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Course: MCAT > Unit 7
Lesson 8: Cellular division- Cellular division questions
- Mini MCAT passage: Tyrosine-kinase inhibitors in cancer treatment
- Cell cycle phases
- Cell cycle control
- Loss of cell cycle control in cancer
- Mitosis
- Interphase
- Mitosis
- Comparing mitosis and meiosis
- Meiosis
- Phases of meiosis I
- Phases of meiosis II
- Cancer
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Cell cycle control
The cell cycle is tightly regulated by checkpoints between the G1 and S phase, and between the G2 and mitosis. Key proteins, cyclin-dependent kinases and cyclins, control this process. Cyclins are produced at specific times, activating the kinases and allowing progression through the cell cycle. This regulation prevents unchecked cell division, a hallmark of cancer.
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- At2:50, Rb protein is mentioned. What does this stand for?(17 votes)
- Retinoblastoma(20 votes)
- What makes the cylcins present?(7 votes)
- 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)(34 votes)
- 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)
- the retinoblastoma protein prevents the cell from replicating if the DNA is damaged. so stops after the G1 phase (can not go from G1 to S).
the cell tries to fix the DNA in order to continue but if the damage is irreparable, apoptosis will be triggered by caspases.
https://www.khanacademy.org/test-prep/mcat/biomolecules/gene-control/v/tumor-suppressors(3 votes)
- 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?(3 votes)
- 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.(4 votes)
- 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?(3 votes)- Cyclin E is most active in the checkpoint between G1 and S however cyclin D is most active between S and G2 but it is active throughout.(1 vote)
- At2:57it says Rb inhibits DNA replication. How does it do this?(1 vote)
- 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.(4 votes)
- might be a dumb question, but when we think about cells performing their normal everyday functions, within the context of the cell cycle, would these cells be in interphase? or more specifically in G1?
For example, epithelial or skin cells, minding its own business protecting, or sending sensations via nociceptors, etc.. I assume this cell would be in Interphase, or would it be right to say G1? better yet if it is in G1, does that mean the cell goes into some sort of "dormant" state while in S/G2 to prepare for mitosis?(2 votes)- If the cells are in interphase, based upon probability alone, they're most likely in G1. Cells in the Nervous System (or at least neurons) don't divide though, so those cells would be arrested in G0(2 votes)
- 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...(2 votes) - if the RB (retinoblastoma) had blocked the DNA replication, does the cell will stop to divide?(2 votes)
- the retinoblastoma protein prevents the cell from replicating if the DNA is damaged. so stops after the G1 phase (can not go from G1 to S).
the cell tries to fix the DNA in order to continue but if the damage is irreparable, apoptosis will be triggered by caspases.
https://www.khanacademy.org/test-prep/mcat/biomolecules/gene-control/v/tumor-suppressors(1 vote)
- do cancer cells skip the interphase?(2 votes)
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.