Lecture 3: Phases of Cell Growth and Division Flashcards

1
Q

The “point of no return” at the border of G1 and S1.

A

Restriction Point (R)

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2
Q

What point in the cell cycle is the cell’s only chance to reset itself if it lacks the size, energy, etc. needed for division?

A

The restriction point (R)

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3
Q

Which tumor suppressor regulates the restriction point and sends the cell cycle back to the beginning if the cell is not ready for division?

A

Rb

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4
Q

Which phases in the cell cycle make up interphase?

A

G1, S, and G2

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5
Q

What happens during G1 (gap phase I) of the cell cycle?

A

Cells grow larger, copy organelles, and synthesize macromolecules.

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6
Q

During which phase of the cell cycle do cells synthesize a complete copy of their DNA and make a duplicate centrosome?

A

S phase

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7
Q

What happens during G2 (gap phase 2)?

A

The cell grows more, makes more proteins and organelles, and prepares for mitosis.

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8
Q

Which tumor suppressor regulates whether or not the cell undergoes DNA replication?

A

Rb

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9
Q

Which tumor suppressor regulates the fidelity of the genome?

A

p53

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10
Q

Where is the second checkpoint in the cell cycle located? What does it check for?

A

On the G2/M border; it checks for DNA replication errors.

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11
Q

Which tumor suppressor regulates the G2/M border?

A

p53

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12
Q

If errors are found in the DNA replication at the G2/M checkpoint, what options does the cell have?

A

1) Fix the errors

2) Apoptosis

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13
Q

What kind of tumor suppressor is p16?

A

It is an INK4 tumor suppressor protein

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14
Q

How does p16 (INK4) stop cell division?

A

If inactivates the Cdk4 and cyclin D1 complex, thereby activating Rb, which in turn inactivates E2F transcription factor/oncogene, stopping cell division by preventing the entrance of the cell into S phase.

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15
Q

What happens in the cell cycle if the Cdk4 and cyclin D1 complex is active?

A

The Cdk4/cyclin D1 complex will inactivate Rb, thereby activating the E2F transcription factor, which allows entrance of the cell into S phase and continues the process of preparing for cell division.

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16
Q

How does INK4 (p16) indirectly activate Rb?

A

By inactivating the Cdk4/cyclin D1 complex that would otherwise inactivate Rb.

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17
Q

What does CDKs stand for?

A

Cyclin dependent kinases

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18
Q

What is the name for the regulatory protein that binds to a CDK to activate it?

A

cyclin

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19
Q

Which cyclin interacts with CDK4 to take a cell through G1 and into S phase?

20
Q

Which CDK interacts with cyclin D to take a cell through G1 and into S phase?

21
Q

Which cyclin interacts with CDK2 to take a cell from G1 into S phase?

22
Q

Which CDK interacts with cyclin E to take a cell from G1 into S phase?

23
Q

Which cyclin interacts with CDK2 to take the cell through S phase and into G2?

24
Q

Which CDK interacts with cyclin A to take the cell through S phase and into G2?

25
Which cyclin interacts with CDK1 to take the cell from G2 into M (mitosis)?
Cyclin B
26
Which CDK interacts with cyclin B to take the cell from G2 into M (mitosis)?
CDK1
27
What are three ways to mutate DNA?
1) Intrinsic 2) Exposure to chemical agents 3) Radiation
28
How can a cell be mutated intrinsically?
1) Spontaneous base modifications | 2) Replication errors
29
What types of chemical agents can mutate DNA?
1) Endogenous agents (oxygen radicals) | 2) Exogenous agents (chemical mutagens)
30
What types of radiation can mutate DNA?
1) Ultraviolet radiation | 2) Ionizing radiation
31
Which structures cause a lot of DNA damage during mitosis?
Centrosomes
32
What is it called when there are centrosomes pulling DNA in different directions from multiple poles?
Centrosome amplification
33
___________ can drive centrosome amplification.
Oncogenes
34
Why are the damages caused to DNA by centrosome amplification preserved in the next replication cycle?
Because in the next cycle, the centrosomes coalesce at just two poles, preserving the rearrangement and stabilizing the genome (and thereby passing on mutations).
35
What is ARF?
a tumor suppressor
36
When is ARF activated?
When it senses too much oncogene signaling.
37
True or false: Oncogenes inhibit ARF.
False; oncogenes turn the ARF tumor suppressor on.
38
What does ARF do when it senses oncogene signalling?
Shuts down growth.
39
If the E2F oncogene is active, what will happen normally?
It will be sensed and shut down by ARF.
40
Which tumor suppressor regulates cell arrest and apoptosis?
p53
41
Which tumor suppressor senses DNA damage and alerts p53?
ATM
42
What does ATM do when it senses DNA damage?
Tells p53 if the damage can be repaired and, if so, sits at the break site and tells the repair machinery where to go.
43
What are two ways by which apoptosis takes place?
1) Extrinsic (by death receptors) | 2) Intrinsic (through the mitochondria)
44
The degree to which a gene or set of genes is expressed in an individual's phenotype.
Penetrance
45
To be penetrant, a mutation must affect one of these 4 things:
1) RNA stability (so that DNA can's become a protein) 2) Disrupt the critical binding region of a protein (so the protein can't perform the same function). 3) Make shorter proteins (change the protein's function) 4) Point mutations (affects the function of the proteins)