and we are going over um cell communication and the cell cycle so if you're taking AP Bio um you're in the right spot so uh I call my students AP biop penguins and I call all y'all AP biop Penguins why because you're dressed for Success so the fact that you're sitting in this live stream right now means that you are ready to be successful you're ready to rock the AP exam you are ready to to do this thing um so in case you don't know I have a ton of different resources that are available on my website um um so just wanted to give you quick review just for anybody who's joining us that isn't already aware of the stuff I have Daily Review that I started on February 1st on my Instagram story so every day Monday through Friday um I go live oh not go live sorry I post every night um questions and then every couple weekends I'll do a live stream like I'm doing with this one um I have a 374 page review guide that I have posted also on the webly where I go through each of the CED topics um with ien statements and I ask topic questions to try to help you to to better understand the information um as well as there are built-in multiple choice and free response questions divided up based on the unit so it kind of gives you a little bit of background there um and then I have explanations for all those multiple choice questions um I do frq Fridays I'm going to put those in air quotes because they're not really ever done on Friday um but I do have a bunch of f frq videos my goal is to get through all of the um fq from 201 13 to 2023 and have them all post as little videos for you um so I'm only three and a half weekends away from that but I'm almost done with all it um there's also 120 plus quizzes games that you have available for you that you can use to review as like quick little games um as well as there's review Powerpoints and there's tons of other things all available on that website so uh ww. apop penguin. we.com or honestly you could just Google AP biop penguins and it'll probably be one of the first hits so today's plan we're going to go over cell communication um the cell cycle we're going to do a couple practice questions um and then I just have uh a way that you can just do Q if there's any questions that you might be having um I am running this you know solo so if you have questions um as we go you're welcome to put them into the chat um and I'll answer them as I go but there is a slight little bit of lag I think it's about 30 seconds to a minute um between when I say it and you hear it um so sometimes I've moved on to the next slide so if y'all want to help each other out in the chat you're welcome to kind of answer each other if I don't get around to the question fast enough um and also I can you know double back and answer some of those questions as they come up so quick cell communication is the big bulk of unit four um but cell communication is a very broad topic so what we'll go over is the different specifics that we can for it but what you're going to see on the exam is going to be something you probably have never seen before um but you're going to be know you'll know the the different components of cell communication to be able to apply it to whatever pathway they put on the exam for you um so there's three different steps to um cellular communication the signal transaction pathway um the first one is reception reception is going to be when we have a signaling molecule which we call the LI it is going to bind to a receptor and when it binds the receptor the receptor is a protein and we know that anytime you bind something to a protein it always changes shape and so we're going to go through a confirmational shape change and so some different examples of receptors out there we've got a g protein coupled receptor which is going to be of course it's a receptor um and it's going to work with a G protein it's going to activate the G protein by binding a GTP to it um and then that's going to then go onto some pathway which is part of the transduction of it you've also got um liated ion channels um which may have a receptor on them and the receptor is going to basically close that ION channel and when you bind let use my keys when you bind the Lian um to your receptor it causes that confirmational shape change so now the ions are going to be able to flow through that channel um we also have a tyrosine receptor chinase um tyrosine receptor chinise is going to be basically having two receptors they'll come to together and they form a dier hence the name dimer because d means two um and then there's going to be kinases so there's um going to add a bunch of phosphates to each of the tyrosines which are amino acids on them and that will then go on multiple U transaction Pathways so now we really need to look real fast at the lians of them so the liant can either be a steroid hormone so going back to our knowledge from unit one and knowing that steroids are non-polar we know that the receptor is going to be on the inside of the cell so it's going to be an intracellular receptor um so examples of that would be like testosterone or estrogen those are all uh steroid hormones um and the way that it comes out of the cell is just by simple diffusion it can go straight across that membrane as well as it can go straight across that membrane to come into the cell my students did a free response question this past week um on estrogen and on antibodies yes I know antibodies aren't part of the curriculum um but antibodies where they had to explain why an antibody couldn't bind to receptor for the estrogen receptor um and so the answer really came down to the fact that the steroid could get through the membrane but that antibody which is a protein is unable to um so we can also have a protein hormone which as I just mentioned um is going to must have a extracellular receptor receptor must be on that cell membrane um because a protein is unable to get through that membrane by any type of simple diffusion it's going to have to be released by exocytosis so if you remember exocytosis we had the little uh plas sorry our transport vesicle moves to plasma membrane and it kind of like opened up to that plasma membrane releasing out the contents um so that's how we release any of our uh protein hormones an example of one of those would be like insulin and so insulin if you know is going to help to uh bring your blood glucose level down the way that it works is that it binds to a receptor on the membrane um which then leads to um your body cells to take up that glucose um so it can be used for uh glycolysis so after we go through reception we have transduction transduction is kind of basically the point between when it starts to when it ends so it's everything in the middle so if you think about like dominoes it's the point where all the dominoes are falling um and so this is just a Cascade it's relaying those signals is relaying the message the actual signaling molecule does not move through transaction um but the actual message will move through um through a series of uh different um my mind's C going blank I'm so sorry U so we have all these different molecules on the inside that are going to help to to relay it in um and so that will help to amplify that signal as well as it's going to help to kind of modify in a way so we'll see a little bit of interaction that might be taking place in that Cascade so there's two main ways that we see the Cascade number one or sorry receive the transaction one is a phosphorilation Cascade and by the name you know phosphorilation there's something getting phosphorated something's going to get a phosphate molecule added to it and so as I mentioned before chinise it's going to have a protein kise in there and the protein can's job is going to be phosphor a protein okay um and so it's going to phosphorate these relay molecules these relay proteins um that are allowing us to move through that transduction another one we can have is secondary Messengers secondary Messengers their job is going to be be small little molecules inside the cytool that will move from one place to the other that will then continue the Cascade so have two different ones we've got calcium and then we've got cyclicamp so calcium is traditionally going to be stored in your smooth the are and so if we were to think about I don't know muscle contraction in muscle contraction there's going to be that uh transaction um it's done as a Electric electrical signal um and that is then going to move an ion gated channel to open that channel is going to be on the membrane of the Smoothie R and so as the um calcium is removed from the Smoothie R which we call cyop plasic reticulum the calcium will then bind to this tronin tropomyosin and all this stuff inside of your uh muscle to allow for that contraction so the actin B mein and all the stuff that you don't really need to worry about too much okay um cyclic is literally CYCC adenosine monophosphate um so there's aen cyclas which is a enzyme aen cyclas is going to convert ATP in cyclicamp so the cyclicamp will then move throughout the cytool to lead to a protein kinase to be activated that then goes to a phosphation Cascade um so as I said this is very vague um you're going to be given some type of diagram and that diagram will allow you to know which pathway you're going to be following um and kind of you're going to be interpreting the pathway and then the final thing the third step is going to be response this is what's going to happen because of it um and so give me a second I'm going to move my camera because I know that um it covers up and for some reason I can't find my camera I guess I can't move my camera sorry y' um so what we're gonna see with the response is that we're going to see uh that the cell can grow one of the things that can happen is the cell grows um another thing that can happen is that that we can secrete different molecules we can see that different components will be um released or they'll be secreted um we also see that it can modify gene expression so turning on a gene turning off a gene um and making it so that it works that way um and then we can also alter the cell function or the phenotype and then last but not least it leads to apoptosis so I do see a question is a receptor an enzyme um sometimes receptors can be enzymes sometimes they're just straight up just proteins um so it all depends depends on which one it is so for example the tyrosine receptor kinas that one is an enzyme because it's going to be phosphor but like the G protein coupled receptor is just a protein that binds to a g protein and through that process activates the G protein um so cylic is similar to ATP the difference between cyclic and ATP um is that ATP has three phosphates and cyclic has one phosphate and it's also got like a an extra Bond on it that makes it kind of cyclic in in structure um talk about AC potentials action potentials are not currently in this thing um okay so here we have Sellar communication so this was the diagram that was on the 2013 exam um and they asked you to tell us what the three steps were and what their functions were so Step One is reception I see that I have the signaling molecule which I know is going to be a protein hormone it's going to bind to my receptor on the plasma membrane I know that it's protein hormone because the fact that it's binding to a cell um membrane surface receptor okay that b finding then cause a confirmational shape change that induces my transaction which is step two step two is transaction this is where we're going to see that Cascade that will induce the signal from one relay molecule to the next relay molecule through these various shape changes so as things bind to those proteins those proteins of course change shape and that changing of shape then leads to the message being sent to the next one okay and then based on this diagram I can see that I must be having some type of um response being uh gene expression so um it's going to act as a trans description factor and it's going to turn on a gene or it could inhibit a gene um so what we're seeing is that this protein is now interacting with DNA to turn on or turn off that Gene and so that would be those three steps that I would see in that signal transduction or in that cell communication so now I wanted to show you two other more recent examples that we see with cell communication so this is the 2021 exam number one um and this is just one component of it um and so they gave you this diagram and they asked you a couple questions just about the experiment first um but then they asked you about that there's this experiment the scientist added an inhibitor for uh PCH so this thing right here we're going to have an inhibitor of it um exposed to these certain cells So based on the figure this figure predict the change in relative ratio of irk to perk in the Oban treated PKD cells now you don't really need to worry about what PKD is but it's a certain type of disease kidney cells um and so compared to those ones that were treated without the inhibitor and then I need to provide reasoning so what I see here is that I don't have this enzyme this thing that was going to speed up the reaction between irk to perk okay and as we already mentioned it's a phosphorilation Cascade right so what I'm assuming is going to happen is this is part of that phosphorilation Cascade and so since I don't have PCH I'm not going to see irk getting phosphorated to perk um and so the ratio of relative of irk to perk is going to be that there's a low am I'm sorry a high amount of irk and a low amount of perk so my ratio is going to increase um and then the reasoning being because of the fact that that PCH is unable to allow for the phosphorilation of irk to perk um and then so that will lead to a buildup of irk because I'm not making the perk so option one that they said was that the ratio of irk to perk will increase um another option you could have put here was that the ratio would stay the same um just between the two uh different things okay um and then based on those options your justification would diff so you could have said for option one um that the perk is is not going to increase as it does without the inhibitor the irk will not decrease as it does without the inhibitor the cell will continue to synthesize irk and so since we keep making the irk and we're not able to convert to perk then we're going to see the increase of the amount of irk um the phosphorated irk is not being def phosphorated into irk okay so what they're saying is that that kind of goes backwards um so there were the different ones for 2021 so 2018 was again another signal transduction pathway that we see here um yeah the response is always going to be some type of molecular the response um one molecule is going to cause the response to take place so we could see apoptosis we could see um the gene expression we could see because that gene expression a changing in the the function of your cell or a changing in the phenotype of your cell it could lead to apoptosis to get rid of a certain cell so there's all those different uh things that can happen because of the the response um okay so here we've get we have this pathway and the big thing about it is it's talking about bacterial infections don't worry too much okay but they're saying that we have this inactive cast Bas one okay um and that it gets cleaved into active cast Bas one that is then going to come over here and it's going to cleave this little thing right here on the gastrodin which allows it to go into the membrane um and then it also is going to activate the interlukin that will then also be released okay um and so with this I'll answer your question just a second with this we see they they want to know what's going to happen if you inhibited step three okay so in terms of the formation of these pores and the release of the inter Lucan if I inhibit this step here what would happen Okay because that's one of the standards it says asking about if you if you mess up the singal transaction if there's an inhibitor somewhere what would happen and so thinking about that I'm not going to be able to convert gastrodin into this end terminal gastr so I'm not going to be able to create that pore so my first thing I'm going to say is that the pores would not form so pores will not form because of the fact that this gastro German cannot be converted into the end terminal gastr okay the second thing is does step three three have anything to do with step two well no these are two different paths that I see where active C Bas is going to go to both of them so there'll be no difference in the amount of releasing of the active interlukin because this step step three has no effect on step two um and so interlan release will not be affected or the interlukin release will continue um so someone in the chat says how do you distinguish between a paracrine and a synaptic signaling um paracrine is going to be a nearby cell synaptic signaling is specific signaling that you're going to see in a um a neuron so between a neuron to the muscle or a neuron to another neuron or a neuron to an endocrine gland that little space between the axon terminals of the neuron and the uh postoptic cell is going to be your synapse okay now the immune system I'm sorry the nervous system is not in the curriculum anymore it could be used as an illustrative example which is why I mentioned the I'm not talking about action potential um also we can talk about that later uh but so what we see is in that space so that'd be like a kind of a type of paracrine signaling but it's specific to neurons so I don't really like I think if you saw the picture of it you would see a picture of like one cell and another cell for paracrine and then in terms of synaptic you would they would probably tell you it's a synapse um but you would have the long axon and then you would have the next cell nearby um I hope that ansed your question so on to the cell cycle so the cell cycle is of course mitosis and how the the cell can go like basically the life of one cell okay and so there's a couple different steps to it we've got interphase which is made up of G1 s and G2 and then we also have the mitotic phase which is going to be made up of mitosis as well as cyto canis okay um and so the mitotic phase has those two parts of it okay so in interface as I said before there's three steps G1 s and G2 yes sying is a type of parac is a type of par signaling um G1 s and G2 okay now the cell is going to grow through all these traditionally when we talk about we say that the cell is growing in G1 and G2 but the cell technically is growing through all three phases okay so G1 is our Gap one okay this is where we're going to see a duplication of our organel the organel are going to duplicate I make a copy of those organel um and then this is also when I'm going to synthesize the different proteins that are going to be needed for the new cell as well as the signal transduction and the the communication is going to take place in this okay we also make the RNA as well as of different building blocks s is the important part for replication so for me I actually teach my students replication as we're learning about the cell cycle but that's not actually until unit six so I'm going to keep that in unit six for the reviews um but this is where we're going to make a copy of the DNA into the S phas okay so replication of genetic material and the centrosomes um so the parts that are organizing the uh genetic material okay and then we have our G2 which again cell is growing it's called Gap 2 this is where we synthesize proteins RNA we continue to make those organel and then we reorganize the cellular components okay now notice that that takes up a large chunk of it so here this whole thing is our cell cycle G1 s and G2 is a very large part of the cell cycle um g0 is going to be a non-dividing state um we don't really talk about g0 right now um but g0 is when it's exiting the cell cycle and the cell is just being um so cell cycle is really just talking about the when the cell is made to when the cell divides that's just what the cell cycle is so if it's in Z it's exited the cell cycle and the cell is just chilling um so like your neurons are just chilling your muscle cells are just chilling um your liver cell is also in g0 um but it based on environmental stimulus can exit g0 and start growing again um okay so after interface we've got mitosis okay now I have a funny little dance my students laugh at me and it's okay if you want to laugh at me too um and so what we have is we've got prophase metaphase anaphase telophase and then afterward after mitosis we go through cinis okay so that would be prophase metaphase anaphase telophase sesis yeah whatever it's okay um we've also modified that throughout the years and we've done like um adding in you know we've got G G1 then we go through S G2 and then we add in the prophase metaphase anaphase cophase cyesis so we can have the full cell cycle but you know if you're just randomly dancing at your desk or in AP exam someone's just going to think you're weird it's okay no worries I won't laugh yeah no just kidding you're going to laugh at me right now it's fine um anyway so prophase is going to be when the cell is preparing to divide so this is when we're going to see our um chromatids are going to condense um so at this point we have sister chromatids they have now are they're going to condense down and they're going to find their pair okay um and they're going to use cohesive molecules to attach their um Cent mirors together so they're attached in the middle and they make kind of that little little shape okay um we also see that our nuclear envelope is going to kind of disintegrate it's going away and then we see that our centrosomes are kind of organizing micr trules and they're going to kind of come out to attach to these different um sorry chromites okay so in metaphase this is when we see that our sister chromates align on the metaphase plate now notice I'm not saying they I'm not saying it I'm being very specific the sister chromatids align on the metaphase plate when you're writing an F frq question you want to make sure to be careful that you do not mention any pronouns okay you want to talk about things what they are I'm talking about the sister chromis because if you say they the readers might not know what you're talking about so cister chromist align on the metaphase plate metaphase plate is literally in the middle of the cell and you'll notice that they have these little microtubules attached to them okay it's due to a tug of war that tug of war is going to go back and forth making sure that they line up in that middle um so that once we have the appropriate enzyme that separates them separates um we go into anaphase okay and anaphase is going to allow for those sister chroma to be pulled apart to opposite sides okay um and so what's happening is that there that cohesion molecule is being broken by the separas enzyme um and so it separates them two and so since each one is attached to micral they're being pulled to those opposite poles so I can equally divide the cell okay so that's anaphase where they're pulled apart and the reason why I make my hand like that is kind of because it makes that shape right here so I can kind of remember the shape that I would see in case I happen to see it on the exam um and then last but not least I have telophase or tase depending on who you want to talk to um and this is when I'm going to make my two new nuclei so the nuclear envelope is going to surround my two cells um or my two nuclei um and so that's going to then allow for my chromatid who's now chromosomes um to decondense and they kind of become a little ball again um and so now a cell can go through telophase without going through cyesis if it does that it just has multiple nuclei okay um and so after telophase we go into cyto canis cyto canis is going to be the cytoplasmic division so this is how we'll separate our cells um so in animal cells it's just going to be looking at the the cleavage Furrow from the actin ring so there's this ring of actin that gets smaller and smaller and smaller and smaller until you know finally they're two different cells um and then in our plant cell we're going to release these little vesicles and that will build the cell plate which then forms the cell wall so that was our cell cycle but now we have to talk about how things are regulated in this okay so there are checkpoints in there there's things that kind of make sure that everything goes according to plan so I have a G1 checkpoint the G1 checkpoint job is hey should I be dividing so should I actually go through this process and divide okay um so it's due to some type of potentially a growth factor there'll be a signal that a paracrine signal that's going to bind um that will bind a receptor that then sends the signal that says hey we should be dividing is there enough res reserves is there enough resources for the cell to divide um and there Al going to check for d uh damage as I said if it doesn't pass this checkpoint it's going to um go into this non-dividing state so there a type of cycling um that will become activated and it will go through this big phosphorilation Cascade and if it goes through that Cascade then the SAS will begin and that's when we start going through that DNA replication so big picture of G1 is is the cell going to divide if it can get through the G1 checkpoint then that means the cell's probably going to divide so the G2 checkpoint is going to be at the end of inner phase okay number one did my DNA replicate correctly like do I have all the DNA replicated and is there any major errors in it okay so the logically the cell doesn't want to divide number one if it doesn't have all the DNA replicated because then it's not going to be equally dividing um as well as we want to make sure that there's no big errors in it because of the fact that we need to make sure that those errors can be corrected um it's a an enzyme it's just working it's it's going to make errors it happens um and so if if it detects a problem with the DNA that cell cycle will be halted so that we can repair the DNA um and then finish completing that DNA replication this is usually where we see like p-53 coming in to like stop the the gene from uh doing all that um yeah Ana gen and CH suppressor genes we'll talk about those I believe in another section I feel like but maybe not um I'll talk about them just in case um enco jeens are our normal genes um so these are normal cell division genes um and their job is just to make the normal proteins for cell division um if a enkco gene becomes um mutated um then it can be um like hyperactive so the RAS protein is an example of this um where our Ras protein makes the the normal division saying hey time to dive um but it can get hyperactive where it just keeps sending the signal even if there isn't a u a growth factor there and that causes the cell to excessively divide when it should to be dividing um a tunmer suppressor Gene's job is to Halt cell cycles so p-53 is an example of a tumor suppressor Gene as job is to hold so if you have an error in your p-53 p53 isn't going to stop the cell from dividing when there is errors and so your cell divides when there's errors in DNA which then leads to of course cancer right so here we talked about the G2 we were looking at damage p53 coming in so it forms the cdk inhibitor um and the cdk inhibitor then of course is going to stop the cell cycle from going into this so um in case you don't know a cdk is a cycling dependent kise um and so it's a kise something phosphor that uses cycl to do that okay um and so what we'll see here is that it's going to inhibit that enzyme um and then the M checkpoint is going to be during metaphase and the job for it is to make sure that all those cister chromatin are actually attached to microt trules because if they're not attached to microtubule I should not go through metaphase and I shouldn't um I'm sorry I shouldn't go through anaphase and I shouldn't let those two cells divide because I won't make equal numbers of the chromosomes with the in those cells um and so here we can see um that we're ensuring that those are together that Co cohes and holes the chromatids um separates is then going to break them which allows them to separate and be moving to opposite cells so we are a little bit ahead of schedule but that's okay um so multichoice we've got two mul choice questions and then we've got one long F frq to talk about so mul Choice insulin is a protein hormone So based on the fact that we know it's a protein hormone we know that that means it cannot get through the plasma membrane and it's going to have a receptor on the cell like on the membrane okay cool this is secreted in response to elated blood glucose levels when insulin binds to its receptors on the liver cells the activated receptors are going to stimulate a phosphation Cascade that causes the translocation of glucose Transporters to plasma membrane so what this is telling me is that the receptor is going to be on the membrane I have a phosphation Cascade which is part of transduction and then the response is that glucose Transporters are removed to the membrane and so you can can make those little notes as you went through this or as you kind of look through the question you kind of pick these different parts out so based on the information which one best describes the role of insulin in this liver cell so why did I need insulin well insulin was my protein hormone that bound so that must mean that it is a ligant okay it is a signaling molecule is the thing that binds it's not the receptor because the receptor is sitting on the membrane also tells me the insulin binds the receptor so I can immedately tell that that is not correct CU insulin can't be the receptor if it's binding to the receptor it's not a secondary messenger because we're not even looking at secondary Messengers here and it occurred before transduction transduction most that phosphation cascap and I know that it's not acting as a protein Chase because again it's binding on the to receptor on the cell and and so it's not even in that phosphorilation Cascade to be able to um be responsible for phosphor something okay so hope that was helpful now we have the endocrine system incorporates feedback mechanisms that maintain homeostasis which of the following demonstrates negative feedack back by the endocrine system so I put this here because I wanted to talk about feedback real fast feedback has to do with that there's two different ones we've got negative feedback and positive feedback negative feedbacks job is to regulate is to bring us back to homeostasis it's to kind of if there's too much of something bring it back down um is to kind of help to maintain that homeostasis versus a positive feedback is going to build up um and so the product is going to cause the pathway to continue which will then keep building up the response until finally something happens okay so the options I have is during labor a fetus exerts pressure on the uterine walls inducing the production of oxytocin which stimulates the uterine wall contraction contractions cause the Fus to Pur further on the wall increasing production of oxytocin so here you see we've got a buildup right uterus um I'm sorry the fetus is pushing on the uterine wall so there's oxytocin oxytocin then causes more pushing so we see that um there's now an increase in production that is positive feedback okay so after a meal the blood glucose level becomes elevated so I've got a too much glucose beta cells of pancreas release the insulin into the blood excess glucose is then converted into glycogen in liver reducing blood glucose level so it was too high and now it comes down which that is actually my answer but let's keep looking at high elevation atmospheric oxygen is more scarce okay so there's not a lot of oxygen in response to signal that the oxygen is low the brain decreases in individual's rate of respiration to compensate for the difference I don't have enough oxygen so I'm going to stop breathing as much that's not even logical a transcription Factor binds the respiratory Gene of a regulatory Gene of of a regulatory region of a gene blocking The Binding of another transcription Factor required for expression well if you have one thing blocking another that's not feedback at all that's just inhibition so the answer is of course B bringing us back down to homostasis okay so our long frq question we have the 2021 I'm sorry 2022 two number one um they talk about this whole big pathway talking about how there's a Lian binding GTP replaces GDP um it show basically it's talking about what we see in this picture right here okay so let's talk about what we see okay I see I have an extracellular Lian I see that binding to this uh G protein coupled receptor I've got a receptor I've got this G protein it isn't active when that binds I see that the GDP is being replaced with GTP and now it's active so I can see that Lian binding it causes the g g protein to become active once that g protein is active it looks like that it's it's activating the adental cyc see myal cycl was originally inactive now it's activated its job is to convert ATP into cyclicamp and then the cyclic is activating my protein kinas and then that protein kinas leads to a chlorine secretion by the cell okay so they're going to give you some type of diagram they're giving you this pathway and you've got to be able to figure out something from that okay um so they then talk about that there is this uh dehydration that causes when you get the bacterial toxin of Chala um because it's leading to that water to be released as we just saw they wanted to study the effects of that to color toxin are four different samples of intestinal cell membranes containing that g protein signal components as shown GTP was add to samples 2 and four col was added to three and four and the scientists then want to measure the amount of cyclic a produced by the denal cyclic in each of these steps okay so we're measuring how much cyclic a we have whether there is GTP add it or the color toxin at it and we're kind of seeing the differences in the amount of cyclic a because we're seeing that that um signal is being path the pathway is being activated so first step um and notice I'm putting this little I and I I I'm modeling it after the new way that they're doing the exam um where they're actually going to rent it up um where there is actually like there's a and it'll have a little bit of a prompt and then they're going to do one I and then they'll I I because they're going to separate all of the um task verbs so that you can ensure that you answer everything correctly okay so first thing is a is always about content okay so describe one characteristic of a membrane that requires a channel to be present for chloride ions to passively Across the membrane so chlorine ions are negatively charged okay now I know that this hits back to the previous unit but that's what we do in biology we keep building on this right um and so what we see here is that those chloride ions are negatively charged because they're negatively charged they are polar they're hydrophilic they're not going to easily pass through that membrane and so um why do I need a channel I need a channel because my plasma membrane is non-polar it has hydrophilic heads on the outside on the extracellular and intracellular sides and hydrophobic fatty acid tails in the interior of the membrane due to this the membrane is non-polar the membrane is hydrophobic and that's going to lead to this polar chlorine not being able to pass through so the interior of the membrane is non-polar the interior is not charged or the interior is hydrophobic any of those were valid options you could have put here and then 1 a II is explain why the movement of chloride ions out leads to water loss again that's a unit two topic think about this for a second chloride is a solute okay if solutes are moving out of your cell it makes the outside of the cell hypertonic because of the fact that it's hypertonic water is going to float out of your cell to try to make it equal okay it's going to move from the hypotonic cell to the hypertonic environment so the water rushes out of the cell to try to balance the fact that we've now got all these more these we have more ions outside so the space outside the cell because hyperonic or hyperosmotic compared with the cell so the water moves out of the cells you could also say the space outside of the cell is going to have a lower water potential compared to the cell so the water will then rush out of the cells or move out of those cells okay sorry so now we have to identify an independent variable in the experiment so your independent variable is what is the scientist is changing what did the scientists do that would be different that they're testing to see does it have an effect okay so here I can see that they changed the presence of GTP as well as they change to the presence of the cha see sometimes it's not there but sometimes it is there and they are seeing what happens in those presence so the presence or absence of color toxin the presence or absence of GTP and you had to say presence or absence because the fact that sometimes it was absent so you had to make sure that you were able to describe that it was there there or it wasn't there okay um so the second thing we have to identify a negative control the negative control is for us to see does the um independent variable have an effect so it's going to be whatever TS to without that independent variable okay so you can say sample one sample one doesn't have GTP nor does it have C okay so it' be the absence of both of these things that we are testing you could also mention the one uh that is L lacking col so samples one and three both lack um I'm sorry one and two one and two both lack that CH Toxin and so the fact that we could say we could look at samples one and two because they're both lacking the col you could talk about the ones that lack col but that they contain GTP which would be your sample two you could also talk about samples one and three and the fact that it lacks GTP because again if I um was looking at the gtp's presence then that I would pick the one that lacks it okay so there was a lot of options of things you could have put here on bii okay and then the third part of B says to ask uh us to justify why they included sample three as a control treatment in the experiment okay um so why was I able to have three as one of my controls okay well it has to do with the fact that it's got that col there okay it serves as a control so I can compare that cyclic production when I have the GTP present okay so I want to compare it with the sample that has the C Toxin and the GTP as well as just looking at when there is no GTP in just the cola so it allows me to see was the GTP essential for the experiment so what like so we can look at yes we're looking at Cha but does it need GTP in order for that CH toxin to inhibit the cyclic a or whatnot okay so part C based on the data describe the effect of the C toxin on the synthesis of cyclicamp so here I can see that I have no toxin but here I have toxin so if I compare one and three together I see that the amount of cyclic is not affected so call has no effect on um cyclic production in the absence of GTP because notice here that I do not have any GTP so in the absence of GTP col has no effect but if I was to look at instead samples two and four I can see that when GTP is present and I compare no col to CH there's a a significant increase in the amount of cyclicamp so chaoxin is going to increase cyclicamp in the presence of a a GTP okay so those were the two options you could have put and you had to mention about the presence or mention the absence of GTP that was required in your response um so make sure that whenever you're giving responses you give your full answer okay so then part C is asking us to calculate the percent change in the right of cyclic a production due to the presence of the cha toxin in Sample four compared to sample two okay so this is not on the formula sheet you did this math in many of your labs this year but you might not remember it and so I want to make sure that you do know that you need to know this formula this has shown up on multiple years of fair responses and it's never on the formula sheet nor do I give you the formula and students screw this up a lot so percent change is going to be your final minus your initial over your initial I'm seeing the difference divided by what it originally was okay so final minus initial over initial okay so what that means I'm going to compare two and four together CU it told me to look at two and four okay so I'll do 127 which was my final number minus 10 which was my initial number okay divided by 10 which was my initial number okay and that gives me 1,170 per. okay which your brain screams and says no that number is too big and then you have a mini freak out okay so trust yourself if you know your formula they might be giving you something like this where it's an excessive number to make sure you actually know how to do the math okay um and yes there were some interesting questions answers that year okay so a drug is designed to bind to the C toxin before it crosses the inter uh the intestinal cell membrane scientists mix the drug with C Toxin and then add this mixture GTP to a sample of intestinal cell membranes so we want to predict the rate of our cyclic amp in pea moles per milligrams of adal in cyclus per minute if the drug bits all the toxin okay so if this drug drug okay actually has a way to block okay what's going to happen well it's going to look just like this okay we're I don't have the toxin but I do have the GTP so they wanted a specific answer you had to give them the answer that the rate is going to be T I'm sorry 10 okay so now you see that this is in parenthesis because of the fact that the unit was given in the um the question you didn't have to restate the unit um but my brain always screams like give them you know give them the extra information just to be sure and so if it was me I would have still written the units on there um they gave them to you you can't screw that up but if you happen to have the units you were still fine on this one um and then the second part says in a separate experiment scientists engineered a mutant adental cyclas that cannot be activated okay so we cannot activate a denal cyclas it's just not going to happen okay they claim the car toxin will cause excessive water Lo will not cause excessive water loss from the intestinal cells um that contains that and they want you to justify the claim so they're telling you the answer they're telling you that water will not be secreted you now need to tell them why and you need to work through the entire path tell them every single step and why you're not going to see um that water be secreted okay so if I don't have a dycl then I don't have my cyclic being produced from the ATP because remember the job of the dental cycl was to convert ATP into cyclicamp so there's not going to be the cyclicamp and if I don't have the cyclic then I'm not going to activate protein cyas okay protein chinase won't be activated because of the fact that I don't have that cyclicamp and because the fact that there's no protein so I'm not activate my protein cyas then I'm not going to see that chlorine secretion and if I don't see the chlorine secretion then the water will not be released so you had to mention CYCC a not produce you had to mention protein kindnesses and then you had to mention that se the chlorine and how that would then lead to less water okay um no this wasn't a Kai Square um I'll probably see if I can work on putting a Ki square into uh unit 5 I don't know if there's one currently in there but I can work on making sure there's one in there um as well as when I'm done doing the uh FR frq Fridays that I'm building I'm going to go through every formula on the formula sheet and I'm going to make a Tik Tok for each formula so that y'all can have a good idea of how to approach those um if you're needing those math questions already um if you search math applications and Marco learning um then you will find the video that I did with Marco learning where I went through every single one of the formulas on the formula sheet with them in a a review session on YouTube um okay so Q&A what questions do we have um and I know that there's a lag and last time I didn't kill enough time so I'm trying to make sure that I kill enough time so at least the Q&A shows up on the screen and then I'll you know go from there um so somebody asked in the chat um do I know of any review books that have the new F frq format no I don't know any of them that have the new format um that new format was released to the readers um at the AP reading last year um and I don't know when it was globally released um I do know that um they posted it on AP Central like the other day when I went to check it out I did see it there um as well as um like I got news earlier this year and I made a Tik Tok about it I know that um but so are there any questions of about four I'm happy to answer them as we go um you know want to help you um so but in case you don't know AP biop Penguins on Instagram I'm posting you know Monday through Friday daily questions they're insta review um so they're designed is just like quick review questions um if you missed any of them so far they are all available as quizzes is games on my website so if you just go to the website and you do go to the drop down or use the clicking button on the navigation um to quizzes you'll see they're all they're called CED and they're just written out as the hey Miss Smith Clinton um they're written out as that um and then I've got the Tik Tok as well as I got YouTube but you're already here on YouTube so you know about my YouTube so do we have any questions I've killed about a minute and a half two minutes um I'm not seeing any questions coming in the chat um so that I hope that today was helpful um let me know on uh Instagram