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Cell cycle control

AP.BIO:
IST‑1 (EU)
,
IST‑1.D (LO)
,
IST‑1.D.1 (EK)
,
IST‑1.D.2 (EK)
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  • hopper jumping style avatar for user Jacob Anderson
    What makes the cylcins present?
    (5 votes)
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    • blobby green style avatar for user Manuel Menéndez
      Cyclins are made when they become necessary (when it's time to start prepping for the nest phase of the cell cycle) and are destroyed when they are no longer needed. They are actually called cyclin because their concentration in the cell are cyclical!! In other words the concentration rises, then reduces until it is no longer present, so on and so forth! Growth factors (factors that indicate the cell that conditions are appropriate for division) stimulate the cell to activate a pathway of signals that result in the translation of the specific cyclin gene and thus, we have cyclin! When it's time to move on, other factors (usually downstream products) stimulate a pathway that cleaves and destroys that specific cyclin. (hope this helped)
      (25 votes)
  • leaf grey style avatar for user blue
    So in summary the cyclin dependant kinase bonds with the cyclin, producing phosphates to activate different steps of the cell cycle.
    Is that correct?
    (3 votes)
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    • blobby green style avatar for user rahulrthakkar1
      You have the gist of it. Kinases in general, however, don't "produce" phosphates. They usually grab a phosphate group from a high energy compound (such as ATP), and then place it on their target (in this case, it's cyclin). This phosphate group on the cyclin rids of the inhibition (which is set by default) and allows the cell cycle to proceed until you need the next batch of cyclins to get phosphorylated to move even further. It's important to mention that the cell cycle is inhibited by default; this is to prevent the rapid proliferation of cells that is apparent in cancer.
      (9 votes)
  • leaf red style avatar for user maileallisa
    what happens to rb when DNA is damaged? i know what its role is when the cell is healthy but what happens when it encounter damaged DNA
    (4 votes)
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  • old spice man green style avatar for user Crystal
    Is the retinoblastoma (Rb) a type of protein that is supposed to block DNA replication? If so, is the cyclin's function to stop Rb from blocking the process?
    (2 votes)
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    • blobby green style avatar for user realityisjustaword
      Yes you are correct. Retinoblastoma (RB) prevents DNA replication. When retinoblastoma is phosyphorylated however, RB is inactivated and so DNA replication can proceed.

      This makes sense--you don't want to undergo DNA replication unless the cell is ready, so RB blocks synthesis, until cyclins are produced (cyclin E and cylcin D to be specific) when the cell has made the neecessary preparations.
      (3 votes)
  • blobby green style avatar for user cholorabadon
    if the RB (retinoblastoma) had blocked the DNA replication, does the cell will stop to divide?
    (2 votes)
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  • blobby green style avatar for user Kirill K
    Thank you for your explanation)
    What exactly the difference in function of cyclin E and cyclin D because it a wasn't mentioned in the video?
    (2 votes)
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  • blobby green style avatar for user H Riel
    So does CDK2 bind with both cyclin E and cyclin A at the first checkpoint?
    Because it wouldn't make sense to have CDK2 bind with cyclin A (which ACTIVATES DNA replication) at the G2/M checkpoint, which is past the point of DNA replication...
    (1 vote)
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  • duskpin ultimate style avatar for user moonchicken123
    At it says Rb inhibits DNA replication. How does it do this?
    (0 votes)
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    • piceratops ultimate style avatar for user RowanH
      It inhibits E2F transcription factors that promote progression to S phase (such as by upregulating expression of genes needed to synthesise DNA and nucleotides, and other cell cylce controlling genes). I know this is vague, but if I go into more detail, I will end up telling you something wrong. For example E2F is a family of transcription factors, and it seems Rb binds mostly E2F1, but I am not sure if it does or doesn't bind any of the others.
      (3 votes)
  • hopper cool style avatar for user SofiyaMarkova
    do cancer cells skip the interphase?
    (1 vote)
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  • piceratops tree style avatar for user Siyuan Yu
    So he clarified at that CDK4+CycD phosphorylates Rb, but then what does CDK2+CycE do exactly?
    (1 vote)
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Video transcript

Now, the cell cycle is not the sort of thing that occurs in a very unchecked manner. There's actually a lot of regulation in play here. In fact, there are two key places that we have extensive regulation of the cell cycle. The first check point is right here between the G1 and the S phase. So, we regulate before we get to the point of DNA replication. The other major checkpoint is right here, between G2 and the step where we jump right to mitosis. And, there are a couple of proteins that regulate this process. Two main ones are called cyclin-dependent kinases, which as you may recall, a kinase is something that adds a phosphate group. So I'll put a plus in parentheses. It will plus a phosphate group. And it will add a phosphate group on other enzymes or proteins to either activate or inactivate them. These cyclin-dependent kinases will work together with a protein you might be able to guess the name of: cyclins! Right? Because what else would these kinases depend on? So an important thing to notice is that these cyclin-dependent kinases, or CDKs, are always present. All the different types are always present in a cell, but their default form, or their default function, is for them to be inactive. And so they need to be activated by these cyclin proteins. And the point of regulation here is that specific cyclins... I'll just write, "spec," are made at specific times. And again, the reason why they're both so important is that when you have a cyclin-dependent kinase, it is only active when it is bound to a specific cyclin. It's at this point, again, that this guy is active, and the CDK is the business-end of this complex. So that's the reason why in G1 you'll see the production of cyclins D and E. >From there you will see CDK-2 bound to your cyclin E, and at the same time you'll also have your CDK-4 bound to your cyclin D. These activated kinases, then, specifically the CDK-4 cyclin D complex, will phosphorylate a protein called, "RB." So I'll draw just a little reaction over here where we add a phosphate group on our RB protein. So when RB is phosphorylated, it can't inhibit DNA replication, like it usually is supposed to do. The phosphate group renders it inactive. And this is sort of the set up we have as we go further on in our cell cycle. In the S phase we have cyclin A produced. Cyclin A will complex, again, with CDK-2 most directly to activate DNA replication, so it helps to activate DNA replication and in a similar way we have cyclin B only produced in the G2 phase, because the cyclin B CDK-1 complex is able to activate what step, do you think? Mitosis, or cell division. So, it's important to recognize that in order to pass these checkpoints, you need to have these cyclin proteins present so that they can go ahead and inhibit proteins that are blocking DNA synthesis or replication from occurring, or so they can promote the production of proteins that are needed for mitosis.