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BIOM 3500 - Midterm 3: The Cell Cycle > Lecture 19 - Cell Cycle Checkpoints > Flashcards

Lecture 19 - Cell Cycle Checkpoints Flashcards

1
Q

Why might there be a delay or arrest in cell cycle progression?

A

In response to problems completing a specific step in the cell cycle or in response to other cellular problems

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2
Q

What might checkpoints do?

A
  • Pause the cell cycle and promote repair before continuing
  • Induce permanent arrest or apoptosis
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3
Q

When are many checkpoints not essential?

A

Under normal conditions

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4
Q

What are checkpoints essential for?

A

Protecting against cancer

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5
Q

How is SAC recruited to unattached kinetochores?

A

Mad2 component of SAC is recruited to the kinetochore, activated, and released, so it binds and inhibits APC/C-Cdc20

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6
Q

What happens at the spindle assembly checkpoint?

A

APC/C-Cdc20 is inhibited in response to incomplete kinetochore/microtubule attachments and allows the spindle to set up properly before anaphase is initiated

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7
Q

What happens at the G1 DNA damage checkpoint?

A
  • Activated if DNA damage is detected in G1 –> G1 or G0 arrest
  • Allows cell cycle to pause while DNA is repaired
    *A similar checkpoint operates in G2 and prevents entry into mitosis
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8
Q

What is replicative senescence?

A

Telomere shortening –> G0 arrest (senescence)

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9
Q

What does replicative senescence (telomere shortening) protect against?

A

Chromosome fusion

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10
Q

What is oncogene-induced senescence?

A

Hyperproliferation due to oncogene activation –> G0 arrest (senescence)

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11
Q

What do some other checkpoints detect?

A
  • Hypoxia
  • Loss of cell adhesion
  • Other abnormal cellular conditions
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12
Q

What gets recruited to sites of DNA damage?

A

ATM and ATR kinases

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13
Q

What preference does ATM have?

A

Double-stranded breaks

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14
Q

What preference does ATR have?

A

Exposed single-stranded DNA and other DNA damage

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15
Q

What functions do ATM and ATR have?

A

1) Help recruit repair machinery
2) Activate a cell cycle machinery

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16
Q

What do ATM and ATR phosphorylate?

A

Chk1 and Chk2 kinases to promote cell arrest (or apoptosis)
*They also phosphorylate to activate proteins involved in DNA repair

17
Q

What else regulates Cdk2-cyclin A to control S-phase?

A

Wee1 and Cdc25

18
Q

What do Chk1 and Chk2 phosphorylate?

A

Cdc25 phosphatase, targeting it for ubiquitination by SCF ubiquitin ligase and destruction by the proteosome

19
Q

What keeps Cdk2 phosphorylated?

A

Wee1

20
Q

How is the G2 checkpoint activated?

A
  • Cdk1 remains phosphorylated by Wee1 so it is inactive
  • Cells arrest in G2/M
21
Q

In the case of more severe damage, what do ATM, ATR, Chk1, and Chk2 phosphorylate and activate?

A

Transcription factor, p53

22
Q

What does p53 do?

A
  • Induces a permanent cell cycle arrest by activating p21 expression so it can bind and inhibit Cdk2/cyclin A and Cdk2/cyclin E complexes so cells arrest in G1
  • Can also induce apoptosis by activating the expression of pro-apoptotic genes
23
Q

When is p53 inactive?

A

In undamaged cells due to Mdm2 binding

24
Q

What does Mdm2 do?

A

Inhibits p53 activity and ubiquitinates p53 –> proteasomal degradation

25
Q

What happens to phosphorylated p53?

A

It is released from Mdm2

26
Q

What does the cell arrest in if telomeres are too short?

A

G0

27
Q

What are telomeres?

A

Chromosome ends that contain multiple copies of a telomere repeat

28
Q

What is telomerase activity required for?

A

Telomere replication

29
Q

What are telomeres protected by?

A

Telomere binding proteins - sheltrin complex binds to telomere repeats and protects them from DNA repair machinery that repairs double-stranded breaks

30
Q

What happens in most cell types in humans that don’t express telomerase?

A

Telomeres shorten each cell generation (every cell division) and if they shorten too much, there will be no more repeat sequences and sheltrin can no longer bind

31
Q

How is replicative senescence carried out?

A

1) ATM binds to exposed double-stranded DNA at chromosome ends
2) p53 stabilization
3) p21 expression
4) Inactivation of G1/S and S-Cdks
*Induces permanent cell cycle arrest

32
Q

What is oncogene-induced senescence?

A

When normal cells are induced to express high levels of oncogenes like myc or ras (genes that promote cell division), it induces a checkpoint that results in senescence

33
Q

What does myc overexpression lead to?

A

The production of Arf, an inhibitor of Mdm2 so it can bind and cause the ubiquitination of p53 so it is able to mediate cell cycle arrest or apoptosis

34
Q

What transcription factor is the cellular gatekeeper?

A

p53

BIOM 3500 - Midterm 3: The Cell Cycle (7 decks)

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