Lecture 6 - Cellular Reproduction

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[00:00:01]hi everyone welcome back this week we're going to be looking at cellular reproduction from chapter 5.

[00:00:07]so so far we've taken a look at cells how they're built and we're aware that in the nucleus that's where we store all that genetic material and we know from anatomy that you know our cells are going to need to replicate we've just looked at the integumentary system where that basal layer of the epidermis is the site of cell replication right that's where all those new squamous epithelial cells are going to be formed so today we're going to look at the nitty-gritty behind the process of how our cells are actually capable of reproducing then we're going to look at some of the checkpoints to how our cells are able to ensure that during that process of that cell cycle that if any errors were made that we're able to deal with that effectively as you may recall we have prokaryotic and eukaryotic cells the prokaryotic are simple and the eukaryotic much more complex one of the main differences between prokaryotic and eukaryotic cells is that prokaryotes lack membrane-bound organelles and so here what we're looking at is not the dna located within the nucleus here we have their genetic material located free-floating within their cytoplasm in a region known as the nucleoid region now this is going to come into play because the fact that they don't have a nucleus is advantageous for them because they're able to replicate very rapidly one of the big differences between the two is that prokaryotes have a single circular dna molecule and that is what makes up their chromosome within our cells all of our dna is going to then condense to form those 46 chromosomes in all of our cells so in a bacterial cell for example they just have that one single circular dna molecule that they need to replicate now some bacteria also have an additional piece of circular dna it's smaller known as a plasmid and we're going to talk about plasmids and some of the utility in biotech later on next semester so as i mentioned the fact that prokaryotes do not have a nucleus is advantageous for them because that simplifies their cell cycle they're able to simply replicate their dna make the copy and then split to form two separate daughter cells with prokaryotic reproduction the daughter cells are going to be genetically identical to the parent cell now there are other ways that they are able to increase genetic variability and that we'll get into in a couple of slides so looking through here we're looking at our single bacterial cell each circular chromosome has what's known as an origin of replication and then picture it almost as like you're unzipping a zipper on your coat and from that origin of replication they're going to be creating an identical copy so that ultimately that can then produce two of those circular chromosomes and once that process has completed then the bacterial cell can go through what's known as binary fission fission means to split fusion fuse put together okay so binary fission is the process by which prokaryotes are able to simply just split into two identical cells so this as you're going to see is much more simple compared to our much more complicated cell cycle if you recall remember when we're looking at dna dna is deoxyribonucleic acid right remember nucleic acids they are all made up of nucleotides and so the way that we replicate say you have a sequence that is a t t a you know that the complementary strand is going to be t a a t um you know those complementary base pairs well that is the process by which the dna is going to be replicated and they're going to create those complementary pairs to each of these strands that you can see itemized here we're going to get into all of the details surrounding dna replication as well as transcription and translation next semester so for now as long as you're understanding that to replicate the dna molecule what they're having to do is actually create an identical copy and how do you build a nucleic acid you link nucleotides up together to create that new dna molecule now as i mentioned bacteria are capable of increasing the genetic variability in their populations through a number of different means otherwise they would just be creating genetically identical copies of each other and that would not serve them well in terms of being able to survive now there are three different mechanisms that bacteria can use in order to increase that genetic variability and they are known as conjugation transformation and transduction okay so i have identified those here in the diagram first let's start off with conjugation now you have already talked about these structures connecting these two what were those extracellular structures found on the outside of prokaryotic cells that allow them to connect with one another and exchange genetic information those were the pillai so this here is showing you when you have two pillai connecting from two separate bacteria they're able to actually share that genetic information from one to the other and then that other is able to incorporate that dna into its genome another way that they're able to increase genetic variability is through a process known as transformation where they are able to take in dna fragments from other cells and incorporate those into their genome as well and then the last method that they can use to increase their genetic variability is through a method known as transduction now transduction occurs when bacteria acquire new dna fragments from viruses this is a type of virus known as a bacteriophage and now all viruses are essentially just protein capsules which you can see here all in green and then they have their dna located inside that capsule now what the bacteriophage is able to do is able to land on a bacterial cell membrane bind with it and then inject its dna into that bacterial cell and now that bacterial cell is going to be able to incorporate that in its genome as well we don't have to feel sorry for these guys even though they can only use binary fission to be able to replicate they have means by which those daughter cells are still able to increase genetic variability through methods of conjugation transformation and transduction now one thing that makes the eukaryotic cell cycle much different is that eukaryotic cells contain far more dna than prokaryotic cells remember eukaryotic cells outside of protists exist within multicellular organisms and the way that that dna is packaged is much different right we've talked about these chromosomes to this point we've seen an image of them we're going to start to look at them in a lot more detail both this week and next week this here would be one example of your homologous chromosomes okay so one one of those 23 pairs of what we're looking at here now remember at every other time in the cell cycle except for when the cell is dividing all of that dna is in a linear form known as chromatin i remember that was that bowl of spaghetti that i talked about so then as part of our cell being able to divide we we first have to be able to take all of that spaghetti and condense it into these chromosomal structures so that they can then be separated into opposite daughter cells and this number is going to be implanted by the end of this week how many chromosomes do humans have in a single cell 23 pairs all right we have 46 chromosomes in every one of our cells except for sperm and egg cells okay so 23 pairs now eukaryotic cells undergo two different mechanisms in order to divide that dna and create duplicate cells all of the cells in our body except for the cells that produce those sex cells are known as somatic cells so whether it's a nerve cell a skin cell liver cell any other cell in our body besides the germ cells that are going to produce sperm and egg cells those are classified as somatic cells every somatic cell is going to go through the process known as mitosis so with mitosis we're not actually creating genetic variability what we're doing is just wanting to replace the cells that are ultimately going to be dying and meiosis is the process by which the germ cells which are located in the testes and the ovaries are capable of producing those sex cells all right and the whole idea there is that we're producing genetically variable sex cells right we don't want them all to be identical in this process of meiosis there's a number of steps that increase that genetic variability so where are some of those somatic cells well it could be any cell in the body except for the germ cells germ cells are located within the testes in the male and the ovaries in the female and they are ultimately going to give rise to the gametes which are the sex cells now as mentioned previously we have 23 pairs of chromosomes in each of our somatic cells so that would give us 46 chromosomes in total each of those pairs we can assign a number so there would be chromosome pair 1 chromosome pair two three four five all the way up to 23 and 23 would be the sex chromosomes okay so we have 23 pairs each of those pairs contains one copy of that chromosome from the father and one copy of that chromosome from the mother all right so for example here we're looking at let's say chromosomal pair number one each of those pairs are known as homologous chromosomes okay so we have 23 homologous chromosomal pairs now when we go through the process of having to duplicate all of our dna so that we can then divide the cells these homologous chromosomes each have to be replicated so if we were to look at one of them say the one from the mother this would be it isolated here unduplicated and for the purposes here of itemizing these let's call the one from father chromosome 1a and from the mother chromosome 1b all right so we're looking at 1b 1b needs to be duplicated and when you duplicate that homologous chromosome then have two identical copies and so the two identical copies of one homologous chromosome are known as sister chromatids okay it's important that we understand this terminology now because we're going to be using those terms as we progress through this week and also next week when we're looking at genetic inheritance so here again we're looking at the homologous chromosomes let's just say this is chromosomal pair one so we have one a from father we have one b from the mother now the thing about the homologous chromosomal pairs is that they each contain the exact same genes as one another those genes can have different variations from one another for example here let's say this gene is the gene for hair color let's say the father has brown hair and the mother has blonde hair both of those jeans are located at the same place because that is the same homologous chromosome this is chromosome one so the gene is located at that same place but there can be variations in the actual genetic code coding for that specific gene okay and that variation we refer to as alleles so for example here let's say we're looking at the gene for hair color we would have a specific genetic code for brown hair and from the mother we would have then a specific genetic code for blonde hair and so during fertilization of the egg by the sperm the single set of the father's chromosomes and the single set of the mothers are then combined to form the complete set which gives us the 46 in all of these somatic cells in our body now as i mentioned say we're going to look at chromosome 1 from the mother so that's chromosome 1b okay so chromosome 1b is going to have to be duplicated as chromosome 1 a is also going to have to be duplicated okay but we're just looking at one of those homologous chromosomes the one from the mother so when we create an identical copy of both of those homologous chromosomes we're going to refer to the duplicates as sister chromatids so sister chromatids are going to be genetically identical to one another right because we've literally taken chromosome 1b from the mother and we have gone then and duplicated it and so remember we have how many pairs of chromosomes we have 23 pairs that gives us 46 chromosomes so if each of those chromosomes are going to be duplicated to form sister chromatids that's going to yield 92 chromatids in total before the cell divides then once the cell is able to divide those sister chromatids are going to go into opposite cells and we're going to have a complete set in one and another set in the other one so then our 46 chromosomes have been maintained through the process of division there's a structure known as the centromere this is where the two sister chromatids are joined together and the centromeres are important because this is where the spindle fibers are going to attach to before they end up pulling the sister chromatids into opposite sides of the cell this is a karyotype and a karyotype is an arrangement of chromosomes essentially pairing up homologous chromosomes okay so as i was saying before we have 23 pairs right we have 22 known as autosomes and then finally the 23rd pair are the sex chromosomes that determine your gender so the chromosomes are compared based on size the shape of them but also the center centromere location and what they do is they start with the longest chromosomes those are chromosome number one and then for the most part you can see here that they decrease in length as you go through now this karyotype here shows that there are 23 pairs of human chromosomes so that is what is expected now there are certain genetic disorders and we're going to talk about those a little bit later where we're going to take a look at what happens if there's a problem during cell division what if an extra 21st chromosome were to be brought into one of the cells well when that happens that's where you end up developing the condition known as trisomy 21 where you have three copies of the 21st chromosome and that is down syndrome so we're going to take a look at some of those and we'll we'll see the differences between how they can occur in different parts of the cell cycle that are more likely to cause certain conditions now as i mentioned before the eukaryotic cell cycle is much more complex than the prokaryotic cell cycle not only do we have all of our dna located within the nucleus so we have to break down the nucleus when we want to divide it all we also have much more dna than the prokaryotes to have to replicate and divide and so then there's so much more that could possibly go wrong when you're trying to divide a eukaryotic cell now the eukaryotic cell cycle can be broken down into three main phases so the cell spends most of its time in a phase known as interphase right you can see here interphase has a number of different stages we have the g1 phase which is a period of growth the s stage when replication is occurring and then a second growth phase when the cell's preparing to then divide and then the one that gets all the fanfare usually is mitosis right this is just a part of the cell cycle so mitosis where the cell is actually going about lining up those chromosomes and then separating them into opposite ends of the cell so that the final phase known as cytokinesis can take place where the cell will actually divide into two daughter cells so we're going to break this down now and look at each of these phases in a lot more detail the cell spends most of its time in the cell cycle in interphase interphase is broken down into those different phases g1 which is your first growth phase the s phase which is a period of dna replication as well as chromosomal protein duplication and then the g2 phase this is where the chromosomes are going to start to condense right so at this point here when we're replicating dna what form is it in we're going to be replicating dna when it's in its linear form as chromatin once it is duplicated now all that dna is going to be condensed and then ultimately ready to then be divided now g also stands for gap phase i usually just refer to it as the growth phase because it helps me remember and i think you remember what's actually going on during these periods so remember one of the big differences between eukaryotes and prokaryotes is that the eukaryotes have membrane-bound organelles so not only are we having to duplicate all the dna that's inside the nucleus we're also having to replicate certain organelles like your centrioles or mitochondria before you can actually just split the cell into two because what hey if you don't have enough mitochondria in your new cell you're not going to be able to produce enough energy for that cell to even be able to function other organelles are capable of just being distributed through the cell and then the cell can then split into two and then they can produce more as the cell demands so here in the s phase this is the synthesis phase this is where we're replicating the dna but we're also going to be duplicating all of those histone proteins that the linear dna is going to be wrapped around in order to form those chromosomes then once that has completed we move into the second gap or growth phase this is where those chromosomes are going to condense so what that means is all of that linear dna that you've just duplicated you're now going to wrap it all up along those histones to create those chromosomes that we've been looking at and now that they're in that condensed chromosomal form we enter into mitosis now mitosis known as the m phase is made up of four main stages we have prophase metaphase anaphase and telophase and mitosis is where cell division is getting set up okay interphase is where all of the replication duplication has taken place the cell has then condensed that genetic material and now during mitosis this is when we're getting set up to finally be able to divide the cell membrane and create two separate daughter cells all right so during mitosis we have prophase metaphase anaphase telovase during each stage there's unique events that are taking place in order to be able to divide the cell into two now a really easy way to remember the order is pmat all right that'll help you remember which stage comes in which order so we're going to start off with the p prophase looking at stage one so recall where are we coming from when we're moving into prophase well we're coming from that g2 that second growth phase and this is where the cell has prepared for division right we have condensed those chromosomes and so now they become visible what has to happen though is that we have to get rid of that nucleus and so the nuclear envelope that makes up the nucleus begins to start to break down the nucleolus which remember is within the center of the nucleus and houses all of the ribosomal rna it disappears and now all of these chromosomes are going to be eventually lining up within the center of the cell this first initial stage we're getting rid of the nucleus so that we can ultimately separate the sister chromatids into opposite ends of the cell also during prophase we have the centrioles remember those those are those organelles that make spindle fibers those spindle fibers were the microtubules so those centrioles they end up separating in the cell and they migrate to opposite ends known as poles of the cell now the centrioles they have a an outer membrane and that membrane then is going to form a network of spindle fibers that are made up of microtubules if you haven't watched that video yet definitely go and take a look the inner life of the cell you'll be able to really appreciate how these microtubules are not only put together but then also disassembled when the centriole is going to be pulling apart the sister chromatids into opposite ends of the cell the centrioles are producing the spindle fibers which are then going to connect directly to that centromere remember the centromere that holds together those sister chromatids there's a specific protein called a kinetochore and the spindle fibers are going to be attaching to the kinetochore at that centromere and then once they've attached the chromosomes the spindle fibers then are going to align all of the sister chromatids along a region known as the equatorial plane okay and the way that i always think of metaphase is think m middle okay they're aligned up in the middle of the cell okay so remember pmats so we're at the third stage anaphase during anaphase one way i remember what's going on here is to think they all look like sideways a's there's an enzyme known as separase which is then going to break the cohesin protein that's holding those chromatids together at that kinetochore okay so once that bond has been broken now those sister chromatids can separate into opposite ends of the cell and so these microtubules those spindle fibers they're going to then be dismantled starting here so what i want you to picture is that ultimately it's like you're throwing out a fishing line and then you're reeling in your fishing line so when it says that they're dismantled starting at the poles it's meaning that they're going to be broken down here and as they're broken down it's essentially pulling that spindle fiber back in so bringing that sister chromatid in towards that pole and then finally the last stage of mitosis telophase telophase is essentially getting the cell now ready to completely split in two now that the sister chromatids are at opposite ends of the cell so at opposite poles the nuclear envelopes can now reform around the chromosomes at each pole the chromosomes then are allowed to uncondense right so from their chromosomal form they can now go back into their chromatin form and the nucleolus will reappear within the nucleus okay so now the cell is pretty much ready to go except we need to divide it into two separate daughter cells this is that final phase of the cell cycle which is known as cytokinesis what happens is those actin microfilaments now what are they for they're for movement right they're contractile so those microfilaments actually form a ring right down this central portion of the cell and it acts to pinch the cell membrane to ultimately create two separate daughter cells this external landmark that you can see that's created by the active microfilaments is that known as a cleavage furrow so as the actin microfilaments start to pinch off eventually those pinch off into two identical daughter cells and there you go we've just gone through one single cell cycle now hopefully you have an appreciation for how much is going on there every time a single epithelial cell is having to be reproduced to form new skin cells on your epidermis now as i mentioned at the beginning there's a lot that can go wrong here so eukaryotic cells have different checkpoints where we're able to then ensure hey has this cell undergone any sort of mutations that would then be detrimental to the organism as a whole and so these checkpoints are actually set up at each main phase of the cell cycle to ensure that the previous phase has been fully completed before advancing to that next phase and so at these checkpoints we have specific proteins that become involved and is essentially becoming like the checkpoint sleuths they're they're looking around at the dna that's just been duplicated for example here in the s phase at this g2 checkpoint they're going to be looking for any mutations that may have occurred and so you know one example of a mutation could be a substitution where where instead of pairing your adenine with your thymine and pair the adenine with an adenine okay because that is going to interrupt or change the genetic code and that would be one example of a mutation there's lots of mutations we'll talk about next semester but for now just if you understand that if we just mess up just one of those nucleotides that can have detrimental impacts to the cell as a whole and so at these checkpoints we have these proteins and enzymes that are working to be able to ensure um they're essentially able to proofread the work that's just been done so here at the g1 checkpoint that we have just after the cell has just entered into its next cycle g1 checkpoint is there to ensure whether the cell should divide and enter into the s phase now if a cell doesn't because of some mutation that's taken place then the cell cycle is stopped for that cell and our body has a way of being able to program it for cell death which is known as apoptosis now the g2 checkpoint happens right before we enter into mitosis and the purpose of the g2 checkpoint is to ensure that any errors that may have happened during replication that they're caught and that we're able to rectify that if possible and then lastly this one's easy to remember when it takes place because it's known as the m checkpoint the m checkpoint takes place in mitosis but specifically during metaphase and essentially here what we're wanting to make sure of before we go and we create two identical daughter cells here is there anything wrong with this cell where it should not be allowed to proceed and that's where that final call is made and if everything checks out the cell is able to then divide and now we have two daughter cells that are capable of again going through another cell cycle now what can happen is when mutations take place you know even when they occur and these checkpoints fail for us and we have cells with mutations in them our body has ways of being able to detect these mutations you know i always talk about a cancer cell essentially being a cell that's gone rogue right some mutations taken place and now the cell is not being monitored in the same way it doesn't have the same shutoffs and it's able to grow rapidly without being regulated now when we have too many mutations taking place and we're not able to catch all of these cells that have gone rogue early enough sometimes then cells are able to then grow uncontrollably and get to a point at which they can then ultimately spread to other parts of the body all right so the results from that growing cluster of cells is that a tumor would ultimately develop now there are benign tumors and malignant tumors benign tumors are encapsulated so they're surrounded by a healthy layer of cells which means then that they are going to remain in situ which means in that location all right so they don't tend to spread to other areas now malignant tumors such as we've talked about these right the melanomas they are unencapsulated and are invasive which means they can not only destroy the surrounding like tissue so for example the melanoma it's occurring in the epithelial tissue but it's also able to then pass through the connective tissue blood vessels and so on and then spread throughout the body and so the cells are capable with unencapsulated malignant tumors of leaving that location where they started and then spreading to other areas of the body where those cells can then implant into new tissue and form new tumors and that process is known as metastasis so if you've ever heard of anyone who has had a secondary tumor it's likely that it originated from another type of cancer from another organ in the body and then it has since spread so an example here is with with melanoma they tend to readily pass into the bloodstream and then spread throughout the body and one of the areas that they can impact is the skeletal system and skeletal metastasis usually offers a pretty poor prognosis now genes that normally regulate the rate of the cell cycle they're called proto-oncogenes and tumor suppressor genes so the proto-oncogenes we're going to start with first right they're able to code for proteins that increase the rate of the cell cycle during periods of growth um other times that you might need them you know healing of wounds even during pregnancy i want you to think of proto-oncogenes as like a foot on the gas pedal proto-oncogenes are genes that encode for proteins that are going to stimulate cell division so that's great but if there's a mutation to that proto-oncogene that can then cause the cell to then just divide at a rate that cannot be controlled so it's like if your proto-oncogenes have mutations it's like you're putting your foot on the gas okay now your tumor suppressor genes in this image i love this image that's your breaks it's pointing to the handbrake in this case but essentially that's your break if you have any kind of mutation to the tumor suppressor gene well these genes that normally turn off cell division okay they're not able to stop this the rate of cell division that's occurring so not only do you have proto-oncogenes that are going to be further stimulating cell division you've also lost the ability to be able to turn off cell division in those cells and so both of those mutations in proto-oncogenes as well as tumor suppressor genes essentially lead to the development of an optimal situation where cancer cells are capable of developing now one very important tumor suppressor gene is known as a p53 gene and the p53 gene is responsible for stopping the cell cycle at that g1 checkpoint if a mutation is detected and now i can do this by two ways so we look here we're looking at an example of dna there's a mutation there there's a mutated nucleotide improper substitution let's say okay so we don't have the complementary base pair that we should have the p53 gene is capable of then producing dna repair enzymes that can go and take out that mutated nucleotide and then put in the proper one so if that dna mutation can be fixed fantastic that cell is then going to be able to pass that g1 checkpoint enter into the s phase the g2 phase and ultimately through mitosis and cytokinesis and divide normally that's the ideal situation now remember we're still looking at if we have a normal p53 gene okay so the p53 gene is going to produce that dna repair enzyme but if the mutation cannot be fixed we have a way to then arrest the cell cycle okay and then we're going to be able to destroy that cell through programmed cell death which is a process known as apoptosis all right so this is how our body should be functioning if there's a problem we can fix it great let the cell divide if we can't fix it okay throw that cell in the garbage now the problem comes down to if we have mutations as we just looked at on this previous slide mutations in tumor suppressor genes such as p53 that can then cause uncontrolled cell division and so here we're looking at the situation now where we have that mutated tumor suppressor gene mutated p53 if you have a mutated p53 we're also not going to be able to suppress the development and further replication of the mutated cell so two outcomes from that situation either you have a mutated cell that survives and eventually will just die through its normal life cycle or we have a mutation in that cell and ultimately cancer cells produced and capable of replicating now it's not only proto-oncogenes and tumor suppressor genes where mutations can play a role in the development of cancer there are also genes that can increase angiogenesis angiogenesis is the process of creating blood vessels if you have genes that are increasing angiogenesis and there's a mutation in them we have more blood vessels being created to supply a tissue with more blood well now you have an opportunity for growth in an area genes that prevent apoptosis remember that's programmed cell death that regulate the immune response because we have specific cells known as natural killer cells and they're literally think of them as hitman that go around the body they don't necessarily need to know anything about the cell to take them out they just need to know that that cell is not working properly and then it shouldn't be there um so anytime that there's mutations in in our cells our cells have ways of being able to identify to the body hey come here come kill me because i have a mutation and that mutation might be lethal to the body as a whole and then lastly dna repair enzymes okay an inability to repair any mutations at the genetic level would definitely increase the likelihood of developing cancer so i'm sure you've heard a lot about antioxidants and why are antioxidants so great because they're anti-oxidants anything that has an oxidizing effect on our dna can produce mutations all right and as i mentioned before a lot of things in our environment radiation smoking pollution uv light even inflammation has the capability of being able to produce free radicals right so here we're looking at an example here you have your o-h with that little dot that indicates this is a free radical they are unstable molecules and when a free radical is produced it's capable of then binding to our dna binding to the nucleotides changing their structure and function and having a huge impact on our bodies anything that would be recommended that would be an anti-cancer food would either be high in antioxidants because the antioxidants are going to oppose the damage from those free radicals their antioxidants essentially help to neutralize the free radicals and prevent them from damaging our dna anti-cancer foods are also going to regulate our immune response so they're going to help to support the development of those natural killer cells those hitmen that go around trying to kill cancer cells that do develop that pass those checkpoints any food that's going to help to promote your immune system is going to help support those natural killer cells in their ability to be able to detect and destroy those cancer cells now at the beginning of the lecture we were looking at the process of binary fission the process by which prokaryotic cells like bacteria are capable of replicating their dna and then through binary fission splitting into two identical daughter cells this is known as asexual reproduction during this process there's no exchange of genetic information remember we're creating genetically identical daughter cells so the offspring have the exact same dna as the parent and that is not advantageous because we're not able to then evolve right genetic variability is going to be one of the things that is going to allow a species to be able to survive and so we've talked about the ways right through transduction transformation conjugation the process by which your bacterial cells are capable of increasing genetic variability but through the process of binary efficient alone they will not be increasing that genetic variability okay their daughter cells will be genetically identical to the parent now we are capable of sexual reproduction okay where the haploid egg which contains one set of the 23 chromosomes and the haploid sperm which contains the other 23 they are able to then fuse through process of fertilization where we then receive genetic information from the father and genetic information from the mother to create that new diploid zygote which is the fertilized cell and the process through which we go by producing these genetically variable sperm and egg cells is a process known as meiosis okay so mitosis we're looking at the cell division of our somatic cells right every other cell in the body producing genetically identical cells right just the purpose there was replication with meiosis we are looking at the production of our sex cells okay and so remember the germ cells are located within the testes as well as within the ovaries and the germ cells are going to go through a process of meiosis 1 and meiosis 2 in order to produce either one haploid egg cell or four haploid sperm cells now meiosis one and two have some similarities because they have the four stages that we saw in mitosis prophase metaphase anaphase telophase but there are a few differences that we're going to go over that help to increase that genetic variability now one thing that's important to mention is that the germ cell itself is diploid which means it contains 46 chromosomes so dna is only going to be replicated once and it's only going to be replicated before entering into meiosis 1.

[00:39:24]so that first phase here that first s phase that is where you will have the dna replicated we'll have 92 chromosomes but then we go through essentially the process of two cell divisions to then come back to create our haploid which means just one set of 23 chromosomes in those gametes a lot of the differences too exist within meiosis 1 where we have an event known as crossing over where we actually have sister chromatids that are going to be exchanging genetic information and then in meiosis ii this is where ultimately those sister chromatids are then going to separate so meiosis ii looks pretty similar to mitosis it's meiosis one that really we see some differences in how everything is set up so why do why does meiosis occur why don't we just want to create genetically identical well ultimately we're wanting to produce these gametes right the egg and the haploid sperm cell now they're haploid which means they have half of the normal amount of dna so haploid refers to a single set so 23 chromosomes whereas all of our other cells are diploid okay so having 46 chromosomes in total and it's the germ cells that are undergoing meiosis within the testes for the male and the ovaries for the female and the result is sperm and egg are produced and the sperm ultimately can then fertilize the egg to produce that diploid zygote that fertilized eggs okay so we're going to start off here looking at meiosis one again we have the same stages prophase metaphase anaphase telophase but we have two different phases in meiosis okay so meiosis 1 and meiosis 2. so in prophase 1 the homologous chromosomal pairs are going to line up the sister chromatids that are adjacent to one another they are going to exchange through an event known as crossing over genetic information from one another so literally parts of one sister chromatid are going to be switched with parts from another so during metaphase one all of these paratomologist chromosomes are lined up at the equatorial plate remember again we have these spindle fibers that have connected to the kinetochore which is lining them all up and then finally in anaphase one we're going to have then the sister chromatids are going to be pulled into opposite poles and now that they're there telophase will occur but in telophase the individual chromosomes are going to gather at each of the poles but we're not going to have the nuclei condensing at this point now with telophase and mitosis we started to see that the nucleus was starting to re-form and also the nucleolus would reappear but here in telophase 1 of meiosis we still have more cell division to occur in meiosis ii and so as a result you have the division occurring here at telophase to then produce now two daughter cells from that germ cell and so now here in meiosis 2 the process is going to be to then divide all the dna from those diploid daughter cells further into then the individual haploid gametes all right now remember as i mentioned there's only going to be replication occurring but in the s phase before meiosis 1.

[00:42:48]so in the process of meiosis there's actually a very brief interphase between telophase 1 and prophase 2. here in prophase two again the spindle fibers are going to be forming again from the centrioles in opposite poles of the cells and then those spindle fibers are again going to connect to the kinetochores and are going to line up the sister chromatids at the equatorial plane and now we're going to be separating those sister chromatids in each of those daughter cells okay so we have the sister chromatids are going to be separated here and the sister chromatids are going to be separated here but remember because we had crossing over occur here in prophase one we now have created genetically unique sister chromatids that can now be separated into separate individual haploid cells to create the haploid gametes remember duplication of the dna is only going to occur before meiosis one so we've duplicated the dna and now all that dna is going to be condensed into chromosomes and we are going to pair up the homologous pairs so that is because we are going to have this event known as crossing over a curve where we're going to exchange that genetic information from opposite chromatids as i mentioned before each haploid gamete is going to contain a single set of the chromosomes so we're going to have one copy of chromosome one one of two one of three one a four and so on each homologous chromosome has the same genes but there are variations on those genes and so as we can see here now we have segments here where we have completely different alleles than we do on the other first chromosome let's say and so the differences there are what are going to provide us with that genetic variability that we see in our population now sexual reproduction is going to allow a species to be able to evolve very rapidly because essentially we can create unlimited genetic combinations now the three mechanisms that are going to help to produce the genetic variability that we're talking about are independent assortment crossing over and random fertilization before getting into independent assortment and crossing over in more detail with random fertilization remember one of eight million different sperm are capable of being able to fertilize the egg so think about the genetic variability that we just created there in one single cell cycle of meiosis one and two creating four sperm cells and think about how much genetic variability must exist within a population of eight million different sperm cells that would all be capable of ultimately fertilizing an egg now independent assortment we're looking at the idea here that there's nothing saying which side of that equatorial plane your homologous pairs are going to end up on so during metaphase one the arrangement of the homologous pairs on either side of the equatorial plane is completely random and because that's a completely random process it increases the variability of what potential outcomes we could end up with then the other way in which sexual reproduction increases genetic variability is through crossing over that occurs during prophase one so recall during prophase one homologous chromosomes are then going to line up together but now it's in pairs okay so we have the two pairs of sister chromatids and then crossing over is going to occur by the non-sister chromatids so you have the one sister chromatid from the father and the other sister chromatid from the mother and the two that sit right along the equatorial plane are then going to cross over and exchange that genetic information so now we end up with four genetically unique chromosomes now lastly meiosis also has two unique features not found in mitosis okay first off synapsis this is the process of drawing together the homologous chromosomes down their entire length so that crossing over can occur i wanted to bring you back to metaphase of mitosis remember during metaphase of mitosis we were just lining all of the sister chromatids up on that equatorial plane so that then they're divided into opposite poles of the cell we're looking at sister chromatids for one from the mother and then sister chromatids from the father in meiosis we're going to pair those up side by side in prophase one we're going to then pair them up you're going to have your homologous chromosomes both sister chromatids are going to be paired up with one another and then lined up during metaphase one so that then the sister chromatid pairs can then be pulled apart into opposite poles of the cell and then the other unique feature of meiosis versus mitosis is that meiosis goes through a process of reduction division remember in mitosis we maintain the same number of chromosomes from our parent to the daughter cells but in meiosis the whole goal is to take the diploid germ cell remember because we're going through two cell divisions but only duplicating the dna once we end up with half of the amount of genetic material in the gametes which we want because once the sperm then fertilizes the egg that gives us then that new diploid fertilized egg the diploid zygote so i've included this summary chart for you just to organize the main differences in cell division between our somatic cells and our germ cells so remember somatic cells are all the cells in the body except for the germ cells right the germ cells are the ones that are going to give rise to the gametes either the sperm or the egg so the somatic cells go through mitosis where we're producing two new identical daughter cells and during mitosis we're maintaining the 46 chromosomes and so the daughter cells are all diploid now the germ cells once they go through meiosis they're they're producing ultimately the gametes the germ cells themselves are diploid right so 46 chromosomes but once the germ cells have then gone through meiosis 1 and meiosis 2 to produce the gametes we have half the number of chromosomes and so our gametes the sperm and the egg only contain 23 chromosomes okay and so they are known as haploid so they have a single set of all 23 chromosomes and our germ cells and somatic cells all possess two sets 23 pairs or 46 chromosomes so that brings us to the end of our lecture for this week we're going to continue on next week looking at genetic inheritance patterns to see how we're able to pass on these alleles to future generations if you have any questions please feel free to reach out otherwise i look forward to seeing you all in tutorial take care have a great week