Transcript for:
Ch. 10 Understanding Cell Reproduction and Division (YT VIDEO)

hello chapter 10 cell reproduction this covers how cells come from pre-existing cells which we learned about in unit one um they go through what we call a cell division and then cell division ends up being cell multiplication because it's also how cells grow in number so it's a little weird um but when one cell try to hold it up divides it splits into two two so then it becomes two cells and um that's how organisms like us which all sexually reproducing organisms start out as a single cell and then go through a process called mitosis and cyto canis to become multiple cells so one cell to two two cells to four four to eight and so on um and then single cell organisms their division is just how they reproduce when they go from one cell to two cells that's their population size how many they have cell division has multiple functions um for single cell organisms as I said on the last slide This Is How They reproduce essentially a single cell organism is just going to copy its DNA and then split itself into um and the population size can go from one to two the video here is bacteria uh multiplying so all procaryotes or I should say all bacteria are procaryotes all pro procaryotes are single celled so how they grow on population side is size is through their cell division um they do have ways of exchanging some genetic information which we'll touch on in this class but we won't really go over uh and I don't test you on but it does come up a few times uh for multicellular organisms they use multiplication to grow right I said we all start as a single cell and then become a multi- cellular organism made up of trillions and trillions of cells so growth um maintenance and repair if you have a damaged cell you can replace that cell cell replacement under there if you've had a wound you can replace those cells so it can repair tissue um right which are multiple cells of the same kind working together if you have multiple that cells sometimes it can be okay if a few have been damaged um because some are still functioning and we can use those to help repair um there is your book didn't really say it but um it can be used for reproduction multicellular organisms multicellular organisms typically uh often can reproduce sexually and will go over uh sexual reproduction and that type of cell division in the next chapter but a number of multicellular organisms including animals can um essentially grow a bud it's like a growth that is of them that is the same type of cell that they're doing through mitosis and then that breaks off and become it becomes another individual it's just genetically the same as what it started with uh which is different from sexual reproduction which mixes up the genetic variation so um it can be used for reproduction but we don't think of it as much as that but there are some ways of essentially asexually reproducing multicellular organisms that can do that through just basic cell division for a cell to divide the important thing that needs to be done is um to duplicate its genome right it has to copy all of its DNA so that the next cell that comes from this division has uh a full copy of DNA every cell in your body every cell in multicellular organisms have a full set of DNA they have for us we have all the chromosomes uh which we have um 40 two what am I trying to think 40 uh six I don't know why I going to say 4 we have 22 pairs 46 total chromosomes in humans it varies species to species um and every cell except um your sex cells which are sperm and egg have that full 46 chromosomes um so that is the genome that's all the DNA cells multicellular organisms every cell doesn't necessarily use all that DNA actually not necessarily like it doesn't it does not use never is all the DNA used and in UK carots in general a lot of the DNA isn't used at all like ever um and then certain regions are only turned on or off as needed or in that specific type of cell as used um but they all have it and in procaryotes they have um kind of large circular DNA that's bundled up in the nucleoid region um and then they have little plasmids which are smaller circular DN um and they can exchange those it's that's a way they can kind of almost sexually reproduce they can exchange plasmids with other bacteria they can incorporate plasmids into their chromosome into their DNA bacterial genome to um turn on those gen use those genes to make proteins and so whatever type of cell it is it has to copy this genome before or it goes through cell division so that there's essentially two copies to go into each of the two what we call dotter cells um and it's a little bit different the way procaryotes and ukar do it so I will talk about procaryotes first and then ukar procaryotes divide through a process called binary fion think of binary as two andion separating um so they start as one and it divides to too um there are more steps and we're going to come back to Binary fion next unit when we talk about DNA replication so how they're actually replicating their DNA but we're not going to go into that here it's just that they have this circular DNA they have like that big long circular chromosome um where they use most of their genes they do turn genes on and off as needed but most of their DNA is coding and they want to copy all of that cuz it's very important for them before they uh divide to make two cells so they start at what's called an origin of replication it's kind of shown here but it's really already started working it starts and what happens is the um uh what do I going to say the enzymes which we're not going into here move out and are going to copy going two ways going two ways around from wherever that origin of replication is and and copy it around and essentially make two large chromosomes which is shown down here so it'll copy all the way around and it'll go around the chromosome in a circle when it gets back to where it started has a um side of termination where it's going to end the copying um they have these proteins the ftsz fits proteins these proteins help with their cell division essentially um separating a cytoplasm and uh where their cell membrane's going to be pinched in and their cell wall is going to be built um so these proteins help them form a septum and we're going to see what that is on the next slide where we're continuing uh with binary fion something else that I hope you notice is happening is that the cell elongates it kind of which they're often kind of oval shape anyways bacteria are kind of a lot of bacteria are pill-shaped but they'll elongate further whatever shape they are um in preparation for the division so they will get longer a bit a bit bigger in size they're going to replicate their circular genome to have two genomes and then these Fitz proteins are going to move towards the middle of the cell so that's the the green things are the proteins we're going to see them where they'll move more align in the middle uh and we'll see that on the next slide as well the chromos will separate so the cell's pretty elongated now as you can see the chromosomes right each of these what was a duplicated chromosomes will separate from where they were attached and moved to either end of the cell it's still a single cell here and those fits for proteins um will kind of make a ring the ftsc proteins make a ring in the middle um that ring is going to form what's called a septum septum is where the cell membrane is going to be essentially elongated and grow in and the cell wall is going to grow from and then once it's complete once the cell membrane has completely been pinched in and the cell wall has grown um to separate it will finally separate after that septum is complete or it has it all the cell separates into two and it has two cells so in summary procaryotic cell division is called binary fion um it replicates its circular chromosome starting at an origin of replication the enzym zip around make a copy so that there's two those separate on the elongated cell going to either side of the cell the ftsz proteins move towards the middle to make a ring to help build the septum which is um makes up accumulates the material that make up the cell membrane and cell wall once that gets finished the cell then separates in as two daughter cells the UK carotic genome is a bit more complicated um we have linear chromosomes so UK carots have multiple chromosomes how many they have varies among species but they have their DNA wrapped up on these multiple chromosomes that all need to be replicated before the cell divides so really we have to replicate that genetic material in the nucleus separate them and then the cell can divide so as a little refresher over here on the left is our cell and I've kind of uh left things in that are going to show up with our cell division remember the nucleus is where our DNA is held the DNA is held there um in chromosomes but I'm going to note we'll get to it in a little bit chromosomes is one form of how the DNA is wrapped up typically during a cell cycle while cell's doing its stuff it's not in a chromosome form it's actually in what we call chrom and we will get to that but the DNA is held in there um mostly in the chromatin form DNA plus some proteins um of the side remember our cytoskeleton materials microtubules are really important in cell division um this say forms the mitotic spindle so they're essentially going to make Little Fibers you like threads that will attach to the chromosomes to separate them and the centrosome this is a bit specific to animal cells um is animal cells microt pual organizing centers plants have something similar uh but organize the microtubules so that essentially there'll be two centrioles on either side of the cell the microtubules will come from there to attach to the chromosomes and then pull them separate them so they go to opposite sides of the cell we are going to do a mitosis lab which is great where we look at the different steps of mitosis so the these are onion cells or they look like onion root cells to me and when you see here this is what I mean by the chromatin form this is when that DNA is very loose inside the cell and squiggly and can't see it but during mitosis when these chromosomes duplicate and are going to separate you can see them and they're much more visible and you have different like stages so when you're kind of here this is might be a prophase or PR metaphase where they start what we call condensing and you can actually see the chromosomes here they're lined up this is showing the different chromosomes lined up in the middle and you can kind of this purple spindle fibers are the microtubules well groups of them that come out and reach those chromosomes and are going to separate them to either side so we're going to look at these in lab as well let's see fun La I did already say this but I'm going to go into some things about uh chromosomes and chromatin try to help you understand these differences but in UK carots um the DNA molecules right the DNA is the full molecule that is on a chromosome it is one long polymer of nucleotides right the the N they have different nitrogenous bases a TCG and then they all have the sugar phosphate backbone they're coal bonded on that backbone double Stranded the double stranded is hydrogen bond with the um nucleotides forming the rungs of the ladder that's the long you can think of it like a long string that's a double string of the DNA molecule it is wrapped up around proteins to fit inside your nucleus there is a lot of DNA in all your chromosomes like five feet Worth or even more um of DNA wrapped up in every cell in your body so well I guess not your blood cells but other than that and only half of it in your gametes but other than your sex cells and red blood cells you have all this DNA wrapped up and so the chromosome is how it's wrapped up when it's wrapped up in the form where we can see it like on that previous slide that is a chromosome although there are some differences to that um when it's in a more looser stage we call it chromatin the number of chromosomes a species has varies it's typically the same across a species So within one species most individuals have the same number there can be variation things happen um and we'll talk about that next chapter but for now within a species they have the same number of chromosomes but between species the number of chromosomes can vary um and there can be some differences as it says here uh with developmental stage and then like your sex cells have half the number um so this is the stereotypical chromosome but this is really a copy of a chromosome so chromosomes are linear but when they make a copy of themselves before they divide they're attached at a region and so they tend to look like this x shape um that's when the whole DNA the chromosome has a copy of itself attached to it and we'll get into that in a little bit as I've already said and was written on the last slide um your chromosomes can vary by cell and cell type so let's differentiate some cell types within multicellular eukaryotic organisms um somatic cells are any cell in a ukar that is what we call called diploid has it's does normal functioning it has the two full sets of chromosomes so um most ukar have some type of way all multicellular ukar have some type of way of sexually reproducing um not all always do it many species can reproduce asexually and sexually but most have a way to do um sexual reproduction and so what they have is two sets of chromosomes half they got uh from their paternal lineage and half from their maternal lineage and so um those come together and then they have two full sets that's why earlier I said humans have 23 sets of chromosomes that is what we call diploid 2N we have 23 chromosomes and we get 20 well we have 46 but we get 23 from our biological mother 23 from our biological father and so together that makes the 46 and I'll talk more in a slide about what that looks like gtes which are sex cells um usually egg and sperm although not all species do that and I'll get more into sex next chapter um because we'll go into how gametes are formed in that chapter we're not talking about how they're formed in this chapter um so mainly gamet sex cells which are often egg and sperm have half the number of chromosomes they're haid they only have one n so egg and sperm for humans only have 23 chromosomes each and then when they fuse they make a fertilized egg which is that single cell we all start out as um which for us is 46 chromosones and then th those go through mitosis cell division they'll start specializing into different types of cells and all those other types of cells that aren't sex cells are somatic cells so somatic cells are diploid they have the full set of chromosomes um they make up the different tissues of your body except sex cells sex cells or gametes here's a picture that I hope will help explain some of this when I say they have two sets of chromosomes being diploid versus being hloy so with sexually reproducing species they have homs um let me back up a second to go to the slide arrange the title of the slide arranging the chromosomes by size produces aype kype is essentially a picture of the chromosomes of a species so this is for a human this is some humans um chromosomes I said there were 20 three so we have 22 what we call autosomal chromosomes and then we have two sex chromosomes chromosomes that determine sexual characteristics again I told you we'll get into the sex stuff next chapter but uh it is important to see this so we have 23 total pairs which makes us have 46 um total chromosomes so if you counted each one of these 1 2 3 4 5 6 you would get up to 46 but what we have is 23 pairs meaning we have these homologues the homolog is essentially the same sized chromosome that has the same genes on it in in the same place so this chromosome could have came from this person's biological mother and then they got this chromosome let me use a different color from their biological father and the DNA is wrapped up on there but in the same region is the gene for like if it's a gene for eye color if it's here on one chromosome it's going to be in the same spot on the other chromosome so the genes for all of our traits are in the same spot on all the chromosomes now what that Gene says like what the eye color or hair color and skin color what proteins that Co for to make it that can be different the DNA sequence can have changes in it that make things different but the gene for these different traits are in the same spot so homologues are chromosome pairs that are the same size have the same genes um a carot type is when they are ordered by size so we number our chromosomes right we know we have 22 what I said autosomal chromosomes which are essentially nonsex related and then we have a pair of sex chromosomes so 23 total we don't count the sex chromosome because one of our sex chromosomes is very big and the other one is very small but separate from our sex chromosomes we order our chromosomes by size so and this is for any species the first chromosome if you take a picture of their chromosomes in the cell the largest one is what we call the chromosome one so we have two chromosomes ones one from our biological mother one from our biological father and that is the largest chromosome with the most genes on it and then they decrease in size until we get to 22 which is our smallest chromosome pair and of course they're homologous one from Mom and one from Dad um they don't have nearly as many genes on them and then um sexually reproducing species have chromosomes that contribute to their sexual characteristics and so we call those sex chromosomes the sex chromosomes aren't really homologous we have two sex chromosomes what we call an X and A Y um biological chromosomal biological males are what we call X Y they carry they have one X chromosome and one Y chromosome the x is very large but lots of genes many genes that aren't related to sexual characteristics the Y chromosome is very small with very few genes but it does have the genes related to male sexual characteristics characteristics um biological chromosomal females are what we call xx and that they have two X chromosomes they have two of this larger chromosome and they do not have a y um and that causes female sexual characteristics to develop um there's a lot of differences and things that go into that that I will talk about next unit but they're considered the sex chromosomes are considered heter logous because they're not the same size with the same genes the XX are um but the XY are not so they're not considered homologous but for the purposes of what we're going over for this chapter you don't really have to worry about it it next chapter may come up slightly um so here's the human chromosome this would be a biological chromosomal male with the XY um and his that person's autosomal chromosomes as well hopefully you understand um the homologous chromosomes and we have these sets of chromosones which makes us diploid in all our cell and then the way the DNA is wrapped up on those chromosomes matters too um the terms we use chromosomes chromatin and there's going to be another one chromatid coming up all kind of refer to the way the DNA is how it's wrapped up and how many copies there are so right we have 23 pairs of chromosomes 46 total chromosomes and that DNA is wrapped up really tightly it's not just the DNA the DNA is there so start here you have your DNA but that DNA that double stranded DNA like a string is wrapped up around these tiny little um balls called histones they're proteins histones are proteins um that the DNA is wrapped around really tightly and then essentially eight of these histones get wrapped up in sort of a bigger ball called a nuclear zone so when the histones are wrapped up the DNA is red on the histones and those there's like eight histones that make up a nucleosome and it looks like what we would say beads on the string we can actually sort of see our DNA like this with really good microscopes in the cell where they look like the nucleosome looks like a little bead where it's wrapped up and the DNA is kind of a string between it um because there's some little space between those nucleosomes fold up themselves they kind of wrap up more and are folded in a particular p pattern like here um and then here so we're getting we're starting small with our DNA and we're getting bigger as we're going down zooming out some I guess you could say wrapped up um really tightly to make the chromosome and really this is this side is one chromosome the other side is an exact copy which I'm going to get to here in a minute um but it's all wrapped up really tightly and so when it's wrapped up tightly where you can see it like like the the way you this is shown here and on those previous karot karot types um this is the chromosome form so really what a chromosome is is when the DNA is wrapped up really tightly and you can actually like see it in a cell like on those um images from the onion cell and you're going to see these in lab which is cool too you'll get to see wrapped up so chromosone is are wrapped up form DNA is wrapped around histone proteins those histone proteins are grouped together groups of eight to make a nucleosome and that helps fit the 5T worth of DNA um into these tiny cells all right so these are two uh the bottom are two images kind of showing the different versions so this is the beads on a string over here in the left uh where the DNA is wrapped around the histones in these uh balls of eight see if you see four and four eight histones to make a nucleosome and then you have some DNA stretches in between when DNA is kind of loosely wrapped up we call it chromatin you see chromatin fiber so the majority of the life of your cell called a cell cycle um the DNA is in the chromatin form where it's Loosely wrapped around these proteins and that makes it accessible to the enzymes that need to access it to make proteins they have to get that information from the DNA so in most of a cell's life their DNA is Loosely wrapped up in the nucleus as chromatin and so on a when you actually like stain a cell and look at it the nucleus looks like this you can't particularly see any specific chromosomes because it's in this loose chromatin form and it kind of all stains somewhat universally when a cell is going to divide shortly before it divides the that chromatin condenses into what we call the chromosomes where you can see it and that's the more X shape where it's it's really two it's one side with its exact copy which we'll get to and so this is the condensed form the condensed form when the DNA is wrapped up really really tightly is chromosomes and this happens when a cell is going to divide and you can actually see the chromosomes again this is an onion cell those are right next to each other this one is getting ready to divide um and you can see that the different chromosomes are kind of hard to make out where one ends and one starts but they're all condensed in there so it is the DNA is very tightly wound up around um the histones and nucleosomes and put in very tightly now we're finally getting to the cell cycle so how the DNA is important because I'll use some terms later later when I'm talking about the mitotic phase um because like in the different stages the DNA is wrapped up in different ways whether it's kind of in the chromatin or chromosones and when it has its uh exact copy attached to it so let's look at the stages of mitosis oh no sorry I don't know why I said mitosis the stages of the cell cycle so this whole thing is the cell cycle we'll kind of start here this would be from an a cell has divided and there's two new ones it starts in what we call the G1 phase or Gap one um and the cell grows here doing its stuff whatever type of cell it is doing its reactions being a nerve cell being a muscle cell whatever it may be or if you start as a single cell it's not really any specific cell yet it just starts as a cell and is mostly dividing it's just growing and dividing we're taking its food doing its cell respiration it needs to do cell respiration uh and generate lot of ATP to keep growing um and if it's going to continue to go on and divide go into the next step what we call the S phas um it will need a good amount of ATP so G1 and then it will go into What's called the S phase where DNA is copied so all those chromosomes you have each one is making a copy of itself but it's still attached to that copy but it's also in the chromatin form here so it's very loose so this is called DNA synthesis it's only going to do this if the cell is going to divide and then it goes into a G2 phase um and this is the end the DNA has already been copied it's going to get ready to divide now do do some stuff which I'll talk about in the next few slides um still grows some uh and then if it's ready it can go into the mitotic phase which will is how it actually like separates the chromosomes something I want to note though if you look around this G1 s and G2 they all have interphase by it because interphase the cell really has two main two main phases what we call as inner phase and then the other one the mitotic phase and those make up the cell cycle but then when within each of those there are substages so the G1 G2 s and G2 excuse me are the three substages of interface and they go in that order G1 sg2 so there's cuz there's specific stuff happening interphase is just the cell Cycle's life right the cell is normally an interphase that's when it's doing its thing but there are some differences s really kind of breaks up the two Gap phases the G1 and G2 because that's when it's copying in its DNA so it kind of gives it this separate thing that we can say it's doing but through all of interphase a cell is functioning as that cell doing what it needs to do to help the organism maintain homeostasis and survive and potentially grow Andor reproduce reproduction cell division for reproduction is a separate process we're going to talk about in next chapter um but the normal cell is doing this so interphase is its kind of normal cell stuff but then it has those three substages that are characterized by specific things happening uh mainly the the S phase and that DNA synthesis really kind of separates it okay and so then the other phase the other of the two main phases is mitotic Phase mitotic phase has its own two substages mitosis and cyto canis so mitosis is it's essentially nuclear division the nucleus actually goes away so it's separating mitosis is to separate the chromosomes you've already duplicated them in SASE of interphase but you need to separate them now um in mitosis so that when the cell divides and you have two cells from it you have made uh each cell has all the chromosomes has all the DNA because all your cells have the same DNA except your sex cells and your red blood cells because they don't have a nucleus and then cyto Kinesis is just the very last step where the cell divides it's actually the cell division and I'm going to go over all these and I'm going to go over each of the stages of mitosis because mitosis itself has its own five stages in it so we have the cell cycle interface my itic phase inner phase has three substages mitotic phase has two substages mitosis and cyesis and then mitosis has its own five substages so we've got a lot of stages to know here different levels let's look at those three substages of interphase a little more closely so this whole thing from when essentially the cell starts around to before it's going to divide and go through mitosis um is interface but and so interface is the reason that's that big circle of this Pi is because that's the majority of the cell cycle the mitotic phase is very small it may take an hour or less out of a cell cycle and when multicellular organisms start as a single cell they are going through the cell cycle very quickly so they're growing quickly but as they get larger and kind of form into the organism they're going to be it slows go down um and you don't have as much Division and even some of your cells once you reach maturity um will stop going through it at all and they'll just essentially stay in interface and we'll talk about that at the end of here but so interface is the majority of the cell cycle then we have these three substages G1 stands for Gap one up here and the cell's active doing what it's going to do and it's usually growing if it's in a G1 it's probably going to be growing in size there's a little thing later where when it's done it may just stay where it's at um so cell growth there may be I think I not it in the speaker notes Here there may be some organel reproduction here too but it's not for division it's just for the cells so say like your muscle cells are forming as you know you're developing um a muscle cell is full of mitochondria but when two muscle cells go through division from the one muscle cell they came from um they might not have all the mitochondria in it right when they're formed so they might duplicate a mitochondria to make more mitochondria mitochondria and the Smoothie R are really important in muscle cells so it could grow may increase in some organel if that cell needs more of a type of organel and is doing active if it is going to divide if it yeah divide if it has intentions of going through a division it will go into the the S phase which is synthesis think of synthesis because it's DNA synthesis DNA synthesis means copying the DNA I want you to remember this because it's coming back next unit you do need a note for this unit but we get in to that whole process of copying DNA in the SASE next unit it's a big part of next unit so all your chromosomes and this is for any living thing that is copying a UK carote that's going to be uh has a nucleus and needs to copy it DNA before it separates will copy the whole chromosome that whole large DNA strands and you vary from like um what was it vary from I think 50 million base pairs on your smallest chromosome or around there to like 300 million base pairs on your largest chromosome uh so you have lots and lots of base pairs um to go through when you're copying your DNA and all that gets copied um and they're still attached so the chromosomes are attached and what they're attached to is called the sister chromatid um and that's that X shape because I kept like circling one side because one side was the chromosome but it's attached to its sister chromatid when it makes its copy and they join at a region called a centromere and I have an image on the next slide to to go over that specifically because it's kind of confusing but you're going to need to understand that to understand mitosis during the S phase though when they're C when that sister chromatid is made the DNA is still in the chromatin the loose form so it's still kind of loose in the nucleus after the DNA has been copied the cell will go into its G2 phase second Gap this is where it is preparing for mitosis it's going to look um for any DNA damage or mutations that was done when copying the DNA in that DNA synthesis uh checks that we'll get to that later organel here are reproduced or duplic at so that um when the two because this is like getting ready to go into mitosis so when the two cells are formed they each have at least one nucleus um sorry at least one of each organ now they actually don't have they will have a nucleus but the nucleus doesn't get duplicated here the nucleus is actually going to come apart for us to separate the chromosomes and then it'll reform at the end so other organel that are not the nucleus are going to be uh duplicated and the cytoskeleton breaks down um we use those the microtubules for separating the chromosomes and the cell's going to have to elongate to separate so there's not a strong cytoskeleton during the mitotic phase which is what we're going to go into after the G2 all right let's talk about sister chromatids and how they relate to homologous chromosomes and chromosomes these These are really important terms that you should know that get a little confusing the better you understand them the easier uh it's going to be so um SASE DNA synthesis they make a copy you have um this really should say like I would rather to say holus chromosome so like these two they say chromatids but really what they are are homologous homeus chromosomes just put Chrome there we'll just put that um like one the yellow one let's say came from Mom and the SEC the the blue one came from biological father so this is both let's just say chromosome number one for humans they're the same size they have the same jeans on them there's a jean here for hair color there's a jean here for hair color there's a gene here to make the lactase enzymes to break down lactose there's a gene here in the same spot to either make make or not make the lactase enzyme maybe one makes it and one doesn't I don't know so they have the same gene same position they're both the chromosome one the center mirror is where they're held there's always like not quite in the middle but sort of towards the mid region a center mirror that uh pinches the chromosome and that's going to be used to make the copy so during S phase DNA is going to copy this whole chromosome right and it's going to do all of them it's going to do this one as well and it's going to make a copy and the centrosome is where those copies are held together so make a copy and then let's go over here after replication it has made an exact copy and that's where we get that X look when this happens the chromosome is really in its chromatin loose form but when it's going to go into mitosis it'll condense into this this chromosome form where we say it is with its sister chromatid anytime the exact copy is attached to a chromosone it is called a chromatid so you have two sister chromatids here one two they're both chromosome one but you have two sister chromatids that are held together at their Centum mirr that's this not quite Center but near center part that holds them together with a protein a cohesin protein it's going to hold them together until they separate in mitosis to get each on either side of the new cell so your DNA has copied itself in sphase we will go over that replication again next unit you don't have to worry about now you just need to know that it happens in s phace we'll go over how it happens and that when it happens you have these sister chromatids all your chromosomes all 46 of your chromosomes have a sister chromatid attached and they will look like this through mitosis until they separate and then your one your chromosome number one from Dad did the same thing the biological fathers our blue chromosome over here so they're homologous chromosomes they're considered and this is where it gets kind of confusing while we have two sister chromatids attached they are considered one chromosome as long as they are attached at the Cent miror so this is just one chromosome so you would still say even though they all have a copy chromosome even though every all 46 of your chromosomes have their copy attached your sister chromatid you still say you only have 46 chromosomes they they are not considered separate until they actually separate during mitosis they will separate into two and then you actually have a double for a short amount of time which we'll talk about that there so I have a picture of this how it looks for humans a human kot type with the sister chromatid showing on the next slide so here's a uh cotype of human homologous chromosomes each with their sister chromatid attached so like for your chromosome one one of these was from biological mother and the other is biological father but they've each copied right they've made their copy so that's one and then the other held at the uh Center mirror so they've copied itself um and so these are homologous all of these are homologous but these are the sister chromatid and it is still considered one chromosome so at this stage if we saw a cell like this this is a cell with its chromosomes but it still only has 46 chromosomes even though it has 92 two sister chromatids because every chromosome has a sister chromatid attached um technically this for since this is a chromosomal male here um it would be uh not that's not truly homologous but we are showing them together so the X and the Y the sex chromosomes so hopefully that makes sense if it doesn't um watch some the extra resources video watch this over again make sure you kind of understand the difference between sister chromatid chromosomes and chromatin um I'm going to be using those terms throughout mitosis and meosis next chapter and next unit and so it's important you kind of understand what they mean interphase makes up the majority of the cell cycle right G1 s G2 s is when it copies itself after G2 um it's preparing to go into mitosis uh with which is where it's going to separate all those sister chromatids that it has copied in the S phase and then go through a cyto canis where the cell actually divid um so Kinesis is essentially mitosis your book uses that term I'm just going to say mitosis because that's the way you probably heard it and everybody refers to it it's not really only referred to Kinesis in like scientific papers um so this is a nuclear division the nucleus itself goes away but we're separating the chromosomes that may that are where the DNA is held inside that nucleus and it happens over its own five phases that will go over each of those at the end after mitosis the end of mitosis it's going to go through cyto canis cyto canis is the actual cell division cyto meaning cell um so we're getting this is where at the end of cyto canis you have the two daughter cells everything the mitosis separates the chromosomes so it can divide but mitosis isn't the actual cell division the cell the true cell division is cyto kinesis when the cell divides and you'll get two daughter cells so there's different stages of mitosis we're going to go in them so interphase um is when that the DNA is in the loose chromatin form even after the sister chromatid has been made when it goes into mitosis it's going to condense where you'll start seeing it more clearly U they line up in the middle of the cell and then they separate and we can actually see that we're going to see it in both animal and plant cells in lab and then at the end after the chromosomes have been separated cyto canis is going to happen where the cell actually divides into the cytoplasm splits and the cell membrane is pinched in to then make two separate cells so now I'm going to go into those five phases of mitosis um there is this image that I got from your publisher Open Stacks um they're showing interface here G2 of interface because that's what's right before mitosis I want you to note that that is not part of mitosis G2 is getting ready for mitosis but mitosis really starts when certain specific things happen which we call prophase and that is where mitosis starts um so we have five substages of mitosis I'm going to erase that so don't confuse people maybe we have prophase prometaphase you may or may not have if you've learned mitosis in the past you may or may not have heard of prometaphase um sometimes it's not used and what happens in PR metaphase some Publishers just kind of put in prophase but there's kind of specific stuff that really separates prophase from Pro metaphase certain things that are happening this is how we define the phases so um I do like the having them separate because there's like very distinct things happening uh and then metaphase anaphase and tease is the last stage mitosis cyto canis is not part of mitosis it is part of the mphase or mitotic phase that second part of the cell cycle but cyto canis itself is not mitosis um it's when the cell divides right after mitosis uh this video over here on the right I do highly recommend watching it and especially after I go through the stages I would come back and watch it we're going to see images of cells of these different stages in lab but you don't actually see it happening and so it's cool that we have real video of this happening um because this is a process it's more like a movie that's happening and we're just pausing it at certain parts and calling it these phases we're giving right the the the names are really arbitrary we're giving these well they're not completely arbitrary because stuff is happening but like we've just said this is a stage like you know when one ends and the other starts is sometimes tricky hard to hard to say we've we've divided them by specific stuff that's happening so usually when a certain thing is happening now we say this one's starting and the other one is ended but it's a really it's a movie that's continuing so um it's hard to like differentiate them and I think that actual footage on the right this video on the right of a cell dividing is cool because you see that yeah this is just like continuously going through and we're essentially pausing at points and saying okay that's this phase after G2 the cell is going to go into mitosis the mitosis has five substages it starts with prophase um I should have said on the last five some people like to remember the five stages by PP mat prophase prometaphase metaphase anaphase tease PP mat it's the first letter of each stage um profase has some specific stuff happening that is written here on the left and semi shown again it's sort of a process so it's hard to show it as an image which is why I think those videos are really good um so nuclear envelope is going to bring break down the nucleus actually goes away where you um the the phos filipus that make it up kind of break down and go into the cell so that's broken down showing there that red I'm going to erase that in case that looks confusing nuclear envelope breaks down the membranous organel these membrane bound organel move they've most have already been duplicated um so they move toward the edges of the cell so that hopefully um they go to opposite sides like you know you'd have a a smooth a g g and a smoothie on one side and GG and a smoothie AR on the other so that when it divides the new cell has at least one of each organel that it needs um nucleis disappears so you don't really see the nucleis anymore remember that's that smaller organel within the nucleus where ribosomes are made uh that it kind of goes away during the cell cycle centrosomes we talked about those in unit one when we were going with self structure and I said they would come back croomes is where the microtubules are organized and so you have these pairs of centrioles that are 90° angles those are the centones those move towards the pole as well they're going to move in opposite directions uh opposite sides of the poles and microtubule spindle fibers will start coming from them microtubules will start growing out from them so they look like the we call them spindo fibers and they are microtubules those are going to work their way to attach to the the Cent mirror of your uh chromosomes which each have their sister chromatid attach so now the chromatin condenses to chromosome so this is where it has that X shape that we can see now we're in the actual true chromosome form where it's very tightly condensed and wound and you can see it they're kind of these are in the X shape here but they're showing both chromosones like right next to each other so there would be one and then in blue I'm going to do the other one it's hard is like right next to it and they're attached at the Cent mirror um so major things nuclear envelope breaks down centrosomes migrate towards the pole spindle microt tual spindle fibers start to form from the centrosomes and the chromatin condenses to chromosomes and you can see the chromosomes with each having a sister chromatid attached Pro metaphase your spindle fibers or I should not say spindle FIB the centrosomes with those centrioles at 90° angles have reached either pole and what defines prometaphase is that the microt tual spindle fibers are attaching to each cister chromatid um they're going to attach to essentially the sister chromatids are held together uh at their centrr centrr is just a region where they're held ciric region over here that's really cir is just that region uh shown in the black rectangle here where the cister chromatids are held together they're held together by this um protein called cohesin that's going to come up and the microt tual fibers are coming from either side and attaching to What's called the kinetic core the kinetic core is um where the microtubules attach the specific spot where the microtubules attach at the centr region of the cister chromatids so microtubules are going to be assembled to get there and some disassembling um there's a bit more disassembling in the next stage they're mostly being assembled to attach and if one if this sister chromatid on this side is attached to here there's going to be a microtubule growing from the other side that's going to come and attach here so it has to grow to get there and once they're all attached every pair is attached on like each sister chromatid has a micral attached on both sides at their kinetic core remember that fancy word kineticore reason it's Metalized and underline there then there's going to be some excuse me some assembling and disassembling to work to line all these chromosomes for there the sister chromatids up on the center What's called the metaphase plate it wants to line them all up essentially perpendicular to where the centrosomes are so like for this one this microtubule is going to have to be assembled to be longer to get it here but once this one attaches now it's going to have to be disassembled a little bit to pull it back so that it can line up at the center so it's working to line them all up at the center because they need to be lined up at the center to separate so PR metaphase is defined by those spindle microt tual fibers attaching to the kinetic core so the microt tual fibers are going to be assembled to get to attach to each cister chromatid at their kinetic core and then there's going to be some assembling and disassembling to start moving them to line up on that metaphase plate metaphase is defined as now all the chromosomes the sister chromatids are all lined up on the metaphase plate it's a relatively short phase because once they get lined up they're going to start separating um but once the centrosomes have adjusted all the microtubules so that they're kind of all lined up perpendic to them on the equator of the cell um and remember we're looking at this as a 2d thing on a picture it's really 3D this is a ball so they can be going through it it's hard to see but like right there can be like on a line on the inside of the basketball if you put a like a sharp metal thing that went all the way through the chromos zones could be lined up anywhere on that the sister chromatids are attached U still attached to their cohesin protein so right now for us we would still have 46 chromosomes total all 46 are going to be lined up on the metaphase plate there in the middle for us attached to each other by their cohesin protein and each cister chromatid being attached to a microt tual um fiber protein at their kinetic core um and so now going into the next step the the micral are going to start to disassemble to pull the sister chromatids apart but they are together in metaphase still the diploid number uh 46 chromosones for us soon as those sister chromatids are separated now we are in anaphase what happens is the cohesin that protein that was holding the cister chromatids together gets this kind of broken down degenerates it's not holding them together tightly the microtubules will start disassembling so that they're pulled towards either pole and that will cause the sister chromatids to separate so now we no longer have sister chromatids sister chromatids ending in a d s are um only when they're held together soon as they separate now they are separate chromosomes and the DNA is still condensed here highly condensed so it is the chromosome form and this is when you would actually again now double your number of chromosomes because we had 46 lined up when they separate in anaphase for a very short time not very long very short time in that cell you actually have 92 chromosomes because they all all 46 were there and they separate and they move to either side and you're still one cell you're still one cell the cell is usually kind of elongating at this point elongating it's shown better here is the elongation but maybe a little bit in the picture on the right um notice how they have like the doubling of organel or on this left picture they've doubled the organel so you have multiple organel on either side um and the chromosomes are being pulled towards either pole so anaphase starts as soon as those sister chromatids separate they are now chromosones and they get pulled towards each pole pole going towards those Cent zomes being pulled towards really the the pole with the by the croome the last stage of mitosis is telophase or tease can say either think of telephone and to end tilo is end that's going to come up again later as well so tilo phase is our last step of of mitosis it's pretty much the opposite of prophase prophase starts so you think of pro pre it's the first one starts off mitosis and so the stuff's going away and whatever's happening there the opposite is having a Tila phase at the end so the chromosomes have reached the poles once the chromosomes are at their poles that's the end of anaphase and the start of til or telophase they've reached the end now that they're on either side um some things are going to happen the spindle fibers will disassemble you don't need those um the C Zone with their cental perpendicular pair these have all essentially been disassembled they've been disassembling as they're pulling um the chromosomes to either pull they get shorter and shorter so they're disassembled in Tila phase where you don't see the anymore that's the opposite of prophase where they assembled the nuclear envelope you'll get two nuclear envelopes forming kind of in sections around each set of chromosomes so if you look here this is a nuclear envelope forming and this is a nuclear envelope forming because of um around each set of chromosomes because you have the full two diploid sets on either side um the it doesn't do I say it here it doesn't look like oh no I do begins to decondense that's what's the fcy word I was looking for right your chromatin condensed to chromosomes in prophase so in tilas the opposite is happening the chromosomes are going to decondense back into chromatin they're going back into that loose form ready to make the proteins needed um and then you you your cell is fairly elongated at this point because it's getting close to splitting and there's a little bit difference in animal and plant cells which I'll show on the next slide this is uh showing the animal cell version a cleavage Furrow will often be starting to see in telophase and will deepen sometimes you can even see it in anaphase um on some of the cell slides we'll look at that'll be hard to see you can't always see that too well plant cells don't really have the cleavage F so you don't see it when we look at the plant ones the animal ones we look at can but sometimes that's hard to see um so I'll talk about that on the next slide that's as it's going from tease into cyto canis where actually separates but the big things for Chase the chromosomes reach the poles will decondense back into chromatin nuclear envelopes will reform to around each set and your spindle fibers are completely disassembled and the kind of not they're used those pieces are now used for the cytoskeleton that's going to be be built in the two new cells and cleavage Furrow or a cell plate forms if we're talking about a plant cell which will be shown on the next slide after cyto canis oh sorry after telophase the cell is going to go through cyto canis which is actually this cyto is the cytoplasm divide so this is where cytoplasm is going to separate and a cell membrane will come down to form between so that you get two separate cells this is the actual cell division right the the Tois was to separate out the chromosomes each copy the chromosomes animal and plant cells are a little bit different and animals we say we have a cleavage Furrow sometimes uh you can even see the starting in anaphase it's usually shows up to some extent and telophase it will deepen and deepen and it keeps deepening and deepening like going in more and more this contractile ring you don't really need to know the details but there's proteins that are helped doing this that are essentially elongating and pulling down the membrane from the edges pulling it in towards the center until it deepens enough that the cells split and you have two daughter cells plant cells remember that they have a cell plate so they essentially build their cell plate in Little Steps vesicles typically starting towards the center of the cell and then moving out and adds more and more until it goes all the way through and separates the two after they're chromosomes have split to either side so they build a cell plate in steps they don't really have that cleavage fur they build a cell plate that's going to separate um the cell um and that and then you have two daughter cells something I want to note which is not shown here but we're going to compare it to meosis next chapter at the end of mitosis you have two genetically identical daughter cells so they might be slightly different in size they roughly are usually smaller because you've gone from one cell to two cells so after you start these two new cells they generally smaller than what that cell started is and then they'll go into their G1 and grow and may go through my you know go through the whole cell cycle again if they're going to divide as they get bigger um but the daughter cells are genetically identical they have the same copies of chromosomes in there in all cells the cell cycle as it goes through these steps of interface and goes through mitosis has is regulated it has checkpoints things it's doing that will allow it to go to the next step um I want to note here right we as humans made these steps looking at what happens in the cell the cell doesn't know that it has specific steps it's just if it's going to do something if there's a trigger essentially an internal external trigger it causes certain proteins to be made that then allows the next thing to happen and so when we see this stuff happen we have given it these names um so to make a new cell you have to duplicate the original cell so we're making that that same number of chromosomes with the same DNA um and so there's three regulated checkpoints throughout the cell cycle that look for particular stuff before it continues on to the next one so there is a checkpoint what we call the G1 checkpoint that looks for specific things which I'll go over Al also called the Restriction checkpoint at the end of G1 so essentially as a cell gets to often a certain size that will trigger these proteins made at the G1 checkpoint that look for stuff if everything looks good that allows it to then go and copy its DNA and then there's another checkpoint what we call a G2 check point before it goes into mitosis that looks for specific things that has happened in the cell before it's going to go through mitosis and then there is an M checkpoint towards the end of metaphase of mitosis and I'm going to talk about each of those checkpoints on the next few slides controlling the cell cycle the cell cycle has to be controlled because we don't want cells to duplicate um unregulated that causes a problem which I'll get to later but we also need them to duplicate when we need new cells and so it's not a good thing if they're not duplicating when we need them to um so it's controlled in essentially how long a cell is an interface and how if it's going to divide and there are different things that control it external internal triggers um death of nearby cells can cause that um growth hormones are a big thing growth hormones are released to um get cells to divide to make more and that um rut is what we do as we're growing because we all start as a single cell and so early on we're just doing a lot the cell cycle is very short and going very quickly as we're getting bigger and bigger and then it kind of slows down so you're releasing lots of hormones in the beginning um cell crowding how much there is I will talk about that in a few slides as well and cell size how big it gets when it gets a certain size it can't really get bigger because it'll become too inefficient so then is it going to divide to become smaller cells or is it going to uh just stay at the large size and not a lot of cells so we talked about the cell cycle a lot of cells will go into what we call a g knot Gap zero Gap notot phase we say G notot um where when it would be in G1 the the cell just doing it things before it's duplicated its DNA if it's not going to divide it can just stay in the Gen not phase like um and I'm going to talk about that on the next slide but that's what this little thing over here is is when a cell's staying in G KN and not going through the cell cycle and it just essentially stays in a stasis G1 phase G not can be cells can be triggered to stay there just essentially it's like saying in G1 but when it stays in there for a prolong time we call it g not and it may be triggered to go back in the cell cycle something can cause it to then go into the cell cycle and go through cell division at a later time so a little more information on the G not phase this is showing where the G not is when the cells are not actively dividing um so growth factors are essentially our main trigger for cells to divide if those grow factors are not being released or blocked um the cell typically stops in the G one checkpoint which then we just say stays in the G knot it can be triggered to come out of it how long a cells in G knot can be from days to weeks to months to Forever well after some certain period of time so you start as a single cell cells are going to divide and you'll become this multicellular organism um you'll keep growing you pretty much you're still growing until sexual maturity usually around or after puberty when sexual maturity is reached a lot of of your cells stop dividing that's when you're you stop growing so it slows down right it's very fast from a fertilized egg as it develops through to a fetus and then it's slowing down but still happening quite a lot right as a baby babies grow quite rapidly with adequate nutrients because this all takes a lot of energy and then that grows uh and this is you know for mammals and general and really animals and plants do this too as well and then when sexual maturities reach uh right there's a lot of hormones there's a lot of hormones releasing all the time but a lot of hormones around puberty to develop SE secondary sexual characteristics and um growth hormones people do grow uh and then once that happens some of your cells pretty much stop dividing most of your heart and nerve cells um this brain cells don't do much dividing we used to think they didn't at all that like once you kind of reached adulthood they didn't divide we do know that some do but most don't there's not a lot um and they just stay in that Gene not phase for the rest of your life other cells like your skin cells do stay in it I mean do stay in the cell cycle and keep regularly dividing but it is controlled they um right they're kind of like they say your skin cells uh are replaced about every 3 weeks weeks so they go through it but it is regulated when they do it so they'll kind of be hanging out in a gnot for a while before going back into the cell cycle um but they also like skin cells can be triggered to go the cell cycle in less time like when you have a wound right when you have a cut that releases specific type of growth hormones that are going to cause the cells around that wound to start growing back and go into mitosis or go back into the cell cycle and through mitosis until they have um essentially hit each other so sealed sealed back and healed that wound so there is triggering to come in and out um and even the ones that are staying in the cell cycle could be triggered to go back in uh more than it earlier than it would because of things like a wound let's look at the checkpoints individually now G1 checkpoint determines if the cell is going to divide so a cell's growing maybe it gets to a certain size um and now it's getting too big it can be triggered to go past G1 into the S phase but um it is going to check for certain conditions to make sure it's ready for this so what something it's looking for is DNA damage from after that cell right this is would be sometime after mitosis and cyto Kinesis from the cell it came from and so it wants to make sure that it has all the chromosomes and all the DNA is there and all those chromosomes and that there wasn't like chromosomal damage where you only got part of one um so looking for DNA damage it's looking that there is energy either's some food stores in that cell it's able to make ATP because there's a lot of energy that goes into cell division so cell respiration needs to be um happening with available food to keep it going to get it through um dividing so making sure there's adequate fuel reserve and this is why starvation will halt the cell cycle so if you don't have enough nutrients if you're not getting enough food your cells aren't going to go through cell division and this is why um when you've seen like images of starving children they're very small right they're they're always very small for their age um if they've gone through starvation conditions because the cell cycle was halted and they didn't have the nutrients to be able to grow and go through mitosis um so that cell cycle will be inhibited from survation um the cell will try to fix the conditions um to go forward if there is an issue it may be able to to repair DNA damage there's a variety of ways to repair DNA damage um get adequate food reserves if it gets enough nutrients that it deems able to do cell division it can go forward but if it doesn't get these it's going to stay in the G knot um there are there's another thing it may do it may if things are really bad it could potentially just kill itself uh which we'll talk about later but typically it's just going to stop there and stay as it is and not go forward if things are working right that is what it's supposed to do um if a cell goes through the G1 checkpoint it is making a commitment to divide right a cell stays in a g not if it's triggered because it's not going to divide and at certain times of life um like I said a lot of your cells are just going to stay in G knot the cells that are going forward have the intention to the five like a cell isn't going to go forward and copy its DNA unless if there is the trigger the intent to um divide the G2 checkpoint is after SASE so this would be after all that DNA has been copied all the chromosomes so the major thing here is DNA damage DNA damage is both being looked at at the G1 and G2 um but this is you've copied it so now it's making sure that copied DNA was copied correctly not too many massive amounts of mutation or if a section of a chromosome didn't get copied um it will Halt and not go forward and try to repair the damage if it can if it can't it may kill itself and again we'll get to that in a little bit um if things are working well um it can potentially go on without repairing the damage and that is a problem which we'll get to later but the checkpoint is looking for looking at the DNA and looking for damage and either repairing it if there is or if there's not proceeding on to mitosis the M checkpoint is at the end of metaphase so remember our mitotic phase metaphase is in the middle the M checkpoint is towards the end of metaphase before the sister chromatids are going to separate this is checking to see that all the microtubules are attached to the kinetic core of each sister chromatid right so I'm going to kind of draw this out here you have have one sister chromatid which is exact copy over here that c in the middle and then let's draw microtubules in green so it's looking that each a microtubule is attached to each sister chromatid um if there's not if you have something I'm going to go over here on the right if you have something like this and only one sister chromatid or one microt tual is attached when this one pulls it'll pull both chromatids this way and they will separate later but that means that that that daughter cell will have an extra chromosome an extra full chromosome that's an exact copy of that one so it could to have like the an extra first chromosome that's a problem the cell doesn't like extra chromosomes it has trouble dealing with them in its regulation so M checkpoint is making sure that the um microt tual spindle fibers the spindle checkpoint this m checkpoint is attached to e cister chromatid if it doesn't that is called non-disjunction non-disjunction is when they don't separate and those chromosomes both go to one side of the cell and end up giving that daughter cell will have the extra chromosome the cell that's going to come from this side is going to have an extra chromosome but the cell that the other side that should have gotten that cister chromatid will be shorter chromosome it won't have it it would lack one of its first chromosomes and again your cell in its regulatory processes have problems with that so if it's shter chromosome or longer chromosome has an extra one one cell both of those causes cells issues so spindle checkpoint is just to make sure that there is a spindle fiber attached to each um cister chromati okay the regulation how how this is kind of regul we have these checkpoints and what they're looking for this is just going to be a little bit summary your your book goes into a bit more detail but you will learn this more deeply in future classes um but there's two kind of General ways of regulating what we call positive regulation or positive regulators and negative Regulators so positive Regulators are things that are promoting going to the next cell cycle they are specific proteins that are made these different points um in the cell that look for this stuff and allow the cell to go forward negative Regulators stop the cell cycle they're not trying to promote it they're trying to keep the cell from going forward so cyclins and cyclin dependent kyes what we call cdks are the major component of our positive regulation cyclin are specific proteins they're little proteins that bind to a larger enzyme called kinases kinases are enzymes that phosphorate things and so kinases often will activate although they can also deactivate proteins so often they're activating the enzymes that are needed to make the proteins to make the cell go forward to the next cell cycle like like at the G1 checkpoint the specific cycle independent kinases activate the enzymes that are needed to do DNA replication to do that DNA synthesis and copy the D DNA so they regulate specific types of cyclin and their specific cdk cycl KES regulated each checkpoint the cyclin have to be made they have to attach to the kyes that's why those kyes are cycl dependent they need the cycl protein to attach to them and then they can activate the proteins or enzymes needed in the next step of the cell cycle that is positive regulation I'll talk a little bit more about cycle independent kinases on the next slide so cyclin are these proteins that change predictably over the cell cycle so we essentially know we they're different types and we see when they go up in the cell and then they go down as it goes into the next cycle so we can see where they're used um different signals trigger the making the production of specific cyclin so um cycl e is the specific cycl that activates that G1 right so size cell getting too large can trigger a production of this protein making this protein cycl e and then this cycl e attaches to a specific cdk that it can attach to when they bind together that causes them to activate a protein that then may make the enzymes to do DNA replication or they're activating the enzyme itself that does so uh DNA replication so cyclin attached to the cdk the kise that gets activated and essentially is going to get phosphorated um and then once it has that cycl and cdk are attached and have their phosphate group they can activate a protein itself that allows the next step for the cell cycle to happen so there was a bit complicated you don't need to worry about too much of the details you just need to know that cyclin and cdks the cyc independent kinases uh regulate each checkpoint they regulate the cell cycle they're the combination enzyme that is activating the proteins or enzymes needed to do the next part of the cell cycle so they need to be produced to then have what needs to be done to go on to the next step up the cell cycle cyclin and cdks are positive Regulators because they're promoting going forward right they're produced because the cell has a trigger that it intends to divide and so goes to the next stage um and they're checking they're doing the stuff at that checkpoint or they're they the cyclines and cdks are essentially activating or helping to make the enzymes and proteins that are needed to do the next part of the cell cycle um so that's promoting going forward a cell can also be kept from going forward with a negative um regulatory mechanism these are mostly at the G1 because remember I said G1 is where it's kind of committing to divide so if it's not going to be div if the cell should not or it's not supposed to divide it can essentially be inhibited from going forward um so transcription factors are little proteins that like turn on genes like your cdks are often activating a transcription Factor activating A protein that then it's going to turn on the enzymes that need to make um the enzymes for DNA replication so these transcription factors allow the cell cycle to proceed are blocked in negative regulatory proteins so it's like block the protein um that will turn on a gene keeps from going forward it's look at these as double negatives they're like right they're blocking something and then that keeps it from happening your book talks about a specific one you don't need to know the specific one um if you do read about this it kind of helps it make sense um like this molecule protein is blocking a transcription factor from binding to an enzyme that allows the cell to grow um if a cell gets big enough that will trigger see how it's phosphorated the Cyclone's probably phosphorated um that would allow it to be released and now it's going to make the enzymes to go into the next part of the cell cycle but if it's blocked it can it blocks that transcription Factor it keeps it from turning on the enzymes to go into the next stage and that's a type of negative regulatory it's blocking keeping it going forward um but then there's ways to unblock it certain triggers that allow it to proceed forward we've been talking about the cell cycle or I've been talking about the cell cycle and how it's regulated things can go wrong where those regulations the positive and negative controls are broken down those checkpoints don't do what they're supposed to do and the cell cycle continues when it shouldn't and that can lead to tumors cancer which we've all heard of and is really many different diseases that can be triggered by different agents a basic definition of cancer is uncontrolled cell growth so it's when something has gone wrong and those checkpoints aren't met but something is wrong or there is damage to DNA or something's wrong with the cell and the cell cycle checkpoints have been broken down and the cell continues to divide and passes on the problem the mutation or issue um when it shouldn't and so that can lead to cancer because you have uncontrolled cell growth we want to control the cell cycle when we don't control it that is where we get tumors and cells become cancerous so a mutation in a gene so the genes are the section of DNA that code for specific proteins you have all these regulatory proteins if a mutation in these regulatory proteins happens where now it doesn't function properly or maybe at all it's not doing its regulatory job that leads to tumors because you're not regulating the cell cycle tumors happen when these reproduction of these cells that have the mutation in them um surpass or become more than your normal cells so like they'll just keep growing an example of this of what we see when we can grow cells out in Petri dishes it's not hard and we can see a lot of stuff and how different things interact and drugs interact you can do a variety of things with cells and Petri dishes and something that we see is normal cells if you put normal cells here a health the growth medium so they have nutrients to be able to do their cell respiration and grow they're separate they're not touching each other you're just normal non-cancerous cells they'll grow to fill in the space in the petri dish but once they fill a layer and they're all touching they stop they have this thing called Contact inhibition they are density dependent when they become dense enough that they filled it in and they're all touching that inhibits cell the cell cycle and cell division cancer cells don't do this cancer cells have the mutation where they don't have that contact inhibition it's not exhibited even when they're touching each other they're not the cell cycle isn't stopped it just keeps going and they keep growing and that are those are cancerous cells and that can become a tuor and those cells can potentially spread to other cells in within the organism I'm going to talk more about cancer in the next slides as well this is not all of it but to set us up so tumors happen when you have this uncontrolled cell growth and that can come from essentially kind of two ways increased cell division where you have lots of cell division happening or reduced apoptosis so I haven't talked about apoptosis although I have seen some students in some my classes mention it apoptosis is called is defined as programmed cell death so earlier I mentioned cells killing themselves so something's wrong if damage can't be repaired the cell has mechanisms to go through apoptosis and essentially kill it self break down that cell and then use the parts of it to be used to make other healthy cells so apoptosis is a way of preventing damage if there's a DNA damage if there's multiple mutations on the DNA that can't be fixed cells can go through apoptosis and normally they will be triggered to do this it's a good thing it's what they want to do um when a proptosis doesn't happen so decrease this is the bottom one decrease apoptosis normal cells divide and some have normal apoptosis if something's bad's happening it let me go at the top here it kills those bad cells and you're kept with the functional cells and you're maintaining homeostasis let me go to the bottom with the apoptosis if you have decreased apoptosis so that um you're not killing off all your um cells that have a mutation they get passed on if that's not being controlled they get passed on and they can become tumors overgrowth you can have so then the next one that I'm talking about you also can have um increased cell division if cells are just dividing apoptosis is still happening in some cells but you have increased cell division happening too rapidly you can also get tumor so increase cell division or or decrease apoptosis um increases your chance of getting a tumor and having cancerous cells where you have this unregulated uncontrolled cell division now these come from your cells as they divide having a mutation which means these regulatory proteins that check the cell cycle aren't being made correctly and aren't functioning right or at all so they're not regulating the cell cycle meaning it's uncontrolled cell growth or they're the cell is not being triggered to do apoptosis so it doesn't stop dividing I just want to make a side note here because it's going to be important for next the next two units we think of mutations as bags we think oh things that cause mutation are bad which they are and can be if they increase the mutation past the normal level not all mutations are bad really every time your DNA copies itself on all those chromosomes there is going to be a mutation it just happens your cell goes back and checks for it and FES most but some it won't most of them aren't bad and have almost well really no effect on you because a lot of your DNA is non-coding meaning it doesn't make a protein so it doesn't affect it mutations that happen in your germline cells the cells that are going to become your sex cells could be good bad or neutral they are differences in that genetic sequence that get passed on to offspring potentially but it's not always a bad thing and we will get into that in the future so we are looking at mutations as bad in this chapter but I want to note here they're not always bad I also want to note that um mutations like I said do happen every time your DNA copies so I'm going to talk about Agents that increase the chance of mutation the more mutations you have throughout their life the more likely something like this is going to happen um that could cause cancer so this is why cancer does increase with the age and then there are agents that you can be exposed to that increase the chance of mutation cuz like I said mutations happen naturally and they could just happen naturally a faulty mutation not caused by anything um but just happens when your DNA copies so you can get cancer any time in life but there are different things that increase the chance and I'll talk more about those later your cells um you have genes that make proteins that help regulate the cell cycle some of these genes if a mutation happens it leads to a breakdown in the cell cycle and essentially promotes cancer and causes cancer we call these Proto onogen so enogen are genes that make a protein that cause cancer that lead to this cell cycle regulation if those Proto onco genes genes that are supposed to regulate the cell cycle become mutated and now they're not regulating a cell cycle they become enogen so some Proto onogen are like the genes that code for growth growth factor receptors so growth factors are released received by a cell and then that triggers the cell to go through cell division but it won't do that unless if the growth factor is that hormone that's growth factors are hormones uh is received but some receptors can be have a mutation that causes them to always be on where they don't need the growth factor hormone to then cause cell division they'll just go they'll just tell the cell to go through cell division even without that hormone and then that's not a good thing because now you have unregulated cell division because it's telling the cell to divide when it shouldn't um so protooncogenes are these genes that when a mutation happens essentially lead to tumors and cancer we have a number of tumor suppressor genes and these are the genes that codes for the proteins that will go back and repair the DNA damage or chromosomal damage help copy that DNA fix mutations that were made or will activate apoptosis like hey we can't fix it let's let's activate the proteins that are going to cause this cell to kill itself and do a proptosis so when activated these prevent uncontrolled cell division instead of passing on the damaged DNA the cell will kill itself and wouldn't pass it on um unfortunately those genes the proteins that make that help promote the things you want to cause apoptosis can be mutated where this is again that tble negative where now they're not stopping the cell cycle and the cell cycle is going to continue um cervical cancer often comes from a tumor suppressor chain being mutated that doesn't stop apotosis and pass it on on the next slide I'm going to talk about the common a common Gene that um seems to be damaged in a lot of types of cancer so p53 uh genes are often ital are italicized when you have you see that p-53 is a well-known Gene that is a tumor suppressor Gene it's a gene that when working normally will cause the cell cycle to stop repair the damage and then the cell can go back in the cell cycle or it is a major Gene that will trigger apoptosis if the cell cycle will stop the cell cycle and if it can't be fixed the cell does apoptosis we have found that in many cancerous cells that Gene p53 has had a mutation and um that mutation makes p53 where it doesn't trigger apoptosis and so the cell cycle continues when it shouldn't and those cells can become cancerous so p-53 is a major tumor suppressor Gene that in many cancers so we look at cancer cells we see that there's bit of mutation to that Gene um and it breaks down essentially regulating apoptosis when it should have happened and it doesn't last few things to touch on related to cancer that your book didn't really um go into as much that I just want to make sure you're aware of carcinogens are Agents that increase the chance of developing cancer so cancer cells happen in your cells it's your cells you're not getting cells from elsewhere that are cancerous they are your cells that have a mutation in them that has caused a breakdown in the cell cycle certain agents can increase the chance of mutation two very well-known well studied well documented agents are tobacco smoke and UV radiation tobacco smoke um is breathed in so it is hitting the lung cells a lot and that increases the chance of getting lung cancer of those cells having a mutation and um becoming cancerous it also increases a variety of other cancers throughout the body because um those molecules in the tobacco smoke are breathed in through the lungs and into the bloodstream and circulate in the body so it increases lots of types of cancer but lung cells is the major one we think about because it has such uh proximity it's hitting it's hitting that and increasing the chance so the longer you smoke and the more you smoke the greater your chances are and again they're chances it doesn't mean that everybody who smokes is always going to get it but you are definitely increasing your chances because you're increasing the chance of a mutation happening the longer you do it and the more you do it um it also doesn't mean if you don't smoke you won't get lung cancer non-smokers get lung cancer they're higher when they've been around cigarette smoke but but your cells are still dividing in your lungs and just when they're dividing a mutation can happen on its own so these mutations can happen at any time in your life in any cell that's dividing if it just happens to happen early or in a specific tissue type not because of anything you've done or any genetic component any reason you have it can just happen um so they are more likely cancers are more likely later in life both because your cells have been copied right you've been copying your your trillions of cells for decades now so just having a mutation is likelier the mutations to accumulate to get cancer later in life you've also been exposed to a lot more things throughout your life that could have also increased the chance of a mutation happening so like UV radiation um does DNA damage to your skin and can increase skin cancer genetic also play a role certain cancers um there are a high genetic predisposition and certain people with a mutated Gene uh are often very likely to get certain types of cancer uh breast cancer caused by certain mutation in the braa genes and two of the braa genes are well known right so like a braa gene is a tumor suppressor Gene if people have a certain mutation that we have identified that is common in certain people they are much more likely to develop breast cancer if they have that mutation so there are genetic um components to it and there are also infections we know that certain viruses HPV human Poma virus is the um wellknown one because we have a vaccine for it uh it's a FAL infection that can lead to um cancer right so the virus can essentially affect the cell and increase the mutation rate that can lead to cancer so there are different ways of getting this cancer though anybody can get a cancer anytime during their life just by chance alone of doing mitosis or really doing DNA this S phase of copying that DNA and we'll get into more of that next unit I'm sorry the slideshow has been so long um there's just a lot to say in here and I do usually do this lecture over two days in class um I hope you found it helpful take your time with it know your stages of mitosis know the cell cycle that will be a big part of the test um this is a video uh it's not anything you have to know but it's an interesting video you might want to hit the watching YouTube cuz I feel like my audio is going to be over it if you try to play it um but it's an interesting one related to your immune system trying to find and kill cancer cells um and cancer cells do try to hide from these as well um so hope you find that interesting and please take your time with this chapter let me know if you need help