and the griffith experiment so he had these dead mice and so they um they recovered the s strain from dead mice so they also said um it's dna not protein but up until this point they didn't really have a definitive answer like they they couldn't say 100 that it was dna like they couldn't hold it in their hand and say this dna this is what causes inheritance and this is what holds our genes um so hershey and chase they actually were the ones that finally said that dna is the actual dna is the genetic factor um they used bacteriophage bacteriophages are viruses that infect bacteria and so they had radioactive sulfur and phosphorus which attached to protein and attached to nucleic acid i forget which one was which but anyway they could track where the dna went so a little bit about a bacteriophage bacteriophage looks like this right so the outer coat is protein everything in red here is protein and then inside is dna and so they could track where the dna went through through tracking the the radioactivity because the dna attracted sulfur i don't know which one it will save sulfur so dna attracted sulfur they could track where the sulfur went protein attracted phosphorus and they could track where the phosphorus so they hershey and chase were finally the two people that could say dna is the genetic factor and then watson and crick came along and they discovered the structure of dna with the help of rosalind franklin who was also part of that rosalind franklin kind of got shafted away from a nobel prize she died you can't give a nobel prize to somebody who's dead but so watson and crick received the nobel prize for discovering the actual structure of dna before they could figure out the structure of dna chargaff figured out the a to t c to g rule so the percent of a the percent of a equals the percent of t and then the same for the others percent of c equals the percent of g and what he ended up finding out in addition to that rule it's a very important rule he found out that every individual of a species has the same percentages so um both bozeman showed you octopus it was like 32 percent to 32 percent and i think it was like 18 and 18. my math might be off but um for every organism that belongs to the octopi species the ones that he was looking at would have that amount of a and t in that amount of c g so humans we all have the same percentages of a t c and g roughly the same this person or these two people here meselson and stahl so messelson and saul came up with the idea that dna replication is semi-conservative dna replication is semi-semi-conservative so when we make a new strand of dna there's one strand of old and one strand of new so this might be the old and this might be the new and then we would have another set of the same thing so we would have new and old so the old strand gets ripped in half and then we add one new strand to each of those to make two helixes so they figured out that it was semi-conservative um the other the other um theories that or hypotheses that they had was that it was completely conservative which is what this is showing you so if it was completely conservative this would be old and this would be new um that wasn't the case and then another hypothesis that they had was a dispersive replication which was like a banding pattern of old and new so something like this is kind of strange but um so what they figured out was that that was the um conclusion there is a nice um ted talk that goes over oh oops no wrong one there is a nice video on youtube that goes over besselson installs experiment if you want to look at how they reached that conclusion but we don't need to learn the experiment per se just kind of what they found from their experiment so semi-conservative replication we're not going to get into replication today we'll get into replication on wednesday but we are going to talk about dna um pairing and how dna looks so i hope we can do this part first before we get into how dna looks um so using chargaff's rule so what is chargaff's rule a to t c to g and we're going to synthesize a strand of dna so maybe should have made these red and red and um orange like our old old and on the last slide but anyway if we have a strand of dna and we need to make a complementary strand the new strand is complementary complementary complementary this is old that is old so how are we going to match them if a goes a matches b c matches with g if we use our gaps rule um what what would we end up with so if you can write on your screen you can enter these in or how about this i'll do um i'll put these in segments so choose a segment to write on how about that there you go you can click your screen you can um use the writing handwriting feature or you can use the text feature and match those complementary strands or make a complimentary strand to the to the original strand so far so good okay so i entered in the new strand oh nope that's not right i entered it on the wrong the wrong strand anyway here's me being proactive i did it wrong um all right so yeah so ggc looks great okay cta looks great a-a-a great a yep e let's see atc yep e-a-t-e [Applause] yep all right awesome so we made a new strand of dna to go with our original strand in our semi conservative fashion right and we have no errors so that's great um so on the bottom strand what you will end up seeing is that the complementary from the original will look like the new strand and the new strand will look like the old strand from up here and then if we we like continued these they would be exit like that we would have like this thing called a replication bubble so again we're not going to get into the replication bubble today but we did a good job at matching those strands of dna so there you go so there's the answer on the next slide if you want to come back to it all right let's talk about the structure of dna so dna we've already learned about um nucle nucleic acids right back from chapter three nucleic acids are polymers which are made up of these nucleotide monomers nucleotides that are connected end to end make a nucleic acid right nucleic acid is the polymer that we learned about in chapter 3. so it's one of those bio molecules or those macromolecules from chapter 3. nucleic acid can be either dna or rna or they can be atp but we're just learning about dna and rna so dna and rna they are a type of nucleic acid dna for rna dna is found in the nucleus the nucleoid region or in some organelles so you might be thinking well how can it be found in all those places all right there we go so dna if it is a linear linear chromosome or if it's organized in like a linear fashion it will be found in the nucleus of eukaryotic cells okay if we're talking about circular circular dna it will be found in the nucleoid regions of prokaryotic cells so remember prokaryotic cells they do not have a nucleus right they don't have an organelle that encloses their dna it's just found in a region called the nucleoid now some of our organelles have little bits of dna in them so that would be like the mitochondria mitochondria and then if we're talking about plant cells that would be the chloroplast they have some bits of dna left over those bits of dna help regulate processes that are um exclusive to that organelle so that's why they still contain some dna and remember mitochondria and chloroplasts are likely bacteria that cells took up a really long time ago through something called symbiosis so they retain some of that dna all right so that's where we can find dna so rna can be found throughout the cell so it can be found in the nucleus it can be found in organelles it can be found in the cytoplasm and that helps to relay messages from dna to other parts of the cell we're not going to talk much about rna this week we'll talk about rna mostly next week but just to let you understand the difference between the two since we're going over nucleotides i figured we would talk about it um so there are different types of rna um we're not going to learn about them right now um dna contains genes which code for your proteins by the help of rna so we are we already learned about genes and mendelian genetics last week so now we're kind of getting into what what is dna what our genes looking closely at them all right so nucleotides are made up of three things three parts one of them is a phosphate another part is a five carbon sugar and then another part is a nitrogenous base so let's talk about the phosphate first so each nucleotide contains at least one phosphate it might have upwards of two or three phosphates attached to it but if we're looking at a nucleotide on a dna strand it would have one phosphate that's how they would be found the phosphate is connected to this bicarbonate sugar so in dna five carbon sugar is a deoxyribose so that's what the d stands for in dna and then it's called ribose in rna the difference between the two is an oxygen so ribose contains an oxygen an extra oxygen deoxy ribose has lost that oxygen head's name um this sugar you'll see these numbers on it they're pronounced as like five prime four prime three prime two prime one prime and they just help tell us the location of the carbons on that sugar and they help us um learn like the attachment sites for certain things so if you look the phosphate here is attached to the carbon or the five carbon sugar through the five prime carbon and then the nitrogenous base is attached to the one prime carbon so this nitrogenous base can be one of four things if we're talking about dna any one of four things the one that you're looking at here is adenine and the other three this here this is adenine the other three can be thymine cytosine and guanine and then in rna we have uracil instead of thymine okay i'm going to switch to the next slide are there any questions yet we're going to talk about how these are arranged into a polymer so again we are looking at a monomer right so this is the nucleotide here made up of three parts so remember when we learned about like fatty acids they had like this um glycoglycerol part then they had like these fatty acid chains and they were made up of like four parts um this nucleotide just has three parts right phosphate carbon um sugar and a nitrogen base and that nitrogen base is what makes the nucleotide different when we talk about our a t c and g a t c and g still have these parts connected to them we don't bother saying those parts though because they're always the same depend on no matter which is attached to those parts so um we just say atcg we know the sugar and the phosphate is always there so what you'll notice is that the structure of these nitrogen bases different from each other juanine and adenine are what we call curings let's see if i have it written i don't purines and the other two i mean and cytosine are pyrimidines aroma um the way i remember which one's bigger is that added mean and guanine have a nine and i and e at the end of their name um and so that nine is actually both because there are nine atoms that make up those um molecules um but anyway um the nine just helps me realize that it's bigger and that's the larger one so purines have two rings they have a five carbon and this are they have a five atom and the sixth atom ring and then the pyrimidines only have a carbon ring um so some other things that you'll notice about it is that when a and t go together and c and g go together there's these dot dot structures between the two right those dot dot dot structures are referring to i oh my goodness if i could write hydrogen bonds if i can type it those are hydrogen bonds so hydrogen bonds are the weakest kind of a bond or one of the weaker bonds that form and they form between separate molecules so that like that's how water is held together so water molecules are held together by hydrogen bonds and um what helps is that it keeps the structure together right so it keeps this like three-dimensional structure together but hydrogen bonds since they're so weak they're easily broken and then we can copy a gene or make the more dna or or rna or whatever and then put them back together and they'll reform so when these hydrogen bonds form here they form a double helix pattern and the way that the double helix is made is called the right-handed model so it's going up to the right i don't know if you can notice that there but it's going up to the right on all of these so it's never going to go up to the left um i don't know why it forms that way i think it has something to do with the bonding patterns between the backbones of the of the ladder the um outside the vertical parts of the ladder um but i'm not quite sure why it's a right-handed model versus a left-handed model but anyway it's only ever found as a right-handed model and let's see what else then i go over right-handed model it's a 3d helix you might hear parts of the helix called um like referred to as a ladder so the vertical sides are made up of phosphates and sugars whereas the rungs of the ladder are made up of bases and the hydrogen bonds so the vertical sides of the ladder are made up of the non-important parts right phosphate in the sugar so not really important doesn't code for anything just kind of adds protection um and then the rungs of the ladder the insides are made of the important parts the nitrogen bases that actually code for your genes let's get to it all right so this is our dna replication figure we're going to be on this figure for quite a while here today um let's see so first dna replication takes place during what phase of interphase might take you a second but it takes place during s phase of interphase right so g1 remember is gap one there's a little that goes on the cell gets bigger it regains some biomolecules during s phase is when dna is going to replicate right so we're going to make another strand of dna so that during mitosis the daughter cells can have the same copies of dna right so during s phase is when all of this occurs okay um each of these things here are enzymes right so enzymes typically run are typically n in a s e a s e look at all of them so these are all enzymes enzymes remember speed up reactions and they might build or break down components so if we look at all of these what are they doing dna polymerase is building dna polymerase building building building building um philly cases breaking and this one's not doing either of the two but we'll talk about that one in a second so enzymes again they speed up reactions and each enzyme here has a different job we're going to talk about each of those different jobs okay let's see let's talk about helicase first helicase so it's this enzyme here helicase breaks hydrogen bonds so remember each of the strands here so the strand on this side strand on this side they're connected by weak hydrogen bonds each base is connected by a hydrogen bond here and that hydrogen bond is broken by helicase and so helicase breaks the hydrogen bonds so that these bases are exposed and so that another enzyme can add new bases to the strand now let's see let me type up here pillowcase hydrogen bonds okay okay so let's go on to the topoisomerase topo isomerase is that circular enzyme there and you might be able to guess what it does topoisomerase prevents super coiling so remember dna is organized into coils so it coils around um histones and then those histones coil around themselves and they make this big um condensed structure of a chromosome by supercoiling now topoisomerase undoes the supercoiling so that the dna strand is accessible by other enzymes okay so if we write up here at the top oh isomerase prevents supercoiling you can also say that it like unwinds the dna or uncoils the dna if that's simpler for you to remember but i'm pretty sure you're going to see that super coiling term in the textbook and the quiz that's coming up so it might be better to write that definition instead okay so now that topo isomerase has undone this super coil and helicase has split the hydrogen bonds what we're going to do next is let's see i'm running out of colors let's talk about primase so primase you can see this is like light blue ring here and it's creating something right um it's creating an rna primer so take a look at the colors here this rna primer is orange whereas there's a red strand right so the original dna backbone is going to be red this rna backbone is represented by this orange color because it's different so primase makes an rna primer and that rna primer is the attachment point for dna polymerase three okay so primase creates rna rna primers so um the rna primer again is for dna polymerase iii to attach to you can see there's a lot of primers here on this side right there's not that many primers on this side it's all just one red strand so let's talk about what's going on here if you notice over here there is a lagging strand and a leading strand remember what we said earlier dna replication runs from five to three prime meaning that dna polymerase yeah you can re-watch this after the lecture is over um dna polymerase adds new bases to the three prime n so if this is the five prime end of the new strand the other end would be three prime right let's let's make a note about dna polymerase so dna polymerase three the dna polymerase iii add new nucleotides to e3 prime end of the new dna polymerase iii adds new nucleotides to the three prime end of the new strand so on this leading strand all is right we're moving in this direction the old strands are being broken apart by helicase so it's going to continue in this direction we can just add one nice solid strand five to three prime now on the other strand remember these run anti-parallel so we have one strand one old strand that runs three to five this old strand runs five to three if dna polymerase can only add new nucleotides to the three prime end of the three prime end of the new strand let's take a look at this so this would be five prime three prime five prime that's the three prime n that's the five prime end of that strand if they can only add in the three prime and it's going to create some problems right so it's going to have to create a strand five to three prime and once that three prime strand matches up like it did over here with the the segment of dna it has to jump up here and start creating another new strand so these on this side of dna replication is called the lagging strand because it takes more time for dna polymerase to create these segments or these fragments of dna and then it has to jump ahead and create more fragments all while primase is making more primers so every time dna polymerase 3 has to jump this primer has to be ready for it so these fragments are called okazaki friends takazaki is the scientist who found or discovered the fragments and he described he described them first so he gets the name of them and of course scientists like name things after themselves right so these are called okazaki fragments now when the fragments restart or they reach the um old segment here they aren't exactly attached um and they're not attached because this is remember this is rna right a primase created that rna primer and now we have like snippets of rna backbone dna backbone rna backbone dna backbone what you see down here is this guy dna ligase let's talk about him dna ligase is a little enzyme and he glues the akasaki fragments together um let's see like clues make sure i spell his name right together so those fragments are going to be glued together by the ligase so ligase is like our glue and dna polymerase one which we haven't talked about yet let's see what color has an iv red dna polymerase 1 is going to do something before ligase act on the fragment dna polymerase one is going to replace the rna backbone with a dna backbone rna or the rna primer with dna nucleotides so the rna primer again rna backbone rna nucleotides dna polymerase has to replace that if we want a viable strand of dna the dna polymerase one replaces those little segments of primer with dna nucleotides and then ligase can come in and glue those meeting places together they can stitch them together okay question so far um let's see one other thing i haven't talked about yet is the single strand binding protein you might see it written as s s e protein you can see it's pointing to these oval purple things um and you might think it's like weird looking or like it doesn't make sense why they're there um the ssb protein they help keep the strand apart from each other so once gila case breaks those hydrogen bonds between the old strand nucleotides the strand is now open but it's going to try to form back together and those ssb proteins are going to keep it apart from each other keep the strand open so that dna polymerase three can access those nucleotides so that's why they're only located here where there are unbound nucleotides and you're pretty much going to only find them near helicase so once dna polymerase iii gets close to those ssd proteins it'll come off and then it'll jump ahead we'll like keep frog the next open bait keep it apart okay so let's go back over this really quick before we play quizzes i'm not gonna hit erase yet um but all right so let's go over we talked about helicase and topology first so helicase unzips the old strand of dna by breaking the hydrogen bonds between nucleotides topoisomery prevents super coiling so that nucleotides are accessible once helicase breaks those hydrogen bonds now we have two strands one strand is called the leading strand and the other strand is called the lagging strand on the leading strand dna polymerase 3 can create a new strand of dna complementary strand of dna by adding bases to the three prime end of this strand right three prime all is well and good on the lagging strand since these strands run anti-parallel right new um new segments of dna can only be added to that three prime end still but it's running in the opposite direction so dna polymerase three has to keep jumping and adding a new strand and jumping and adding a new strand now in order for dna polymerase 3 to attach to a site on dna there has to be an rna primer that rna primer is created by primase so it's not shown here but at the origin point of replication there was a primer here that's probably already been replaced by our enzyme that does that so primase creates that rna primer the primer is the attachment type for dna polymerase iii dna polymerase iii reads the old strand makes the complementary new strand by adding bases to the three prime end once it reaches that end it can jump ahead so next dna polymerase one is going to replace these rna fragments with dna fragments which creates gaps and dna ligase can glue those gaps together to make a nice solid strand okay are there any questions are there any questions about what we've gone over is there any part of like any enzyme or anything on here that you don't quite understand or you need me to explain again um i don't mind explaining something again if you're unsure of what it does okay all right so we're going to i'm going to take a picture of this feel free to take a screenshot i'm going to take a screenshot okay so we're going to play quizzes here in a sec um so i'm just warning you that if you're taking a screenshot say something i won't exit my screen just yet talk about the difference between eukaryote and prokaryote replication um not a whole lot different dna is still going to replicate there's going to be a semi-conservative so it's going the new strand will go um one old one in one old one new just like in our other dna right so we have this this would be our old and then this would be like our new strand that's forming here we'll get two new strands or we'll get one old one new one old one new anyway so what we're looking at on this slide is is a table from i think it's 14.5 i want to say chapter 14.5 table out of the textbook so eukaryotes remember we have a nucleus in our cells that contains all of our dna our dna is also linear and prokaryotes have circular dna prokaryotes don't have as much dna that we have um so they don't have i mean they don't have a lot of dna to replicate so it goes pretty quickly um and in eukaryotes we have much more dna and plus they're linear so our our enzymes have to skip around from dna to dna or from chromosome to chromosome to copy them um so in prokaryotes there is a single origin of replication and what that means is remember prokaryotic dna is circular um and the way that it replicates is by making like a little bubble here so it'll start at like one origin and it'll work its way out away from the origin on either side until we get let's see until we get like a whole nother strand of dna down there so that would be our new that's our new strands that we've made this is our old strand or you know one old one new one old one new so um prokaryotes they just have a single point of origin and it goes around the circle until we get a new one and then it divides you can also see that the rate of replication in prokaryotes is very fast so that's one reason why prokaryotes like bacteria can replicate and they can divide and make new bacteria so quickly because they can replicate their dna so quick eukaryotes can't do it as quick 50 to 100 nucleotides per second um there are different types of enzymes that are used in each um each replication so you can see dna polymerase 1 and polymerase three are used in prokaryotes that's what we've been talking about but there are other kinds that eukaryotes use because there are different enzymes in prokaryotes versus eukaryotes we can target those enzymes with like with chemicals like drugs to stop the replication and stop them from growing so you can so kind of um sort of like an antibiotic um telomerase okay so we haven't talked about this enzyme yet telomerase is present in eukaryotes not present in prokaryotes for the reason being that prokaryotes let me erase everything here prokaryotes they have that circular dna so they don't have they don't have an end to their dna it just loops back together eukaryotes remember we have linear dna so the ends of our dna are exposed so remember like during mitosis the nuclear envelope breaks down meaning that now our dna is exposed to other parts of the cell so a lot of the time it will get damaged by bumping into things or by other chemicals reacting to it so that's not good because that can cause mutations and it can cause cancer but we have some things called telomeres on the ends of our chromosomes that are just repeating segments of dna i think it's like six nucleotides just repeating over and over and over they don't code for anything but because they don't code for anything it doesn't matter if they get locked off or they get damaged it protects what is inside the are inside the chromosome here so the good stuff now telomerase is the enzyme that puts telomeres on the chromosomes but it's not active in every cell telomerase is only active in stem cells um stem cells there's another cell but cancer is um typically activates telomerase so that's why cancer cells can grow rapidly and not get damaged over time um so stem cells your adult stem cells and then like embryonic stem cells are where telomerase is active um adult stem cells can be found like in your bone marrow um and then germ cells but so every other cell in your body doesn't have an active telomerase so as these telomeres get lopped off at the end and our chromosomes start to shorten what ends up happening is that our dna will get damaged and that causes aging so if we find a way to activate telomerase in all of our body cells we might become immortal um but that might not be a good thing because um cancer could and those cancer cells will never die because their telomeres are never getting getting shortened so something to think about for the future so telomerase is kind of that immortal enzyme but um not always a good idea to activate it okay so i think that kind of sums up eukaryote versus prokaryote replication you don't need to know the differences like we didn't even talk about these enzymes here so it doesn't i'm not going to quiz you on those we're just interested in dna polymerase 1 and polymerase 3 which we've talked about already how mistakes during dna replication um dna replication does create mistakes but there are some ways to correct those mistakes um dna polymerase is one of those major correctors let's talk about that one first so remember dna polymerase is the enzyme that reads the old strand and makes a complementary new strand by adding bases to the three prime end of the new strand it not only does it add new bases to the new strand but it also corrects errors so it proof reads what it what it's done it proofreads the bases that it added here and then it will correct it so you can see already these go together these go together these go together but there's already some errors here right so it's going to correct those errors and then um hopefully the new strand will be okay but if the new strand still has mistakes in it there are some other ways that those mistakes will be corrected still so dna polymerase is kind of the first line of defense between or first line of defense for correcting mistakes i can spell okay so dna polymerase this is polymerase three is the first one dna polymerase two we're sorry dna polymerase yeah dna polymerase 2 is another one that will help correct um help correct mistakes but that happens down the line hopefully we don't get to the point where dna polymerase 2 needs to be activated um dna polymerase one will also help correct mistakes oh i only put one and two up here dna polymerase one two and three dna polymerase one remember one helps with um removing rna primers with dna so as dna polymerase one is removing those rna primers it's going to double check that the base pairing is correct okay so another mechanism that can happen is mismatch repair mismatch repair happens after the strands have been created and you can see here that mismatch repair will correct a base pairing so a lot of the time when we get mistakes what happens is we get like a bulge or like a divot in our dna so remember we have um four four bases overall which are purines and then there's pyrimidines purines are the big ones and those are adenine and guanine and then um here pyrimidines are thymine and cytosine so um first if there are like two purines that match up like if a and g were here let's just make this an a for right now if that were an a there would be a giant bulge in the dna strand and that's going to cause this match repair to come in and correct it um so but you can see here that there's an a and t or it's an a a t and a g so that t and g they don't normally match up um they're going to kind of be distorted because the hydrogen bonding isn't working correctly and so that'll create a bulge in dna as well and then this mesh repair will come in so when we have a mismatch like in this case a and g or g and t it creates a bulge or it creates a divot in dna and then mismatch repair will see that quotation marks c and that bulger did it and it'll correct what uh whatever's gone wrong so hopefully the mismatch repair will correctly place the correct space in there so it replace that t with the c and if you look on this strand c c g it should have been a c right right here so that's correct um and then you can also see it up here too but sometimes mismatch repair does not put the right space in so let's say instead of instead of a replacing the t with a c let's say it replaced the um let's see we had t so let's see if they replaced it with an a so that's going to create probably a new protein um or maybe it doesn't create a new protein or it just creates a new amino acid um which could cause mutations could cause problems so hopefully mismatch repair does it correctly where it replaces the the t with the c in this case but sometimes that doesn't happen and it's the opposite basically it's replaced which causes mutation um there's another thing called nucleotide excision and nucleotide excision helps to repair what's called a thymine dimer i mean dimer so thymine sometimes reacts and bonds with itself in dna um and that creates you can see like a weird bulge in dna strand and that could um that could stop dna polymerase 3 from copying the strand correctly so dna nucleotide excision removes that weird bonding so that it lays flat again so there's a um if you want to look in the textbook there's a gross picture in the textbook i'm showing you the skin lesions that could happen when there's a lot of timing dimers in your dna um and it's finding dimers can happen when you're usually like exposed to uv light so if you have sunburn over and over and over again your dna reacts to that uv light and you get these dimers like on mutation types and that creates like these lesions on your skin um pictures in the textbook if you want to look at it but i saved you that i'm not putting it in the powerpoint but it's kind of um so uv light is the biggest cause of those dimers okay so let's see we already talked about telomerase and telomeres but just to show you visually what a telomere is it is um over here so that's bone marrow so here is a telomere so g g t t a g and you can see g t a d so it's just a six pair or six base pair um just repeating over and over and over it doesn't code for anything so if it gets locked off no big deal but eventually enough of it gets locked off but it starts damaging dna which causes aging okay so usually when a cell runs out of telomeres it starts to die causes aging as well um so back in 2009 is uh is when we actually figured out what telomeres a what telomerase does but not too long ago there and we're still making these crazy um scientific discoveries okay so oh we've already gotten the mutation cool so let me show you i'm gonna do a full question really quick before we move on there's that so the question is a scientist randomly mutates the dna of a bacterium we did it on purpose she then sequences the bacterium's daughter cells and finds that the daughters have errors in their replicated dna so the parent bacterium likely experience the mutation in what enzyme okay so most of you said b or d so b or d would be correct um b well i would say d would be more so the correct answer um dna polymerase one is the enzyme that's replacing those um rna primers right after dna polymerase three comes through so i guess if we're talking about like the sequence of dna fast checking um it would be dna polymerase 3 followed by dna polymerase 1 and then dna polymerase 2. dna polymerase one would have caused a lot of those errors if it if we were just picking from those those choices all right cool let's see let's get back to powerpoint okay so mutations we already talked a little bit about mutations in dna so a lot of the mutations are point mutations meaning that there's just one base that incorrectly copied through dna replication sometimes there's um more than one base that inserted or deleted which causes the frame shift so let's talk about point mutations first um point mutations um can be silent they could be missense they could be nonsense um silent point mutations like a substitution so let me see i'm gonna type where it was a and we accidentally put a t in there um a substitution really doesn't cause or this this kind of substitution didn't cause any damage so it is still coded for the same protein um a miscent point mutation would cause a change a nonsense mutation would cause the protein to get cut off so point mutations or like a substitution in this case are the most common uh most common errors in dna replication and substitutions have caused most of the changes in population over time um let's see trying to think of one so cystic fibrosis is caused by a substitution so just one base pair is off which causes the disorder cystic fibrosis um so substitutions are very common um i think i want to say insulin um if you were if you have type 1 diabetes i want to say that insulin gene is also also substituted or a wrong base pair substituted which causes defects in the insulin gene i want to say that's correct but don't quote me on that but definitely cystic fibrosis um so most common in the population causes the most changes over time there are some things like frame shift which causes a change in every protein or every um amino acid down the line from it so those are usually caused by like an insertion or a deletion insertion or a deletion so we deleted t and a from this first one so those uh every base pair after that moved over two spots which causes the frame shift mutation in a frame a reading frame is typically three nucleotides long so if we delete two of them that's going to change our um reading frame right so typically frame shift mutations are really really bad and that causes a huge change in the resulting protein which might cause like death of that cell or death of that i guess fetus in case of replication or um case of reproduction so frameshift is the most deleterious um but if we have a frame shift of three nucleotides it would not be so bad i don't think i have a picture of that but i guess if we deleted um g t and a it really wouldn't cause too much of an issue because we don't we're only missing one amino acid probably won't cause too much on too much of a change but um yeah i think you get the point okay let's go on here these are all the different types of mutations that we could have we're going to look further at these next week when we talk about how we get protein from dna sequences um but first we're going to look at some dna sequences and i want you to tell me what types of mutations we have so i'm going to write them at the top here we could have substitution we could have insertion we could have deletion um substitution and search and deletion yep those are the only ones um i don't think i put anything else in there no okay so if we if we're looking at our normal dna this is the sequence that it has the a t c a t c t a a g g t a so let's say our dna gets mutated and after the mutation it looks like that so what type of mutation would this be or what um yeah so it would be substitution so and it happened right here at g so instead of cct it was cgt which could cause a new amino acid in that case but that doesn't change the other amino acids right okay so let's look at the next one mutation two where is the mutation and what is it yes so we had an insertion insertion good job and maybe you could point it out because there's an extra one here at the end so where was that insertion right here again right so we put a g in instead of the substitution like we had earlier so that causes a frame shift right so now every amino acid after that point we had aag now we have t a a which probably codes for another amino acid and the same thing we had gta now we have gt okay so last one is what yeah deletion so we're missing one here so that's a big giveaway deletion where was it let's see right here it should have been an a right yeah so there was there should have been an a and now if you look there's a frame ship you know while the amino now the um the frames have changed the amino acids probably change okay cool i think that kind of sums it up there is a really nice um ted talk that goes over um like neanderthal dna and how we can look at the anderson genome and compare it to ours and we can see like what mutations have happened over time since these men ruled the earth and now we're here um so there's a really cool video that goes over that if you want something about genetics um but you don't have to totally up to you um all right so that is all i have for you today