Lecture 3: Phases of Cell Growth and Division Flashcards

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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?

A

Cyclin D

20
Q

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

A

CDK4

21
Q

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

A

Cyclin E

22
Q

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

A

CDK2

23
Q

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

A

Cyclin A

24
Q

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

A

CDK2

25
Q

Which cyclin interacts with CDK1 to take the cell from G2 into M (mitosis)?

A

Cyclin B

26
Q

Which CDK interacts with cyclin B to take the cell from G2 into M (mitosis)?

A

CDK1

27
Q

What are three ways to mutate DNA?

A

1) Intrinsic
2) Exposure to chemical agents
3) Radiation

28
Q

How can a cell be mutated intrinsically?

A

1) Spontaneous base modifications

2) Replication errors

29
Q

What types of chemical agents can mutate DNA?

A

1) Endogenous agents (oxygen radicals)

2) Exogenous agents (chemical mutagens)

30
Q

What types of radiation can mutate DNA?

A

1) Ultraviolet radiation

2) Ionizing radiation

31
Q

Which structures cause a lot of DNA damage during mitosis?

A

Centrosomes

32
Q

What is it called when there are centrosomes pulling DNA in different directions from multiple poles?

A

Centrosome amplification

33
Q

___________ can drive centrosome amplification.

A

Oncogenes

34
Q

Why are the damages caused to DNA by centrosome amplification preserved in the next replication cycle?

A

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
Q

What is ARF?

A

a tumor suppressor

36
Q

When is ARF activated?

A

When it senses too much oncogene signaling.

37
Q

True or false: Oncogenes inhibit ARF.

A

False; oncogenes turn the ARF tumor suppressor on.

38
Q

What does ARF do when it senses oncogene signalling?

A

Shuts down growth.

39
Q

If the E2F oncogene is active, what will happen normally?

A

It will be sensed and shut down by ARF.

40
Q

Which tumor suppressor regulates cell arrest and apoptosis?

A

p53

41
Q

Which tumor suppressor senses DNA damage and alerts p53?

A

ATM

42
Q

What does ATM do when it senses DNA damage?

A

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
Q

What are two ways by which apoptosis takes place?

A

1) Extrinsic (by death receptors)

2) Intrinsic (through the mitochondria)

44
Q

The degree to which a gene or set of genes is expressed in an individual’s phenotype.

A

Penetrance

45
Q

To be penetrant, a mutation must affect one of these 4 things:

A

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)