doubling to start with initially for the first few Cycles there won't be very many so one two four eight that's not going to give you this a big high reading on the fluorescence meter then you start getting into the exponential levels you can start seeing that line start to really expense sheet go upwards in terms of the fluorescence intensity and then we do still have a leveling off so this is because normally the primers have run out so the primers are things that are going to be the most limiting in your reaction mixture you will have put excess nucleotide in so they should not run out and obviously it's just going to be about if you don't have enough primers to bind anymore you've used them all up then that's normally when we get that Flatline and no more DNA copies can be made the use of graphs like this and being able to plot and see what's actually happening the reaction is sometimes called rtpcr or real-time PCR because you're tracking in real time the PCR product that you're making and you can see how much you have as well so it also might be referred to as quantitative PCR so you can see how much product you're making as the reaction is happening and this graph is being plotted in real time so Gene probes or DNA probes are singles founded pieces of DNA which are complementary to and therefore bind to a known a sequence these probes are labeled with a radioactive marker or more commonly with a fluorescent probe to detect its presence so they're made to be able to sample DNA and be able to tell you whether a gene is present or not for example so we get some DNA that we've taken from someone a blood sample whatever it is we will DNA to that DNA so we would split it open those hydrogen bonds are broken so that we can expose the bases on the DNA because our DNA probes are also going to bind to a complementary sequence so we need to denature it we can use heat like we do in the polymerase chain reaction for example then we have our DNA probe so short sections of DNA that are complementary to the gene or the allele or just the sequence that we're looking for to know whether that Gene is present and in this case I've got a little pink fluorescent tag on there so that means that it will glow under UV light for example or it can be read by a laser like in the gene sequencing we looked at it can be red brownies which can detect the color that's emitting from it and so that is going to bind to the complicated sequence of my DNA sample and show me yes okay that sequence is present so that could be a gene it could be an allele so it could be a mutation that we're looking for that might be causing a disease whatever it is when we mix these together that's what happens what can we use them for so as we said locate specific alleles of genes to see if the person carries a mutation or a mutated annual that causes a genetic disorder like cystic fibrosis help to determine how patients will respond to drugs so certain mutations are more responsive to certain drugs than others since there is a breast cancer treatment which responds to certain mutation in that brca1 or two Gene and so if you don't have that and that's not what's causing your breast cancer there's no point having that drug so being able to screen for that is really important identifying health risks so being able to identify whether you have genes or mutations in genes that currently aren't causing a problem but could increase your chances likely said about those mutations in the brca1 and two for breast cancer so having this information being able to screen your DNA and know what health risks you are potentially more likely to have because of that then it gives you the options and the choices about reducing the risks so how do we actually do it then so normally a DNA sample is taken and then it's digested into fragments using restriction enzymes to look for the sections that we know where those chickens are going to be present most likely or it could just be chopped up into sections to make this part easier the DNA is separated by geoelectrophoresis so that we have those bands because again we're mostly looking to see sections of the DNA where the genes that we're looking for are most likely to be present and then you use a nylon membrane and you put that on top of the gel so when we run our gel electrophoresis we're going to get those bands on that gel then in order to kind of transfer the DNA off the gel because the gels have quite obviously difficult to move around and it's not very stable so we transferred that DNA onto a membrane that can be manifest a bit easily and sort of moved in and out of liquids so the DNA is bound to that membrane now and then we do what we call a probe hybridization so we wash over that membrane the labeled probes so our short sections of DNA that are going to bind to the genes or the C Secrets we're looking for and they have that either fluorescent tag or they have a radioactive tag and then once that's happened you then wash off the probe liquid that you added so that anything that wasn't bound to any DNA will wash off and then you can look at that membrane either under a UV light either put it through a machine with that color-coded laser that can identify the colors or obviously if it's used a radioactive tab you use an auto radiography where we put a piece of radiographic film over it and where there is radiation it will create spots or bands will show up and so then we can know yes or no whether we have the genes that we're looking for we obviously looked at the in Vivo method of cloning and amplifying a gene and so this obviously is not always going to be just done with human samples or it could be that you can use this method to actually look for to see whether you're transformed bacteria that we've made using the recombinant DNA method we talked about if they actually have the gene you want them and this is a way of doing that so instead of using marker genes for example and instead of like growing them on different types of nutrient what you can do instead is just do your recombinant technology techniques in order to transform your back bacteria grow them understand and then we do basically the same thing so we take a nylon mesh we press that on top of the plate some of the bacteria from each of the colonies gets transferred onto the nylon mesh you then make sure that the cells are killed and that the DNA is denatured and hybridized or broken open and so the bases are exposed same as what we said at the start and then you wash over your probes they will bind to the DNA sequences if they're there then you rinse it or wash the DNA probe liquid off so that anything that's not bound to any DNA disappears so then all that's left will show up either on auto radiography paper or through fluorescence will have any colonies that left will have have your Gene eye that you wanted and then you can compare your membrane so hopefully you'll have done it in such a way that you'll be able to know which colonies are glowing what your sheet match the ones that are still on your plate so then you can scoop up those convenience because you know that they contain your Gene and then you can go on to grow them up further and you'd ignore the ones that didn't glow or didn't show up on the auto arachiography on your membrane that you took off the plate okay so those are the main two methods of how DNA probe to use the main thing to understand is that you understand that you need a section of DNA that's got the Gen unit that you're looking for or the the complementary secrets to the probe you've got the probe that's labeled say how it's labeled and then the idea of kind of this transferring of DNA to some kind of membrane where you can wash over the DNA probes they will bind where the sequence is complementary and then you rinse anything off that's not going to bind to the DNA so then only the DNA sequences that have a probe bound to it will show up and that's how you know for the check for the presence of these either Secret this is jeans alleles mutations whatever bit of the DNA is you're looking for with your probe okay so genetic counseling the use of this technology so this ability to be able to screen DNA and be able to identify what is in it what's part of it whether someone has mutations or not is also very useful but it needs to be managed carefully because these can give patients a much better information about their health risks but guidance will be needed by a doctor or a counselor to make the best decision with the information that they're being given and support those patients with their options once they've found out this information so they do make it very clear if you do send off any of these kits where you can send your DNA away and obviously when it comes back they do kind of give you warnings about the health screen you want to say do you want to proceed with this because obviously they will tell you whether or not you have say a bcra mutation and they could tell you whether you have an increased chance of heart disease for example so if you find out some of these things it can be you know life-changing and really serious news and they'll be really serious consequences about how you might choose to act on this information so having someone that can really explain these test results to you and explain your chances is really important and that's what genetic counselors do so they guide people to make informed decisions about matters related to genetics that may come up itself so it could be that someone was diagnosed with early onset dementia in the family and there's a chance then that you can be genetically tested to see if that was caused by the mutation and whether or not you've inherited that so it could be about genetic disorders it could be about whether or not you've got something that you could pass on to your children it could be about decisions based on the outcome of a genetic test so let's think about an example of this we've kind of talked about breast cancer already so screening is available for genetic mutations which can lead to breast cancer so you can actually screen to see if you have those mutations that we've mentioned such as the mutations in the brca1 or two genes so genetic councils could then use this screen to explain the chance of a person developing cancer so explain their probabilities explain the risks and they can help patients decide if they want to take surgical steps to reduce their risk of breast cancer which for example will be a mastectomy so removal of the breast tissue this is obviously a serious kind of life being decision but if you can have someone explain to you that dramatically reduces your risks of getting breast cancer in the future and it's sort of a preventative measure then that can be obviously really helpful to have someone to talk you through those options the other thing that Gene probes and this technology is going to lead to potentially is then personalized medicine so as well as being able to give people options like surgery to help them with their health risks we could be able to screen for these disorders which means that once we able to do that we may be able to find out what mutation is causing the disease so then we can personalize medicine to Target different dosages or compounds because it depend on the genetic makeup dependent on what they need so right now it's in its infancy still this technology but it has the potential to revolutionize the effectiveness of different medicines for different conditions so if we go back to the breast cancer treatment if someone is trying to have a mutation that's causing the breast cancer and we know where the mutation is there are some drugs that are able to Target specific mutations so by using the screening and by being able to tell people that their cancer is caused by this certain mutation it means that some drugs are more likely to work for them than others so instead of giving everyone the same drug so same chemotherapy treatment if there are some drugs that can be targeted to specific types of cancers then every individual person based on their genetic markers or their genetic condition can get a different type of medicine and this is obviously a very exciting and a very new way that we could be doing medicine in the future so in this video we're going to look at genetic fingerprinting but before we look at your fingerprinting we have to know how we can actually produce the genetic blueprint and the first step of that is to understand that we need to use gel electrophoresis so gel electrophoresis is using an electric current to separate sections of DNA or RNA or it can be used to separate proteins as well and it separates them by size because these molecules are polar it's using the electric current to attract them DNA and RNA fragments can be separated by the length or the number of base pairs and proteins are normally separated by mass a tank is used to set up an electrical gradient much like an electrolysis in chemistry however the samples are located in a guard gel so we load them in so they're sort of inside the gel and it's the same agar gel that you use for growing bacteria to make plates with but the gel itself is kind of a mesh or web of fibers that we obviously can't see but that's what makes the kind of gel structure and that means that they have to move and navigate through that gel structure which slows down movement of molecules and that's what helps to spread them out it means it takes time to the sound be drawn to the anode or the cathode depending on what we are using and this Define is directly proportional to the size or charge of the molecule so as we get bigger less distance is moved the smaller the molecule the more distance is moved so the further it will move along the gel so the distance they move along the jam allows them to be separated DNA if we're loading DNA into these Wells then it has an overall negative charge so it's going to be moving towards the positively charged end of the anode of the gel the gel is covered in this buffer that you'll see you'll see that the electrical current to distribute or a tank and around the gel evenly okay so let's have a look in a bit more detail then at the actual method for gel electrophoresis so to start with the DNA fragments which have been Amplified using PCR are mixed with a loading buffer and perpeted into the wells of the agar gel so the welds have been like pushed into so they're kind of little dips that have actually been put all kind of boxes that have been pushed into the well so that they can withhold it they can contain the solutions that we're pressing into them and they will sit in the bottom of these Wells so you can see they're kind of halfway down into the gel so that means that when they move they're going to move through the gel and they're actually going to go through it this way so we put a loading buffer in and what the loading buffer does is it's denser than the running buffer so the liquid that's covering the gel and means that it sinks down into the well and the DNA doesn't just float away step two is that we the gel is obviously in the tank it's covered with this alkaline buffer and it has ions that carry the current and maintain maintains a constant pH and the current Supply this comes from power source and it's about 18 volts so it's not super High level voltage you don't want it to be really dangerous but you could still obviously get an electric shot from this so it needs to be enough of a current to actually attract the DNA the DNA migrates through the gel towards the positively charged end or the anode smaller proteins or DNA fragments will migrate furthest because they're lighter so they will get to the end of the gel here whereas the larger ones move more slowly so they won't move as far in the gel and you can see here I've got my bands of DNA fragments that have moved along the gel from each well and then finally we take the gel out of the tank after depending on the electricity obviously and we can photograph it under UV light now the loading buffer could have fluorescence in it but what really we want is the fluorescence added to the primers that we use to amplify our secrets using PCR that stains the DNA so all of those DNA fragments that have primers in them will have that fluorescent tag that goes under the UV light that means that we can visibly see the bands in the gel so we can see how far each one has moved we know and take a photograph of it and you can see these bands kind of glowing so you can keep photograph because the gel will not keep for very long the bands are compared to the ladder so normally we put a sample of known Bay sequence fragments into the end well it doesn't matter which vent you can do both ends if you're doing quite a large gel that means that all of these fragments here on this row we know how many base pairs how long each of those fragments represents it's made of custom sequences different lengths so a thousand base pairs 800 base pairs 600 base pairs 400 base pairs 200 base pairs and then down to like 50 base pairs so that means that we can now compare if this is our ladder so this is our known sequence then each band that is in the same distance has moved the same distance as that band in the ladder we can say oh well that band is 5000 bases long that band is 100 bases as long but ever it is and so we can use that to help start to identify our fragments so genetic fingerprinting relies on this feature of DNA called variable number tandem repeats they're repeating sequences that occur in different places in the Genome of eukaryotes they can also be called microsatellites so the probability that two individuals will have these same lengths of repeating base sequences in the same place in their genome is very low so that means the position and length of the vntrs between coding genes because obviously they're in non-coding sections because otherwise they would interrupt genes and then they can cause disease we're just talking about the ones that are in non-coding sections between genes and the position and length of those is sort of pretty unique to every person except identical twins closely related organisms will have more similarities between the length and position of their bntrs because they are inherited so you will have inherited some of your vntrs from your mom and some of you'll be interested from your dad and so between those you can start to look at how similar the branding patterns are in the genetic fingerprint between the different individuals so each of the bands on this gel here represents a vntr the thicker the band normally the more of that secrets that you have and obviously the distance of the band tells you the length of it so the length of those sequences is going to be able to be determined by how far they've moved in the gel and so different lengths of different sequences and then have been cut out with restriction enzymes from places that we know in the genome contain these vntrs and it's to do with the length whether they're there or not only because obviously some bands they don't have the same bands in every fingerprint and whether they are the same length in which case they have moved the same distance on the gel so the method is just as we said so restriction enzymes are used to make the DNA fragments that contain vltrs from each DNA sample that we're looking to try and compare the fragments are then Amplified using PCR the DNA fragrance is separated by size using gel electrophoresis and then we can compare DNA fragments either next to known samples so like example like the ladder we said or next to sample that we want to compare it to for identification so let's take my sample down here and have a look at it as an example so say we were looking to try and match someone to a crime scene so maybe this is the sample that was taken at the crime scene so it was taken from a sample of blood maybe that was found at a crime scene or some DNA that was picked up somewhere else and then we're looking to try and see if any of the DNA from these three other Suspects is going to match the DNA from the crime scene so I have suspect a b and c so all we really need to do is look across the bands and see which of a b and c has the most similar banding pattern to the crime scene so obviously this one is the same in fact these two are the same this one we don't have there is a slight band there but it's not the same in terms of the amount this one is the same and this one is the same and this one is the same so here we have one two three four five there's six bands in common which is quite a lot so I would say mostly I'm leaning towards suspect six if we have a look at a we've got one but it's not really in the same place so actually I would say that's not one this one and that's it for B there are no vans in the same place for B so we know or we can be confident that suspect C has enough shared DNA fragments of the ntrs with the sample that's found in the currency into suspect C has likely been in the crime scene it obviously does not say if they committed the crime or whatever it is that we're looking for but they were there and that DNA that was found that the crime scene is most likely to be this person's because it's very unlikely that they would have this many the ntrs in common this is how we would use these DNA fingerprints for various uses so we just looked at example of forensic techniques using genetic fingerprinting but there are other uses of genetic fingerprinting that you need to be able to describe so for medical diagnosis so we have talked about the fact that there are repeating sequences that can be found in certain genes that are linked to genetic diseases like Huntington's for example so being able to compare samples from patients who have the disease with people who are not sure if they have genetic disease and looking for those Long rookie exceptions where we expect them to be in a gene that could cause a genetic disorder will allow us to diagnose it determine genetic variability within a population so taking samples from different members of the population and if they all have really similar genetic fingerprints then they have quite low genetic diversity which is obviously a bad thing so we want to try and if we're aware of that through this test testing Technique we can try and do ways of conserving biodiversity and increasing that genetic diversity in the population or at least we will know that that population is at risk of collapse because obviously if something came long it was like a pathogen for example they could be at risk of all dying from the same disease in animal and plant breeding so it stops inbreeding of plants or in zoosed so if you have an animal a zoo that you would like to breed from that is in the world in quite a small population and you'd like to breed it with another animal either in your zoo or from another Zoo you're able to do this fingerprinting test to see if they're really similar to vntrs then they are too genetically similar and they shouldn't be broken each other to try and stop inbreeding and make sure that we're increasing the diversity in captivity determine paternity and therefore pedigree so if someone's claiming that an animal is a pedigree animal so it's from a specific licensed breeder they're being able to use it as like a paternity test identifying plants or animals with a desired allele or Gene to help with selective breeding so being able to sample population looking for a specific bntr that matches one that we know is linked to resistance or has similar genetic profile to a plant that we would like to come then we can easily find them and then be able to clone them in forensic science as we said it could match DNA that was found at a crime scene with suspects samples that were taken it does not determine if the person carried out the crime that's very important to say and we can't make those claims we can just say it puts them at the scene of the crime or they were present but obviously that could be potentially faked or could be circumstantial that they'd also visited the scene it's one of those sort of gray areas but it is used in forensic science for that reason determining genetic relationships that we've already looked at paternity testing identifying siblings so if you were adopted or if you were the product of IVF and you aren't aware of who your sperm donor is for example or you were adopted and you've potentially found other siblings being able to prove that you are related or not and as we say Advantage should correspond with at least one of the parents so half of your bntrs will be from one parent partly from the other there is a chance through your own replication of DNA that you may have added or changed but there should be the majority of the ncrs would have been inherited from your parents [Music] foreign [Music] [Music]