hello bisque 130 this is the beginning of recorded lecture 32 uh continuing on with chapter 10 cell reproduction in the previous recorded lecture we had talked about the eukaryotic cell cycle and all these different proteins involved in regulating this cycle and pointed out that there are so many checkpoints involved here it's highly regulated cells are only supposed to divide when they need to divide and when they are able to divide correctly this is how things are supposed to work however nothing is perfect nothing ever works the way it's supposed to 100% of the time it is possible to get cells that are not properly regulated that divide when they are not supposed to divide this leads us to the next topic cancer so we could Define cancer as the uncontrolled cell growth which causes harm and it's it's not difficult to cause harm uh it's it's pretty easy for you know uncontrollably growing cells to cause harm to the nearby tissues nearby organs usually uncontrolled cell growth leads to to harm to the surrounding stuff so cancer this uncontrolled harmful cell growth is caused by failures of all the stuff that we talked talked about at the end of the previous recorded lecture cancer is caused by faulty cell cycle control proteins any of the proteins involved in these checkpoints these regulation mechanisms not doing what they are supposed to do so okay what causes these proteins to fail well we we know that proteins can become denatured through changes in PH and and temperature but actually every single one of these cell cycle control proteins there are many many many copies of these in any given cell you don't get disregulation by you know a few denatured proteins what causes bad cell cycle control proteins is mutations in the DNA sequence every single protein we talk about in this entire course comes from a gene it has to have a blueprint there's a gene for cycl a there's a gene for cdk to there's a gene for oh hey there's cycl a down here again just trying to pull out random things there there's a gene for ducks for there's a gene for all these things if the blueprint for cycl a gets screwed up every single cycl A protein that the cell makes is going to be screwed up so these faulty cell cycle control proteins are caused by mutations in their genes mutations in the DNA sequence okay let's continue down this what what causes mutations in the DNA sequence well uh mutations in the DNA sequence are caused by unrepaired DNA damage our damage is being our damage is being DNA our DNA is being damaged constantly by various things we'll talk more about mechanisms of this in a in a different chapter uh but we have ways to fix this damage if our DNA damage is not fix fixed that can lead to a mutation that can lead to these things not doing what they're supposed to do there are a couple of terms here Proto onco gen and enco gen you may recognize the prefix enco onco means cancer so a medical doctor specializing in cancer is an oncologist uh a a medical facility specialized for cancer cancer patients is an Oncology Clinic uh yeah enco enco means cancer so enco gen are uh genes that cause cancer let's see what are the key terms say an enog Gene is a mutated version of a normal Gene involved in the cell cycle can lead to cancer so these are the bad versions protooncogenes are the normal versions let me read the key terms definition a protooncogene is a normal Gene involved in the cell cycle that that when mutated becomes an enag gen so this unrepaired DNA damage leads to protooncogenes becoming anagen so we really don't want mutations which means we really don't want unrepaired DNA damage we can prevent cancer by making sure all of our damaged DNA is repaired properly and in fact mutations are prevented by things called tumor suppressor proteins or tumor suppressor genes again every protein has a gene every house has a blueprint so there are tumor suppressor genes that refers to the DNA that you know has the code for this uh there are also tumor suppressor proteins those are the proteins that come from these genes but either way these are both used tumor suppressor genes and tumor suppressor proteins prevent mutations how do they do that well let's look at one of these in particular this is yeah tumor suppressor genes proteins this is an incredibly important protein with a very humble name uh p53 lowercase p even p53 so what does p-53 do well here's a outline of this p53 looks for damage uh patrols the chromosomes looking for some sort of damage to the DNA if it detects damage it brings in DNA pair enzymes there are many of these for different types of damage that could fix this damage that's not all that p-53 does it also has a very important switch that it can it can pull one way or the other if this damage is repaired successfully p53 can give the green light on cell division and let everything go as normal however if this damage is too severe or there's too much of it or it it just cannot be fixed p-53 also has its finger on the self-destruct button and it can cause this cell if it has damaged DNA that you can't fix to destroy itself which should look familiar this is apotosis from the previous chapter so p-53 can trigger this if the damage is too severe so p53 locates damage to DNA brings in repair proteins to fix it if the repair is successful cell cycle proceeds if the damage is too severe apotosis and so uh yeah I I say my tests are not cumulative I I mentioned apotosis in the previous chapter uh which is part of the previous exam I'm bringing it up again here so I put it in the key terms again here uh apotosis uh programmed cell death so it sounds pretty good sounds like a pretty nice deal sounds like a pretty pretty effective protein uh if if you can you know destroy cells before they accumulate mutations then you'll never get mutations you'll never get uh enogen coming out of protooncogenes fantastic nothing is perfect this is what p-53 is supposed to do nothing works perfectly in a Cell it is possible for DNA damage to sort of slip past the notice to p-53 even with p-53 doing a fantastic job of all of this it is still possible to get a mutation in I don't know cycl A's gene or any of these other cell cycle regulation proteins it's still possible to get an enag Gene that by itself is actually not usually the end of the world uh there are so many of these proteins involved here there is a fair amount of redundancy in cell cycle regulation has having one Ena Gene is not usually enough to cause really aggressive deadly bad cancer uh but again this mutation could happen anywhere it could happen in cycl a it could happen in any of these other things the worst thing that could possibly happen is a mutation you know unrepaired DNA damage a mutation to slip past the notice of P 53 but that mutation is in the gene for p53 itself so if P 53's Gene becomes mutated and this can happen that means every single p53 protein that you build using those damaged instructions is not going to work properly it's not going to be able to bring in DNA repair enzymes it's not GNA be able to trigger apotosis as needed if p-53 goes down uh just the you know everything is Unleashed you get way more uh unrepaired DNA damage you get more mutations you get more enag genes again one enene is not usually enough to cause cancer you get one two 3 four five you get a whole bunch of anaes accumulating if p-53 is not doing its job correctly so if the p53 gene is mutated it no longer encodes a functional protein this allows cells with damaged DNA to divide willy-nilly uh leading to even more mutations and even more onag gen so again p-53 incredibly important protein but it's not immune to mutation uh here's an interesting statistic in about 50% of all cancer that have been genetically studied there's a mutation in p53 protein so there there are a few other tumor suppressor proteins and and genes uh out there uh p-53 is a really big one uh a lot of the time this just sort of starts the ball rolling uh towards the creation of cancer if the gene for p-53 is mutated so that's an example of a tumor suppressor protein what it's supposed to do and sort of the worst possible scenario of how we can get lots of enogen and how we can get a cancer cell okay that brings us to the end of chapter 10 uh we're going to within this same recorded lecture because that was kind of short so far start up on chapter 11 which is actually still about cell division it's just a slightly different type of cell division so this has to do with sexual reproduction so here's a slide from the very first day of class uh reproducing was something that all living things did this was an example of asexual reproduction but now we're going to focus on sexual reproduction so virtually all there are some exceptions but virtually all multicellular UK carots plants and animals are capable of sexual reproduction this is a big deal because sexual ual reproduction as we will see mixes things up asexual reproduction makes a clone of yourself you know binary fion the stuff we saw in the last chapter those made identical daughter cells the big picture point of what we're going to see in this chapter is not to make identical cells it's to have diverse Offspring it's to randomize things it's to mix things up diversity is very valuable in organisms because you don't know what the next year is going to bring what the next season is going to bring if you have lots of offspring that have lots of different combinations of attributes you're sort of hedging your bets and increasing the likelihood that one of those is going to have what it takes to survive whatever the world throws at him down the line so again this is sort of the big picture um sales pitch on on why all of this is needed why we can't just do asexual reproduction for everything sexual reproduction mixes things up creates diversity in Offspring and high diversity and Offspring increases likelihood of survival so what is sexual reproduction well let's let's break this down into the most exciting way possible uh mathematically so at the end of the day sexual reproduction is very simple sperm plus egg equals zygote um this is how it happens in animals this is how it happens in Plants uh yep one cell plus other cell equals this cell the zygote is this this cell here now something I a term that I introduced in the last chapter was the term diploid I told you that virtually all of our cells are diploid the abbreviation for this is 2 N that meant two copies of each chromosome and we we saw that in the slide on on human chromosomes two copies of each one of those so if our sperm are deployed 2 N and the egg is deployed 2 N uh 2 + 2 equal 4 that would make a zygote that is 4N four copies of each chromosome do do we do we double the chromosome number in our Offspring no we we don't actually do immediately cross this out we don't do this this is the reason why I said virtually all of our cells are deployed yes our skin cells are diploid or muscle cells are diploid or neurons are diploid the exception is the eggs and sperm these things are not deployed they are 1 n or hloy that's because we need to generate a zygote that's 2 N we need to make offspring that is diploid and the only way to add two numbers together and have it equal two because each of those numbers has to be one so sperm is haid these cells have one copy of each chromosome eggs are hloy they have one copy of each chromosome so that when they come together the zygote is diploid two copies of each chromosome now the tricky part is we need a way to make these haid cells everything we talked about in the last chapter mitosis is part of the overall UK car itic cell cycle that made identical copies of cells here we need to make haid cells no other cells in the body are haid we need a way to make haid eggs and haid sperm from diploid cells the way that we are going to do this is through a process called meiosis uh some people say meosis that's another ligand liand thing I I say meiosis but meosis is fine meiosis is the process that's going to create these haid cells and this is done by special germ cells so not everything is doing meiosis only germ cells within the testes or the ovaries are able to do this very special type of cell division so yeah here's a you know overview of the human uh sexual life cycle you get to zygote this single cell it's going to divide it's going to grow into an embryo a fetus a baby an adult all these cells are diploid then within the germ line we have meiosis to produce sperm or egg as the case may be one yeah these are haid the sperm is haid the egg is haid here's the 1 + 1 equal 2 fertilization we're back to diploid and it's you know back to the rest of this cycle so um meiosis is the process here and germ cells are the cells that do meiosis again not everything does this so if we want to talk about the process of meiosis I I talked about how much I like this particular figure in in the last chapter so I'm I'm actually just going to modify this so this was mitosis as part of an overall eukariotic cell cycle uh really we just cross these ones out and replace them with uh this so this is what happens specifically in eukariotic germ cells we have G1 s G2 and then we have meiosis one cyto canis meiosis 2 then another cyto Kinesis and so obviously this is going to be a two-step process it's not just one division it's two sets of Divisions two cyto kinisis uh this is going to result in four cells by the time we're done with this it's two rounds of cell division so we'll get some visuals on this soon enough but yeah I like modifying this familiar figure this is how it happens when a cell is doing meiosis when a germ cell is doing meiosis so all right eukaryotic germ cell cycle we got interphase not going to say anything more about that we talked about g1s and G2 in the last chapter I'm not going to rehash any of that again it's the same interface I talked about then copy and paste all that in all right next we have meos is 1 so meiosis 1 has the same PP matat that mitosis had so in in some ways this is convenient that it has so much in common with mitosis uh but in other ways it can sometimes be confusing because it has so much in common with mitosis uh I am going to do my best to highlight the similarities and the differences between the p P pmat of meiosis 1 and the pp matat of mitosis from the last chapter the way that we distinguish these in text is with the Roman numeral one so if we're talking about profase one that means we're talking about the prophase of meiosis one if you see Pro and so on on my multiple choice test questions you have to read these questions carefully I'm not trying to trick anyone ever uh I just want you to read them carefully if the question says metaphase 1 it means I'm talking about the metaphase of meiosis one and you know spoilers for later on if I say metaphase 2 that means I'm going to be talking about the metaphase of meiosis 2 and if I just say metaphase flat with no additional Roman numerals that means I'm talking about the metaphase from the last chapter the metaphase of mitosis so again not trying to get confusing but the Roman numeral is how we distinguish these from mitosis so all right let's take a look at this process we got prophase uh Pro metaphase is not pictured here I think just to save space on this figure metaphase anaphase uh well I'm sorry prophase one metaphase 1 anaphase 1 tease one and then finally cyto Kinesis so let's start in on prophase one so prophase one we are going to have the chromosomes condense the nucleus GG and er breakdown okay this should sound familiar but I guess that's good uh prophase one is very similar to prophase from mitosis nucleus GG ER breakdown chromosomes condens you know so so far so good has a lot in common with mitosis we are going to see the chromosomes oh okay so this is actually a little different now that we look at it back in mitosis uh we had sister chromatids uh appearing at this point we had these two chromosomes partnered up but if we look closely at this that's not two that's that's four total chromosomes if we want to zoom in on this so we can get get a better look at this yeah it's one 2 three four four total chromosomes paired up together this structure of four is you know this is new to meiosis 1 this structure of four is called a tetrad uh and Tetra means four so you know there are four total chromosomes here this consists of two pairs of sister chromatids so yeah these two red ones here these are the sister chromatids the two blue ones back here these are sister chromatids so what are the red versus blue why are these different colors well they're labeled here the red versus blue uh are homologous chromosomes so okay let me let me write this down then I'll explain what homologous chromosomes are because this is a very important term we've got prophase one still we're going to form tetrads which the key terms define as two duplicated homologous chromosomes parentheses four chromatids and Tetra means four bound together during prophase 1 so this the stapor synapsis is the name of this process so synapsis occurs during prophase one and it leads to the formation of these tetrads so okay what are homologous chromosomes well homologous chromosomes are not identical cister chromatids are identical they're exactly the same homologous chromosomes have the same genes but their exact sequences are a little bit different this needs an analogy these are sister chairs these two chairs are exactly the same no differences at all just like these two sister chromatids they just went through DNA replication these are are exactly the same sister chairs are exactly the same sister chromatids are exactly the same homologous chairs are the same piece of furniture but they are not exactly the same these are both chairs they are the same thing they're the same type of thing but you know legs are connected in a slightly different way here the slats run vertical versus horizontal I think this one's maybe a little bit wider than this one they both do the same job they both fulfill the same function of you sit on this thing but they are obviously not exactly the same that's what homologous means they have the same genes they have the same basic structural foundations of four legs a seat and a back homologous chromosomes are the same type of thing but their exact sequences are a little bit different in these textbook figures that's what the red and the blue these different colors are always trying to to to make clear if it's the same color and the same size and they're together they're exactly the same sister chromatids sister chairs the red and blue is meant to show that there are differences here the red and the blue are homologous chromosomes the same genes but different exact sequences and again this is a good summary of what this is homologous chromosomes have the same genes as one another but the exact sequences are a little bit different so this tetrad has two sets of homologous chromosomes and their sister chromatids so two sets of sister chromatids four of these things total okay this I spent so much time on this because this is one of the most important things one of the most important differences between this and mitosis so why what was what was the purpose of doing this what was the purpose of forming this tetrad we didn't do it in mitosis why are we doing this we go through synapsis and we form these tetrads in order to be able to do something called crossover or you crossover there's another term for it I'm not going to use crossover is exactly what it sounds like it's when these homologous chromosomes swap a little bit of information with one another if we were looking at chairs I would rip off this front left leg swap it with this front left leg you're left with two still completely functional chairs uh but you know they've swapped a couple of parts with one another and the purpose of this is to make slightly different chromosomes you think about parents and offspring this chromosome um is coming from one parent this chromosome is coming from the other parent you're trying to make offspring of your own if you're doing crossover here's a slightly different chromosome it's not the same as any chromosome you have it's not the same as any of your parents chromosomes you're mixing things up you're increasing genetic variation and every time your body goes to make eggs or sperm it's doing this crossover in a slightly different way it's not always down here at this exact position so this again increases genetic variation the whole point of this is to not have the same Offspring twice to you know we're not having millions of Offspring but there are other organisms out there especially big trees that can make millions of sperm cells millions of egg cells and you you want to have as much variation as possible so this synapsis allows for crossover the purpose of crossover which I'm sorry I think I forgot to read the key definition of crossover the definition of crossover from the key terms is the exchange of genetic material between homologous chromatids resulting in chromosomes that incorporate genes from both parents uh allows for crossover and the point of this is to increase genetic variation okay all of this was happening during prophase 1 next we've got Pro metaphase 1 um this one's easy microtubules attach to the kinetic cores of these tetrads pretty similar to the last chapter uh microtubules attach but again it's tetrads they're attaching to not sister chromatids got this set of four here during Pro metaphase 1 okay after PR metaphase 1 comes metaphase one and uh yep very similar to last chapter everything's lining up in the middle but there's an important detail about this lining up in the middle so you know metaphase one yeah these tetrads all line up in the center of the cell but importantly it matters which way they are facing so back in mitosis metaphase it didn't matter whether this chromatid went to the left or whether this chromatid went to the left CU these two chromatids are exactly the same the two sides are going to get exactly the same stuff but here it does matter how they are facing we can we could picture you sorry this one's you know horizontal instead of of vertical this figure but we can imagine what's going to happen next they're going to get pulled apart from one another and it looks like the daughter cell up here is going to get red for this chromosome the daughter cell down here is going to get blue for these chromosomes so it it does matter which which way they they line up which way they are facing so how do we you know make sure that each daughter cell gets about the same amount of red and blue how do we ensure an equal distribution of these different these different homologues well the answer is we don't it's completely random which way they are facing so let's you know compare these chromosomes once once again two pieces of furniture so yeah you have two different chairs you have two different tables again these are all homologues you have two different nightstands you have two different chested drawers this is where I got bored of of uh you know Google image searching different Furnitures uh suffice it to say in a human with 23 different chromosomes this would be a pretty crowded room indeed but yeah these line up in such a way that you're going to make an egg or sperm cell with uh this chair this table this nightstand this chest the drawers and a different egg or sperm cell with this chair this table this nightstand this chest of drawers or you know you could do this with this combination of furniture and another cell with this combination of furniture or it could be this combination and this combination it's any of these are possible uh here is a a simple organism with only three chromosomes uh showing all the possible combinations you blue blue blue red red red or red red blue and blue blue red and blue blue red and you see what I mean eight possible combinations if there are three chromosomes I did the math for you in an organism like ourselves with 23 different chromosomes there are over 8 million possible combinations for how these homologues can be sorted that means you could go through the process of making egg or sperm as the case may be 8 million times and not make the same cell twice um the whole purpose of this is to increase genetic variation so in metaphase one these tetrads align at the center of the cell which way they're facing their orientation is random so different daughter cells will receive different homologues they're not going to be the same every time the purpose of this is to increase genetic variation okay that was PPM a t after metaphase 1 we come to anaphase 1 and uh yep the tetrads are pulled apart from one another uh importantly the sister chro chromatids Stay Together they'll get pulled apart in the next one uh but yeah the tetrad is is broken apart and the sister chromatids Stay Together pulled to opposite sides during anaphase one y tetr pull apart cister chromatids go to the same side okay and uh yep here if we want to zoom in on this this was PR metaphase where the microtubules attached and there is anaphase one where the sister chromatids sticking together but the tetrad is broken apart and uh finally Tila Phase 1 uh followed afterwards by cyto canis um it very similar last chapter til Phase 1 chromosomes decondense nucleus GOI ER are going to reform X2 and then cyto canis is going to pinch that cell uh into two so at this point we have finished meiosis one and the first of our two cyto kinesis the question is what kind of cells are these these daughter cells are these daughter cells hloy or diploid don't answer yet because this is a little tricky at first count you may look at this and say oh this daughter cell has one two chromosome one two one two this looks like a diploid cell technically diploid means you have two different things you have two different chairs you have two different nightstands you have two different tables this is our default cells we have two different versions of everything these cells here at the end of meiosis one in the first cyto Kinesis are not actually diploid these two chromosomes are the same a little bit of difference because they're crossover but these are the same chromosome these are the same chromosome these are the same chromosome these daughter cells are and this is an awkward phrase but it it is what it is these cells are hloy with replicated furniture oroy with replicated DNA so uh yeah this is not a diploid room this is a hloy room with replicated Furniture two of the same chair two of the same table two of the same nightstand and that's what these cells are at this point so after this first cyto canis we have two cells they are hloy with replicated DNA cells they're not diploid cells they don't have two different things they have two of the same thing haid with replicated DNA okay back to this we did meiosis one we did cyto canis now it's time for meiosis 2 importantly there is no interphase between meiosis 1 and meiosis 2 you don't have another cell growth you don't have another DNA replication you don't have another G2 after cyto canis you go to meiosis 2 so what happens in meiosis 2 well got another figure to show this so we got prophase 2 Pro metaphase 2 not pictured here here metaphase 2 anaphase 2 telophase 2 cyto canis all right so what's going on here well prophase 2 it looks like the ER GGI nucleus are breaking down the chromosomes are condensing uh becoming visibly distinct um this is exactly the same as it was in mitosis um Pro metaphase to again it's not pictured here but the microtubules attach to the sister chromatids no no tetrads here no crossover is happening here no synapsis here uh this prophase 2 again I'm sorry it's not pictured here is exactly the same as the the pro metaphase from the last chapter metaphase 2 sister chromatids line up in the center okay still no no tetrads no crossover these sister chromatids lining up exactly the same as it was in mitosis anaphase 2 the sister chromatids are pulled apart exactly like it was in mitosis and then Tila Phase 2 in cytokinesis chromosomes decondense nucleus ER Gogi all the same stuff from mitosis so although meiosis 1 had you know several important differences um comparing it to mitosis meiosis 2 it's actually the same every everything that I would write down about prophase 2 is exactly what I wrote down for prophase in the previous chapter everything for pro metaphase 2 is the same you can if you're making your own notes and you want to do this you can copy and paste this in if you want to I'm going to save us all some time and just say each one of these phases is the same as the phase uh from mitosis there are no notable differences between between uh prophase 2 PR metaphase 2 metaphase 2 anaphase 2 anaphase 2 and prophase prome metaphase metaphase anaphase tease exact same descriptions I gave in the last chapter so by the time we finish with this second cyto Kinesis happening right after Tila Phase 2 we are finally left with four hloy truly hloy not hloy with replicated DNA we are truly left with four haid cells so let's go back to Furniture once again we started with a diploid room two copies of each chromosome we had interfase which means we had DNA replication as part of interphase we created a diploid room with replicated Furniture it's starting to look a little messy but this is what happens during interface we replicated everything after meiosis 1 and that first cyto canis that left us with a haid with replicated furniture room we only had one of each type of furniture but we had two copies of it hloy with replicated furniture and by the time we have finished meiosis 2 and the cyto canis that comes after that we have a truly hloy room one single copy of each piece of furniture sorry if this furniture analogies is getting a little tedious uh but it's a good way I think to describe what's going on here by the time we finish the second cyto canis we now have four haid cells if you don't appreciate Furniture if you don't that's fine here's an overview of meiosis compared side by side with mitosis I find this very useful as a visual hey if you can draw this yourself if you could and you know I'm not a great artist even if you're not a great artist you could draw a cell it's just a circle you could draw a chromosome it's just a sausage you can get you know two different colored markers or colored pencils or you know pens whatever if you could draw this out yourself you'll really get a better appreciation for what's happening along the way mitosis was interphase prophase prometaphase metaphase anaphase tase cyto canis done meiosis was interphase prophase 1 prometaphase 1 metaphase 1 anaphase 1 tease 1 cyto canis each of these cells goes through prophase 2 Pro metaphase 2 metaphase 2 anaphase 2 tease 2 cyto canis ending up with a total of four cells all of which are hloy I don't have anything to write down from this slide I think it's a fantastic visual overview of this entire chapter and kind of the last chapter as well uh but I have no new information to add this is just a great visual resource for you and here's another great visual resource for you just sort of breaking down meiosis one and here's one breaking down meiosis 2 again nothing new for me to write I just want to give you as many resources as possible uh to to give you something visual to look at uh a as you're studying so that brings us to the end of this chapter uh on sexual reproduction and meiosis and this is the end of recorded lecture 32