Transcript for: Understanding Cell Cycle and Mitosis
[Professor] Now, the next two lectures are still following this same thing that I was talking
about as far as genetics and hereditary means
and all that, you know, the six chapters that I discussed that we'd be going through. But these next two in
particular are tied closely, associated with one another, because we're going to
talk about how cells divide and then how that applies
to things like cancer, okay. So this lecture, cellular reproduction, is looking at the dynamics
of one cell becoming two. So it's fairly straightforward. There is some new terminology
you're going to have to learn that is probably just the
most difficult part of it, because a lot of the words start with C like chromosome and chromatin and centromere and no,
I didn't make these up. Okay, so, but you're going to have to
learn a lot of this terminology as we go through. But other than that, it's pretty
simple and straightforward as far as this application. But then, we'll see in lecture 13, that this has everything to do with cancer because ultimately, we ride this fine line through our lives of cell
growth and cell death, okay. We're always riding that line. If we go too far to one side of the line where we have too much cell
growth, we have cancer. If we go too far to the
other side of the line, where we have too much cell death, then our organs fail and we die. And that's really what
happens later on in life. We usually have one or the other. We either have the cells
just growing out of control because they've had too
many genetic problems or other environmental
issues and you get cancer. Or on the other side, you know, this is why your skin wrinkles
and organs start failing, because the adult STEM cells that are designed to regenerate
the cells after they die, start wearing out and dying themselves. And now, you can't
regenerate your tissues. So we ride that line all
the way through our life. Even as we're developing as an embryo, we ride that line because cell death during development is as important as cell growth. Now, the death is controlled and we talked about this back
when we discussed organelles, lysosomes are part of a process that's already pre-programmed into the cells called apoptosis, okay. Remember, this is programmed cell death. If we didn't have apoptosis, you would have webbed
fingers and webbed toes and your brain would be
three times the size. Now that's not a good
thing with your brain because you'd be dead. Your brain reestablishes those connections by having some cells dye
and other cells, not. So if you didn't have apoptosis during the formation of your brain and your other organs, you wouldn't develop properly
and you'd dead, okay. So in one case, if you don't have apoptosis
in your fingers, yeah, you're the man from Atlantis and all that, I'm dating myself. That was a TV show a long time ago. Or will show how the difference
between chickens and ducks, where the chickens have three toes and the ducks have webbed feet. And that really comes down to apoptosis. Now, the overall process of cell growth, we call it the cell cycle. A small portion of the cell cycle is the actual cell division process where one cell becomes two. We call that mytosis. So that's really what we're
going to focus on today is what is mytosis, what happens during mytosis and the like. But we're also going to look at a lot of the applications of that. Now, there's another process
later on in lecture 14, that we're going to discuss
related to sexual reproduction called meiosis because in meiosis it's a completely different process as far as what it's for and
what the end results are. Ultimately, instead of creating two cells that are genetically
identical to one another, which is mytosis, you're creating these cells that have half the genetic information, and it's been scrambled
up to mix and match what you've gotten from your parents. That's meiosis. Now, from the moment when the sperm and egg come together and
fertilize one another, that forms that zygote,
that is the STEM cell that makes every cell in your body. From that point, it's pretty much mytosis
throughout your whole life. From the moment of conception to the development of the fetus, to you're growing into an adult and even as an adult, most of what goes on your body is mytosis. But in very specific organs, we do have meiosis going on
during periods of our lives. And we'll get into that in lecture 14. So what's one of the first applications, 'cause this is one of your first questions on this lecture is what is mytosis for? Well, the first application
is growth and development. As you can see here, here's a picture of a zygote and how it splits and becomes two. Each one of those splits and becomes two. And in this process, the cell has to constantly
copy all of its DNA and then equally separate the copies so that each cell gets
the exact same blueprint. That's why identical twins are identical. So if you look at this
about four days later, you get this what's called blastocyst. And on this outer ring
called the trophoblast, this is where the placenta and
the amniotic SAC form from, but this inner cell mass right here, that's what forms you. Now on the occasion, these cells can split early on and form two inner cell
masses that each can develop into all the cells of an organism and that is identical twins. Now fraternal twins are essentially two separate fertilization events. A woman will ovulate two eggs. And there's more than
enough sperm from the guy for the eggs to be fertilized, now- - [Student] And that happens a lot. - [Professor] Yeah, in in vitro because they usually will
cause several fertilized, and they'll implant a couple. And they do a couple
because a lot of times, only one implants, but
sometimes two implant, as well. So yeah, it's more than common to have two or fraternal twins and in
vitro than to have one. Now ultimately, you can
see from this cell mass, ultimately, it starts undergoing the embryonic development and grow. So one of the main reasons of mytosis is to increase in the cell number. You just get more and more. We're made of trillions of cells, okay. We start from one and it
eventually becomes a trillion. So that's where growth and
development come into play. Now, once we reach adulthood
and even before that, as we're growing up, the second reason why we
undergo mytosis is for repair. We're constantly renewing our tissues. Our skin is growing once a day. Our blood is being renewed at about 3 million red
blood cells a minute, okay. So of the trillions of cells that we have, we're constantly regenerating
and renewing them. And that comes from our adult STEM cells. In each of our organs, our
tissues are being regenerated. Now, as we get older, that gets less and less efficient until the point where we just
can't regenerate anymore. But those are the main
reasons why mytosis occurs. Now, there's one more reason. It doesn't occur in us, but it does occur in other organisms like plants and fungi and produce and whatnot. And that is asexual reproduction. This is cloning. This is reproductive cloning. Like I showed you last
lecture with the plant that the cells will undergo
asexual reproduction where they'll regenerate
and renew the whole plant. And they'll do, and fungi will do this. And bacteria will do this where they're only a
single cell organisms. So in fact, their only mode
of reproduction is asexual. So cloning is asexual
reproduction in these organisms. And that is another reason for mytosis. So let's review. We have growth, development, repair, slash regeneration. Okay, so we cut our skin,
we're going to repair it. But even if we don't cut our skin, we're regenerating it on a daily
basis, one layer every day. So these are all the reasons. Notice, that's the majority of things. That's the majority of
life is mytosis, okay. It's only key times and events where you actually have
sexual reproduction, which is not a cloning process. So that's really the
only thing that mytosis is not used for is for
sexual reproduction. - [Student] So is meiosis
sexual? (faint talking) - [Professor] Meiosis is a
sexual reproduction, yep. That's the process that is only involved in sexual reproduction. So here's the picture of
the chickens and the ducks where the chickens have three digits, whereas the ducks have webbed feet. And that comes down to whether
apoptosis occurred or not. So here, like with our hands
and fingers and whatnot, we had apoptosis occur between the digits, whereas with ducks, they don't. And so that's why they
have the webbed feet. This occurs in our brains and in all of our little organs, as well. So again, the long and short of it is cell death is as crucial
for life as cell growth is. Now, let's look at a process
we've already discussed before, but look at its application
to the whole genome, okay. What am I talking about? I'm talking about
semi-conservative DNA replication. So this process where
we take all of our DNA and we copy it, this is synonymous with what
we call chromosome duplication. Now all cells, when they undergo this
process of mytosis first, must duplicate all of their chromosomes. So that by the end, when the cell goes through
the process of mytosis and splits the copies evenly between the two halves of the cell, once the cell splits, the two new cells are
going to have exact copies of the original DNA. There's always going to
be one or two mistakes. In fact, in about 5
billion nucleotides copied, the cell only makes about three mistakes. That's how good it is. So, chromosome duplication. Now, we have to talk a little bit about what a chromosome looks like because unlike bacteria, where their DNA is this big,
long, big, big circle of DNA, big plasma, as we call it, we have linear strands of DNA. Well, there's a problem with that. They could easily get
tangled up with each other and become very difficult to work with. So, the way that our DNA is organized is it'll wrap around these
proteins called histones. And it just keeps wrapping
around these proteins every few hundred nucleotides, of about 200 nucleotides
for each one of these of the billions. So you can see that actually
most of our chromosomes are made of protein. About two thirds of our
chromosomes are made of protein. And the other third of it is the DNA. It's like taking string
and spooling it up. If you don't, it's
going to get tangled up. It's going to be useless. You won't be able to work with it. And the same thing with our DNA. Because it's linear, we wrap it around these proteins for easier management and control, okay. So what do we call it? We call this chromatin, okay. Here's one of those
words I was telling you that you're gonna have to remember. So if we say, what is
a chromosome made of? We say chromosomes are made of chromatin, which is just DNA wrapped around proteins. That's what chromatin. Well, sometimes we like
to delineate even further and say, well, what are those
individual groups called? They're called nucleosomes. Now, don't confuse this with nucleotides. Nucleotides are the individual monomers that make up the DNA, okay. There's the phosphate sugar and base that get covalently bonded
to form the millions of chains, long, of nucleotides
that make up your DNA. Nucleosomes is the double
stranded DNA wrapped around proteins. So a single unit is called a nuclesome. So we could say a chromosome
is made of chromatin. Chromatin is just repeating nucleosomes. Now, not all organisms have
the same number of chromosomes. Humans have 46. We usually know this. But other organisms have more or less. Chickens have 78. Rice has 24. And it doesn't matter how
many chromosomes you have. It's how you use the
genetic information, okay. Because chickens have 78 chromosomes, but they're not as smart as you and I. Trust me, I've got five. They're morons. And so, we have 46 chromosomes. They have 78. Dumb things, try to bite
me when I get the eggs. Alright, but rice has 24. And so it just varies. But remember, only 2% of actually all
that genetic information actually encodes genes. And in fact, there are other organisms that have almost as
many genes as you and I, but are not nearly as complex as us. So a lot of it comes down to how we manage our genes and make splice variants
and all kinds of stuff. So again, more chromosomes doesn't mean more advanced or more intelligent, by far. Okay, so here's the slide showing you about chromatin and all that. - [Student] What would
happen is the human had 45 chromosomes? (faint talking) - [Professor] Good question. I'll give you a prelude to it. We're going to talk
about that in lecture 14, but one less or one more chromosome is more than likely fatal. We cannot vary from that 46. If you are losing any one,
let me just jump ahead, right here. If you're missing any
one of these chromosomes, or even if you have one extra
of almost any one of these, the fetus aborts. It's too much or too
little genetic information. We ride this line, exactly. Now there are exceptions to that. For example, if you get an
extra one of this chromosome, which is one of the smallest ones, that's where Down
syndrome comes into play. And sometimes, we can end up
having extra sex chromosomes, which doesn't cause hermaphroditism. In fact, a lot of men, about 17% of men that they take genetics from
have an extra Y chromosome. And then, it doesn't do anything to have that extra Y chromosome. So in the case of sex chromosomes, that's where you have
most of the exceptions. But in all of these other chromosomes, one more or one less is pretty much fatal. Now, plants have the ability to kind of overcome duplications of
their chromosomes and whatnot. So it's really animals
that have a difficult time with chromosome number changes and duplications and things like that. So this is what our genome looks like. This is what's called a karyotype where we were to take
all of the chromosomes and lay them out and look at them. Notice, they're all different sizes. Some are much longer and
some are much smaller. Obviously the longer they are, the more DNA they have,
the more genes they have. Let's look at the sex chromosomes. On the Y chromosome, there's
about a hundred genes or so. The X chromosome has a thousand, more than a thousand genes on it. So really, the length of the chromosome tells you how much genetic
information is there. You can pretty much assume
that there are more genes on these longer chromosomes and fewer genes on these
smaller chromosomes. That's why, if you get
an extra chromosome 21, that's one of the few exceptions to be able to have a, is what causes Down syndrome. Now, it causes enough
problems in the development, but it's also one of the smallest
chromosomes that we have. So there's not that many genes on it. - [Student] So is it less chromosomes that could cause Down syndrome or? - Extra, one extra right
here in chromosome 21. And we'll cover that when we get into sexual reproduction, 'cause that's really when it happens is when we divide our chromosomes, we end up accidentally giving one more. Now, the full compliment of chromosomes of any organism is what's called
their diploid number, okay. So humans have 46 chromosomes. Now, where'd we get those 46? We actually got half from each parent. So we got 23 from her mother
and 23 from her father. That's why the paternity test
works the way that it does is because if you look at
all of these chromosomes, if you got this one from your mother, then you had to have gotten
that one from your father and so on and so forth as
you go down the line, okay. So, we get one, we have these, what are called homologous pairs. We get one from each parent. So that's our full
compliment is our diploid, di means two, or we have two sets of
all of our chromosomes. So we have 23 types of
chromosomes in total, but 46 because we have two of every kind. Now, this is also why when we
undergo sexual reproduction, that the gametes, which are the sperm and the egg, are what we call haploid. We only pass on one of
each of these chromosomes when we undergo sexual reproduction. And it's a crap shoot on which one. So here, we've got our
chromosomes from our parents. I may pass on chromosome
one from my mother, but chromosome two from my father and chromosome three from my father and chromosome four from my mother. And this is why genetically, the offspring is a mixing
and matching of your genetics 'cause they're going to be
some parts from your father and some parts from your
mother and so on and so forth. So, it's a crap shoot on
which one you pass on. But when you look at
two parents and a child, the child is going to, if it's the biological parents, share one short repeat from
each of the parents chromosomes. So that's why that works. Now, so haploid means half
of the genetic information or one of each of your chromosomes. And that's really only
going to occur in meiosis when you're creating the sperm or the egg. - [Student] It's half (faint talking)? - [Professor] Haploid. - Half way?
Haploid. Right here, haploid.
Oh thank you, haploid. - [Professor] So you're going to make sure you understand those two words. They are going to show
up on a question or two, but diploid is the full
set of chromosomes. Haploid is half or one of
each of the chromosomes instead of two of all the chromosomes. All right. Now, let's look at the cell cycle. Most of the time, the cell spends its time in
what's called interphase. This is where it's transcribing
genes from DNA to RNA,, translating them from RNA to protein, undergoing metabolism,
breaking down sugars and fats and proteins in the mitochondria. It's doing all the things
that a cell is doing to stay alive, to maintain homeostasis, to work and function the way that it does. Liver breaks down toxic materials. Your neurons are
functioning the way they do. Pretty much all your cells spend most of their time in interphase, but a lot of cells will undergo mytosis, which is a very small
segment of the cell cycle, as you can see right here. Mytosis is the actual cell
division process, okay. So when we say the cell cycle, and this is where one of your
questions comes into play. I may ask you, what is the main, which of the following
phases does the cell spend most of its time in, in the cell cycle? And the answer is interphase. So during the interphase, we have what's called growth phases where the cell enlarges, makes
more of the cell membrane, gets energy. Does all the things that a cell does. But if a cell is committed to divide, then it also must undergo
what's called the S phase, which is, this is where semi-conservative DNA replication occurs, okay. Remember, we said that's the part where you take all of your chromosomes, all of your DNA, you split it in half. That's the healer case. The pyrimidine comes in
and copies everything. The ligase repairs those broken strands. That's what we talked
about in the last lectures. That's it right there. This stage, notice it's
a big chunk of it, too. It takes a while to do this. Copies all of your DNA, because eventually, when it
reaches the stage of mytosis, it's going to need to
separate those copies so that each new cell gets the exact same information. And that's really what
the purpose of mytosis is, is to take the copies of your DNA and separate them equally so that each cell gets one of the copies and they're both identical. And that's really what
mytosis is all about. Now, as we talk about what's
going on during these stages, a few more things are going to come up. When we talked about organelles, we mentioned the cytoskeleton. Well, part of the cytoskeleton are a group of organelles
called the centrioles. Now the centrioles are these
churro-shaped organelles. Haven't eaten lunch today. Churro-shaped organelles
that create the microtubules. Now, the microtubules during
normal cell processes, are mainly used to traffic
things across the cell. But in this scenario, it's actually used as a kind of muscle. Now it's not actual muscle, but it's used as kind of
muscles to move things around. This is what's called the mitotic spindle. So these microtubules or this
spider web of microtubules, this net, is a key component
of the mytosis process. So just make sure you understand, when I say mitotic spindle, these are the microtubules,
those large hollow tubes, that are performing a different function, which is to organize the DNA and actually carry out the
separation of the copies. - Sorry, I have a question.
Uh huh. - [Student] So you say that
they occur (faint talking). - [Professor] Mitotic spindle. (student faintly talking)
Yeah. Alright. Now, before we get to that, there's some more terminology
you've got to learn. When a chromosome gets duplicated through semi-conservative DNA replication, the two copies need to be held together during the whole process of mytosis until a certain point. They're held together
by a group of proteins called a centromere, okay. So the centromere will actually connect the two copied chromosomes. Now, we don't call them
copied chromosomes. We call them sister chromatids, okay. So chromatids, or sister chromatids, are essentially duplicated chromosomes. They are exactly the same from
one end down to the other. That's what semi-conservative
DNA replication did. It took one chromosome and
it turned it into two, okay. So here's just a very high magnification electron scanning micrograph showing you, the sister chromatids of
each of the chromosomes. The yellow is the pseudo-colored,
it's not actually yellow, but it's pseudo-colored
to show you the centromere that is holding the two
sister chromatids together for each of the copies, okay. So, here's the terminology
that is going to be in the questions. This is what I told you,
the most difficult part. You have a chromosome. Remember, humans have 46 of them. Discrete lengths of DNA
wrapped around protein. We call that repeating DNA wrapped around proteins, chromatin. When you copy a chromosome, they become sister chromatids. They're held together in the
middle by a centromere, okay. So a lot of C's there. And I didn't name this stuff. Speaking of naming stuff, dependent upon which book
you use, scientists lately, it's changed over the last decade, lately, they're trying to take prophase, which is the first stage of mytosis and split it up into a second phase. And even then, they're
not in full agreeance, agreement with it. In fact, one book may say prophase and or early prophase and late prophase. One says prophase and prometaphase. One just says prophase. You know what, screw it. Prometaphase doesn't exist in my class. So, because it just changes
from one thing to the next. The reason for that is
because prophase is so long, they're like, well,
we've got to split it up. No, you don't. You don't have to, okay. So the four stages of mytosis are prophase, metaphase,
anaphase and telophase. Those are the four phases
that I will test you on. So even though your book, as well as other resources, might try to split a prophase
into two separate things, no, it's just prophase, okay. (student faintly talking) In what? (student faintly talking) Yeah, yeah. Now prophase, let's look at why because this will come up on
another question, as well, when we just look at some
of the relative links of these things. Let's say that, you've got
these four phases and let's say, let's take skin, for example. Skin has a cell cycle of about 24 hours. Well, in that 24-hour period, 22 of those hours is spent in interphase, which was remember, is the growth and it's where the DNA is being replicated and all that stuff. So the remaining two
hours is spent in mytosis. Now, when mytosis occurs, everything else pretty much shuts down. You can't transcribe the DNA into RNA. And you don't translate it into proteins because it devotes pretty
much all of its resources to separating the copy DNAs, cutting the cell in half,
doing all these things. So pretty much, everything
gets put on hold. So this has to occur fairly
rapidly by comparison to the other things that
the cell is going to do. Well, let's say that
this is a two-hour period in which this occurs. Over half of it takes place in prophase. That's why scientists are like, well, we got to split it up into
smaller chunks, you know. No you don't, okay. So, this is by far one
of the longest phases because the building up to getting all of these other things
done, just take so much time. As a result, typically, metaphase and anaphase are really quick. Now, metaphase is by
far one of the shortest of these stages and then
anaphase and telophase, they range in their overall mechanics. But prophase, by far, is the longest and metaphase is, by far,
the shortest of these phases. So let's talk about what
happens during them. (students faintly talking) Well prophase is one of
the phases of mytosis. These are the four phases of mytosis. So if you look at the cell cycle, you can see here that you have interphase and then here's mytosis. And in mytosis, we've got the four phases. - Oh, I see.
Yeah. Now, whether it is, I'll describe what this PowerPoint
is doing, so you'll see. Whether it's an animal
cell or a plant cell or a protease or something like that, it's pretty much the same, that the mechanics of how mytosis occurs does not vary from animals to plant cells. So in this picture, you see
animal plant cells side-by-side, and they may look a little
different, but in reality, what's happening is the same, universally, for all of these cells. Well, at least eukaryotic cells, prokaryotic is a little different, but we're not going to talk about those. Alright. So, the first phase,
prophase, what happens? Well, there's three major events, okay. The first thing that has to happen is because the DNA through an interphase needs to be accessible, it's usually spooled out, you know. It's not condensed. It's very easily accessible
to a lot of proteins and whatnot, but when you want to move the chromosomes around, it's not very good for management. So, in order for you to easily
move the chromosomes around, they have to super coil
and become super condensed. Now, this picture right
here illustrates that. Ultimately, the DNA, the
chromatin is super coiling in on itself and continuing to coil until it becomes super condensed. In fact, so condensed
that you could see it under a light microscope. Now, normally you can't. You wouldn't be able to see
the individual chromatin fibers of DNA wrapped around
protein during interphase, but during prophase and
metaphase and anaphase, you can definitely see
the condensed chromosomes. - [Student] So this would
be the first of the three. - Right.
In prophase. - [Professor] This is the
first of the three events in prophase. So that takes awhile to condense all of your chromatin down, all right. But now that it's condensed, the cell no longer worries
about things coming in and damaging it. It's kind of like putting a big, you know, a seal on your book so nothing can go in and
access that information. As such, it has no problem
releasing the chromosomes into the cytoplasm because in order for the cell to start maneuvering
the chromosomes around and lining them up, it can't remain in the nucleus. So the second thing that has to happen is the nuclear envelope,
essentially disintegrates. So the nuclear envelope. Remember how it protects the DNA and the DNA needs that protection. Well, now the chromatin
is so packed in together that it's not worried about that and it needs to be able to release it, to move it around. So, the second event
is the nuclear envelope essentially breaks apart, breaks into all these different pieces. Now the chromosomes are all
splayed out in the cytoplasm. Now, here's the third event. Remember that mitotic
spindle I told you about. The centrioles essentially
moved to opposite ends of the cell and create this
huge network of microtubules across the cell. I mean, across the entire cell. And the microtubules, essentially attach to the centromeres of all
of the sister chromatids. Coming back to this picture right here. Remember, here's the centromere that holds the sister chromatids together. So the mitotic spindle actually attached to both ends of the centromere. So third thing that happens, mitotic spindle forms and the microtubules, which make up the spindle, attach to all of the centromeres of all of the sister chromatids. That's why it takes so long. You can see huge processes
occurring here in prophase, okay. So again, recap. Chromatin condenses. Nuclear envelope breaks apart. Mitotic spindle forms and
attaches to sister chromatids. That's prophase in a
nutshell, essentially. Alright, so notice that the chromosomes, or I should say sister
chromatids at this point are all scattered everywhere. Well, in order for the cell to make sure that they're separated
properly, it will pull, the mitotic spindle will pull
on all of the chromosomes until they're all perfectly
lined up along the middle. That's metaphase. So metaphase is the sorting process that lines up all of the sister chromatids along the middle, and you
can think M for middle. Sometimes we use the word
equator, like the equator, the middle of the Earth or whatnot. So, the middle of the cell is where all of the sister
chromatids line up, okay. That's it, that's metaphase. That's why it's so short. It just lines up all of
the sister chromatids. Now, this next part is crucial. Anaphase. At this point, the cells ready to split all of the chromosome copies. So what happens is the mitotic spindle pulls sister chromatids
apart from one another. It grabs one on each end
and essentially pulls them to opposite ends of the cell. In this way, ensuring
that the two new cells that are going to be
created through this process have the exact same genetic information. So one copy goes into
one side of the cell. The other copy goes into
the other side of the cell. That's anaphase. So sister chromatids are
separate from one another. Now, here's the easy
thing about telophase. It is the exact opposite of prophase. Exact opposite. Now, it doesn't take as long as prophase, but it is the exact opposite. All right, so let's look at what happens. Now that the chromatids
have been separated, the mitotic spindles is no longer need it. So it breaks down, okay. So prophase, the mitotic
spindle is created and attaches to the chromatids. Telophase, mitotic spindle breaks down. It's no longer needed, it's done. Second thing, the nuclear envelope now needs to reform around these two groups of
chromatids to protect them again. 'Cause the cells going to
go back into interphase and start accessing the DNA. It needs to protect them and regulate access to
that genetic information. So the nuclear envelopes
reform around the chromatids. And the third and final thing is, now, the cells are going to
start entering into interphase once they split into two. And these have access to the DNA. So the chromatids starts
unraveling or unwinding. So in prophase, it condenses. In telophase, it unravels. Now cytokinesis is not
technically a phase of mytosis. And one of the reasons for that is because though it almost always occurs, there are certain situations where cells will undergo mytosis, where they split their chromosomes
into two separate nuclei, but not divide the cytoplasm. So cytokinesis is the process where the cytoplasm gets split up and you get two cells as a result. So what are some of
the exceptions of this? Well, your muscle cells, for example, stretch the entire length of your muscle. And so, it's one long continuous cell. However, due to the small
nature of these cells, they need to be able to
construct the proteins that they need to be
able to repair themselves and maintain homeostasis. So they are what we call multinucleated, where they've undergone
these rounds of mytosis, but not cytokinesis. So, this is a situation
where in your muscle cells, you don't get cytokinesis,
but you do get mytosis. You do get the cells getting longer and undergoing meiosis but
they don't split the cytoplasm. Most scenarios, you do get cytokinesis. Now, there's two main ways
in which cytokinesis occurs, depending upon the organism. If you're an organism
that has a cell wall, which is, remember, how
plants protect themselves, as well as maintain
their overall structure, they can't pinch in half. And so, the only way in
which the cells can split the cytoplasm is to
create a new cell plate, which is essentially a new cell wall and a new cell membrane that will ultimately divide
the two daughter cells into two completely separate cells, okay. So this process is accomplished by the Golgi apparatus in plant cells. Now, in animal cells, because
we don't have a cell wall, we can pinch the cell in half. And these, this is accomplished
by the cytoskeleton. Essentially, there are
these actin filaments, the very thin filaments that
are part of the cytoskeleton that will cause this, what we call contractile ring that will essentially squeeze
the membrane together, eventually, pinching it into
two separate daughter cells. Because of the plasticity of the membrane, it's able to do this. So, though photokinesis,
ultimately, it's the same thing in plant and animal cells, the way in which these cells accomplish it is a little different.