hi in this video, we're gonna talk about G one phase and s phase entry. So we're at the very beginning of the cell cycle here. So G one phase is a growth phase that occurs after interface, but before DNA replication and cell division. So this is the phase that the cell is just growing, it's getting ready to divide, it's helping, you know, create all these things that it's gonna need to divide into two cells. Um So it's just growing a lot. Um and this is a really important time for cell cycle regulation because once the sale says okay, I'm leaving G one phase and entering S. Phase, um it's got to commit to that because once it gets to s phase the cell has to divide or die. So if G one phase hasn't done its job and it's the cell enters s phase, it's either going to divide and it's not going to be big enough or it's not gonna be able to divide and it's gonna die and that's just a waste of a cell. Right? So um this transition here is regulated by the start checkpoint. So just important to know that start, you know, is this checkpoint super important and is crucial in this G. One to S phase. Now, what stimulates the cell to grow. So these are things called my pigeons and my pigeons are just these extra cellular signals that can be hormones that can be chemicals that can be proteins. Just these extra cellular signals that the cell receives usually during interface, that say, okay, I'm getting ready to divide. So we need to start growing and so my regions usually when they interact with the cell, they stimulate some kind of downstream pathway that will activate these cyclones and cycling dependent kindnesses for the G. One phase. But they also inhibit things like S. And M. Face cycling right? Because sometimes the cells have just divided and very fast growing cells or sometimes there might be like residual of these left over but the cells like okay I need to grow before I go into S. Phase or in phase. So if there's any of these lying around either from a previous cell or just low levels of expression, these mighty gens come in and they inhibit them so that the cell has time to grow before um the cell can divide. So this is kind of an example of this. Um you don't need to know any of these particular names but what you see is there some type of Mycogen signal here? And they come in and they activate cyclones. Their cycle independent kindnesses, various transcription factors, other cyclones um that come in and they act at very different places in the cell cycle. The G1 as checkpoint, the G2M checkpoint all of these things are activated by these mighty engines that come in and stimulate the cell cycle but I guess that you don't need to know this that they just sort of know the conceptual image of it. So that's all good right, Because the cell is growing but the cell has lived its life, right? It's getting ready to divide its maybe an old cell. Um and so there's probably some damage to it. And one of the things that it can happen is if there's D. N. A damage, the D. N. A. Is damaged, then the cell is like, okay, I've got to repair this. So when the G one phase is is going to halt and so when it stops in the G one phase, this gives time for this protein called P 53. Um to since that DNA damage. So what is P 53 is going to be a transcription regulator and um it acts to halt entrance into S. Phase. If the D. N. A. Is damaged. Now, you can imagine if this is such a crucial important protein to recognize DNA damage and stop the cell cycle can imagine that this is really important target for cancers. And P 53 is actually mutated in a huge amount of cancers. Because you can think if P 53 isn't doing its job, then the cells going to divide, even if it has DNA damage and a lot of most if not all cancers are based in DNA damage. So when P 53 is active, it's sort of halting this. But if there's some other reason or P 53 or any of these factors kind of get stimulated and the cell decides, you know, I'm not ready for division because I have some serious problems either. I'm not big enough. My D. N. A. Is damaged. I have some you know stress is around me and I just don't feel comfortable dividing. Then it enters this phase called G. Zero. And this is a non dividing state so the cell can remain here pretty much like indefinitely. It usually doesn't it usually will come out of it eventually but it can um and it will sort of repair itself in whatever way it needs to before it enters G. One. Now these cells that like don't divide Things like nerve cells um they actually enter into G. zero and then they stay there for forever, right? Because they they're not dividing so they don't need to be going through all these different phases. So here's an example of P 53 in the cell cycle. So here you have some type of DNA damage that the cell has recognized it then can activate P 53 P 53 will halt the cell cycle, promote DNA repair and stimulate cell cycle restart. If the DNA can be repaired. But if it can't it actually can go ahead and stimulate apoptosis. Which is remember cell death and sort of eliminate the cell. But essentially P 53 is super important in maintaining this stability in the D. N. A. And making sure there are no errors. So it's a super super super important protein and it's a big field, and cancer research is actually studying mutated forms of P 53 how it acts that cause cancer. So now let's move on.
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concept
S Phase Entry
Video duration:
2m
Play a video:
Okay, so now we have a cell that is N. G one phase, it is big, it's grown, its D N. A is not damaged and it's saying, okay, I'm great, let me divide. So then it needs to start going into the other phases now, the next phases s phase and that's where the D. N. A replicates. So the proteins responsible for entering into S phase are called s cycling. Excuse me? S cycle independent kindnesses or S cd case. And these are the proteins responsible for the cell entering s face. So how do they trigger S phase? Wells? S C D K works by activating D N. A healer cases which we may not have talked about yet and that's fine. Just know that these are proteins important for um DNA replication and then it also promotes this replication for formation which if you don't remember what this is from bio 101, it's fine. You don't need to just know that these are things that have to do with D N. A replication. So the S C K s are triggering these all these different factors important and DNA replication. And so these um S C D K stimulate the formation of this thing called the pre replicated complex and this is recruited to these places called origins of replication which are the places where replication occurs, right, it's going to be the starting point or the origin of the DNA replication. Um and then um this is actually not supposed to be here. So I'll take this out of the handout but sort of ignore that for a second. There we go. So if we look at the S C. D. K is, what we get is um activation in S. Phase. So here we go. We have our c. D. K. S. Um They're recruited along with other proteins to these origins of replication and then um once this pre replicated complex has formed on the origins of replication um and it's getting ready to replicate, then it can enter into S. Phase, which is super important. So now let's move on.
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Problem
Problem
What protein halts entry into S phase when DNA is damaged?
A
Mitogen
B
p53
C
S-Cdk
D
M-Cdk
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Problem
Problem
Which of the following is NOT a function of S-Cdks?
