16. Cell Division
Control of Cell Death
16. Cell Division
Control of Cell Death
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Hello, everyone in this lesson, We're going to talk about regulated or programmed cell death, which is also called apoptosis. Okay, so cells whenever they have been damaged in some way or aren't doing what they're supposed to be doing or if they are infected by a virus or something like that and they are told to actually commit suicide. This is a apoptosis and apoptosis is going to be the process of regulated. Okay, cell death, you'll also commonly see programmed cell death. It's gonna be the same exact thing, programmed cell death and regulated cell death is apoptosis and this is where the cell decides that it is going to basically commit suicide and it is going to break itself down into its parts and be destroyed. And this is a very extremely regulated process to ensure the health of the cells that surround the cell that is going through apoptosis. This is a really important process. You will definitely be asked about this process on your quizzes and your tests and it's really important because it balances cell division with apoptosis. So cell division and cell death need to be in balance or we're going to have things like cancer and tumors where cell division gets out of control and cell death is not working like it's supposed to. So apoptosis is controlled cellular death which is going to meet the same number as cell division. So we don't have too many cells in our body and we don't have things like growths and tumors. Now, this is a very regulated death. It's neat and clean and the reason that it's neat and clean is so it doesn't damage other cells. If you think about cells and the different organelles that we've learned about their organelles, license OEMs which contain enzymes that are really dangerous because they break down things like license OEMs are the recycling and garbage center of cells. So they're going to have these enzymes whose main job is to destroy things. Right? So if the license um, is ruptured and then the cell ruptures all of those enzymes whose job is to destroy are released into the body. And that's really problematic because then they start destroying things they're not supposed to be destroying. So apoptosis really get a handle on this because it doesn't allow these dangerous components of the cell. Things like license normal enzymes and stuff like that to be released randomly into the body. So that's why we're going to need this process because it's going to be very neat and tidy and compartmentalized. So what are some major things that are going to happen here are some of the major things, obviously not all of these steps of apoptosis are listed here. These are just some um, major steps. It is more complicated than this, but I want you to know that the cell is going to degrade in to blabs. Yes, that is a scientific term, no matter how much it sounds like it's not a scientific term. I'll show you a picture of a blob in just a second, basically a blob is where the cell, you know usually a cell is nice and round kind of like this. An animal cell. A blab is where the cell kind of starts to pinch off part of its um of its body. And then it's going to pinch off a whole bunch of different places. And basically this is going to be the main way that the cell is broken down into smaller components. Those blabs kind of push themselves out of the cell. Then they will be snipped off and then that will be a component and then it will be broken down in this way. So the cell is going to degrade into these compartments of plasma membrane and these different cellular compartments called blabs. Now the nuclear envelope is also going to degrade, it is going to break down and then the D. N. A. Is going to be cut up and destroyed by different D. N. A. Processing enzymes, the sido skeleton. The micro tubules acting filaments and intermediate filaments are going to be broken down and going to be collapsed so that the cell can be compartmentalized and then the cell is dismantled into a pop topic bodies. Whenever a blab actually is released into this little component that is going to be the a pop topic body. And basically you're going to see this big round cell be chopped up into all these little components called a pop topic bodies. And that is going to be a blab forms into a pop tart body. Now, this whole process of apoptosis can be controlled in two ways. Extrinsic lee or from the outside of the cell and intrinsically or from the inside of the cell. Apoptosis is determined by cellular signaling, as almost all things in the cell are. So the cell has to be given a signal to go into apoptosis. If its extrinsic it comes from the outside of the cell, meaning that an immune cell generally is telling that sell it needs to go through apoptosis. Generally, an immune cell will tell a body cell to do this if it's infected or if it's damaged in some way or for whatever reason, the immune cell doesn't believe that is fit to do its job. It will give us this extrinsic signal or signal from the outside and then that signal will trigger apoptosis. Now intrinsically is where the cell itself recognizes that it needs to go into apoptosis and it is going to have an internal signaling process that begins the process of apoptosis generally, this is going to happen when problems occur with the mitochondria. If the enzymes inside of the mitochondria leak into the cytoplasm because the mitochondria might be damaged, then apoptosis is generally going to occur. There are some other ways that this can happen, but that's one of the most common. So something goes wrong detrimentally wrong, that cannot be fixed and the signaling process begins to happen inside of the cell and the cell goes into apoptosis. So those are going to be the two signaling pathways that apoptosis can be triggered by. I'm gonna show you this image of apoptosis versus necrosis. Now, I haven't talked about necrosis yet, but necrosis is going to be different than apoptosis. It's not regulated cell death, basically, necrosis happens when you have an injury or the cell is diseased in some way or something happens. So, necrosis, if you fall and you scrape up your arm or something like that, those cells went through necrosis because they're physically damaged by an injury that is not controlled cell death. That is traumatic cell death. That's necrosis, It's messy. It's not clean, it's not compartmentalized and it allows the cells to kind of just burst and then the body has to clean it up from there. So apoptosis is a lot nicer, a lot cleaner, more regulated necrosis is going to be a traumatic cell death that was not planned for. Okay, so here's gonna be the process of cellular death. You can see the normal regular cell here that is going to begin cellular death. Here are those blabs I talked about that happen in both necrosis and apoptosis. You can see that they're kind of these little protrusions of the plasma membrane and then they continue out here and get larger and larger until they become these a pop topic bodies. Now, this is very regulated. You can see that these little a pop topic bodies are membrane enclosed and they're closing off all of the things inside of those little bodies. So nothing gets out into extra cellular matrix. That does not happen in necrosis. You can actually see in necrosis the plasma membrane is broken right here and you're going to see all these cellular components enter into the extra cellular matrix which can be dangerous to the surrounding cell. So that's why the body chooses to do cellular death in the regulated way. So the cells around the dying cells are not damaged. So those are going to be the different components of apoptosis. I'm going to go down and we're going to talk about the proteins that actually do this process. Okay, so the proteins that are involved in this process are going to be the Cast base proteins. And for apoptosis, Cast spaces are the proteins responsible for degrading The different cellular components. I believe cast spaces are known to degrade or break down 600 different cellular components which is a ton right now, Cast spaces are going to do the heavy lifting but before they're actually activated, they're called Pro sorry about that guys, they are called Pro cast spaces. Pro cast spaces are in the the precursor form because think about it. Do you want destroying proteins just roaming around the cell all the time. No. So in this, Pro cast basis form. These proteins are not degrading, not destroying anything. In fact, they have to be activated to turn into caste based proteins Because we don't want these dangerous degrading destroying caste based proteins just roaming around the cell all the time. We only want them activated when apoptosis is triggered. So the pro cast base must be activated via cleavage. So basically you take the pro caste based protein, cut some of it off and it turns into a caste based protein which is activated and ready to go. And then certain activated cast based proteins can be utilized to activate other caste based proteins. So some caste based proteins that I do want you to know. So Cast spaces are gonna be too important types. The first one is going to be the initiator Cast spaces. Initiator cast spaces, you can probably guess what they do. They're going to activate other cast spaces so activate cast spaces. They're gonna cause kind of like this chain reaction, activating cast bases and other enzymes that are utilized for degradation and apoptosis. Now, the second type I want you to remember have a really great name. They are the executioner cap space is you can probably guess what they are going to do. They are going to break down the cell. They are actually going to break down the cellular components and begin breaking down that cell. Now, initiator capsizes are going to be activating other caps cases including executioner capsizes telling those executioner capsizes to begin basically killing the cell and breaking down its different components. So those are some important cast spaces, you should know now, what if the cell doesn't want to go into apoptosis most of that time? It doesn't. Right, So how do we stop these processes from happening when the cell does not need to go into apoptosis, we're going to use the inhibitors of apoptosis. These inhibitors bind to and inhibit the cast spaces. So either they're going to stop pro cast spaces from turning into cast spaces or they're going to stop cast spaces from functioning. So if pro cast spaces cannot be cleaved or cut to activate them, they can't turn into degrading cap spaces and inhibitors of apoptosis are also going to bind to already activated cast spaces and turn them off. So, those are very important, especially when the cell does not want to go into apoptosis. Now, down here in this diagram, a lot of it, I don't really need you to know. I just wanted you guys to look at these things that I'm going to highlight here in blue. These two or these two caste based proteins in the pro caste based protein. So, Pro Cast Base eight is obviously a pro cast base and what do pro cast spaces do? Well remember they're going to cleave, they're going to be cut and this arrow here is representing the cleavage event. This is where part of the pro cast space is going to be cut off and you can actually see this cutting happening right here and part of the pro cast space is removed now, what happens? What does it turn into? It turns into this cast space No eight, but what type of cast space is this? Can we determine this? Well look, this cast spaces interacting with another cast space. So it must be some sort of initiator cast space. So this is an initiator. Cast space. Cast Base number eight is going to be an initiator cap space. Now, since this cast spaces interacting with cap space, number three, we know that this is going to be an activation event represented by this arrow right here. Now, what does that mean? That means that cast base number three must be doing something else. And you can see that caste based number three is leading to cellular death. So what type of cast base is going to be cast Base number three, it is going to be an executioner cap space because it is going to be actually breaking down the different cellular components. So there is a pro cast base that is cleaved and activated, turned into an initiator cap space which then activates the executioner cast spaces which bring on cellular death by degrading the different cellular components. So that is a great example of a chain reaction that occurs in these cast based kind of cascades or pathways that lead to apoptosis. I I know I went over a lot everyone, but I hope it was helpful. Apoptosis is definitely something you're going to need to know. It's very highly tested upon. Just remember Apoptosis is going to be regulated in programmed cellular death that is highly controlled so that the other cells around the dying cells do not become damaged. And it is going to utilize different proteins like Cast basis to begin degrading the different cellular components. Okay, everyone. Let's go on to our next topic.
Triggering Cell Death
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Okay. So now let's talk about how a apoptosis is triggered. So there's two ways the intrinsic pathway and the extrinsic pathway and we're gonna go through both of them. So first focus on the intrinsic pathway which is going to regulate and trigger a apoptosis based on intracellular proteins. So the first one I want to talk to you about is the BCL two family of proteins. And this family inhibits apoptosis. So I'm going to walk through backwards what happened? So first there's this molecule called cytochrome C. And we've talked about cytochrome c before, Do you remember when we talked about it? Right? So cytochrome C is important for oxidative phosphor relation. So where is it found found in the mitochondria? But when cytochrome C is released from the mitochondria, that actually will trigger a apoptosis because cytochrome C. Will bind to a bunch of side assault proteins which then will lead a apoptosis. So when a cytochrome C released from the mitochondria, well it's released due to DNA damage which of course if the D. N. A. Is just completely damaged the cell is going to want to die kill itself so that that's not passed on through further generations. So when there's DNA damage, there are two proteins that are released, they're called backs and bad backs and bad act to release cytochrome C into the side of saul which will then bind to proteins and stimulate apoptosis. So that's how apoptosis can be stimulated but it can be inhibited by these BCL two proteins which bind to backs or bad and prevent cytochrome c release. So this is going to inhibit and this is going to activate. So if we look at this pathway, what we get is we get some kind of stimuli maybe DNA damage for instance that tells the cell um it needs to die. So then it can activate backs it can also activate bad. Um and this will stimulate cytochrome c release. You can see here is being released which will result in a apoptosis or cell death. So that's kind of those intracellular proteins. There is an extrinsic pathway where extra cellular proteins also play a role. So they play a role through usually binding something called death receptors. So death receptors are receptors on the plasma membrane um and they when they're activated usually by binding some kind of ligand, they trigger apoptosis. So an example of this is the fast receptor, it combined the fast ligand and when it's bound it will actually activate this special complex called the disc complex or the death inducing signaling complex which will stimulate apoptosis. Now the opposite of that is going to be survival factors when a apoptosis needs to be suppressed. And so these work by inhibiting the bad which remember trigger the interested pathway and regulate the BCL two families which is also the intrinsic pathway but these are the two main extra extra cellular pathways. So here we have the fast receptor. So here we have the fast leg in in the fast receptor and you can see that once it's activated it will form this disc complex and you don't need to know any of these proteins. But you can see here that it activates a lot of cast spaces through here, which will trigger, you know, cytochrome C release into the side of salt. But essentially this will cause apoptosis. So that's how the intrinsic and the extrinsic pathways work to trigger a apoptosis. So now let's move on.
Apoptosis can only be stimulated through intracellular signals.
In the intrinsic pathway of regulating apoptosis, Bcl2 controls what?
It releases cytochrome C from the mitochondria
It binds to cytochrome C and prevents its release
It binds to Bad and Bax and prevents cytochrome C release
It binds to Bad and Bax and triggers cytochrome C release