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Bio344-Cell and Molec > Ch.17-Cell Cycle and Programmed Cell Death > Flashcards

Ch.17-Cell Cycle and Programmed Cell Death Flashcards

1
Q
  1. Describe the cell cycle including the different phases that occur during mitosis
A

G1&raquo_space; S&raquo_space; G2&raquo_space; M (mitosis and cytokinesis)

  • Mitosis: Prophase, metaphase, anaphase, telophase
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2
Q

2A. Describe the processes that occur during the G1 phase

A

= long resting phase; most cells in this stage

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3
Q

2B. Describe the processes that occur during the S phase

A

= DNA replication

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4
Q

2C. Describe the processes that occur during the G2 phase

A

= short resting phase, has 96 chromosomes

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5
Q

2D. Describe the processes that occur during the M phase

A

= mitosis (nuclear division), cytokinesis (cytoplasmic division)

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6
Q

3A. What are cyclin dependent kinases?

A

= protein kinases (enzymes that phosphorylates proteins) that need to bind to cyclin in order for it to be activated

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7
Q

3B. What is their role of cyclin dependent kinases in the cell cycle?

A
  • Control the cell division cycle

- phosphorylates other proteins

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8
Q
  1. What are cyclins?
A

= The protein that controls whether Cdk are active

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9
Q
  1. List the different cyclins involved in the cell cycle and the processes they control.
A
  1. G1 cyclin
  2. G1/S cyclin
  3. S cyclin
  4. M cyclin
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10
Q

6A. What are Cdk inhibitory proteins?

A

= proteins that inactivate cyclin dependent kinases by binding to active Cdk

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11
Q

6B. What does p27 do?

A

= is a type of Cdk inhibitory protein

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12
Q
  1. How else can Cdk’s be inactivated?
A
  • By inhibiting phosphorylation&raquo_space;> phosphorylation twice = inactive
  • Can be labeled with ubiquitin and degraded
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13
Q

8A. What is APC?

A

= Anaphase promoting complex; It is activated by M-Cdk

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14
Q

8B. What does APC do?

A

= Activates separase (cuts cohesive proteins); degrades M-cyclin, which deactivates M-Cdk

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15
Q
  1. How come a cell in G1 phase that has assembled the pre-replicative complex does not immediately go in to the S-phase?
A

A signal molecule is required??

????????

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16
Q

10A. Describe the role of cyclins G1 in moving a cell from the G1-phase to the S-phase.

A
  1. makes active Cdk complex that forms G1/Cdk;
  2. phosphorylates Rb protein;
  3. released more E2F;
  4. increase in G1/S and S cyclin
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17
Q

10B. Describe the role of cyclins G1/S in moving a cell from the G1-phase to the S-phase.

A

makes active G1/S Cdk

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18
Q

10C. Describe the role of cyclins S in moving a cell from the G1-phase to the S-phase.

A
  1. makes active S Cdk;
  2. phosphorylates inhibitory protein attached to pre-replicative complex;
  3. releases from pre-replicative complex and DNA replication starts.
19
Q

11A. Describe the role of the Myc protein.

A

= DNA binding protein that increases transcription of: G1 cyclin gene, SCF gene (which decreases P27) and E2F

20
Q

11B. Describe the role of the E2F.

A

= DNA binding protein that causes an increase in S cyclin, binds to Rb protein to cause “brake”

21
Q

11C. Describe the role of the Ras protein.

A

= Map kinase  DNA binding protein increases transcription of Myc gene

22
Q
  1. What is an Rb protein?
A
  • A “brake” for cell division cycle; it does this by binding to the E2F protein
  • Active G1-CDK complex phosphorylates Rb protein, which causes it to change shape so that it no longer has an affinity for E2F
23
Q
  1. What is the pre-replicative complex?
A
  • Assembled in the G1 phase
  • Specific spot on chromosome where DNA replication starts
  • Many proteins that are inactive when inhibitory proteins are bound to it
24
Q

14A. What is p53 and what does it do?

A

= A tumor suppressor protein

- it increases transcription of inhibitory protein genes&raquo_space;> inhibitory proteins deactivate Cdk complexes

25
Q

14B. How is p53 activated?

A

= DNA damage, excessive mitogenic stimulation

26
Q

14C. Why can mutations in p53 lead to cancer?

A

= p53 gene mutation can make so the cell never stops dividin

27
Q
  1. What is apoptosis?
A

= Programmed cell death

28
Q
  1. What proteins mediate apoptosis?
A
  1. Procaspases

2. Caspases

29
Q

17A. How are procaspases and caspases proteins activated?

(INTRINSIC pathway

A

= Cytochrome c is released from mitochondria&raquo_space;> procaspases form aggregates&raquo_space;> results in activation of first group of caspases

30
Q

17B. 17A. How are procaspases and caspases proteins activated?
(EXTRINSIC pathway)

A

= Killer lymphocyte has membrane protein that binds receptor in target cell&raquo_space;> Trigger activation of procaspases

31
Q
  1. What are mitogens?
A
  • Signal molecules that induce or stimulate mitosis, causes cell division
  • Binds to enzyme linked receptor
32
Q
  1. Why would an activated blood platelet secrete mitogens?
A

So other blood platelets can undergo cell division and create a primary plug

33
Q

20A. What is a Ras protein?

A

= Map kinase&raquo_space;> DNA binding protein increases transcription of Myc gene

34
Q

20B. What is a myc protein?

A

= DNA binding protein

35
Q
  1. What is a growth factor?
A

= Protein or steroid hormone that stimulates growth, proliferation, healing and cellular differentiation

36
Q
  1. What is a survival factor?
A

They bind to receptors&raquo_space;> kinase activated&raquo_space;> phosphorylate and inactivate proteins that cause apoptosis

37
Q
  1. How does an organism ensure that each nerve cell is attached to a target cell?
A

Target cells will release survival factors to make sure nerve cell survives to attach to it

38
Q
  1. How does an organism ensure that extra nerve cells are eliminated?
A

-Target cell will release survival factors but only the nerve cells that are closest to the target cell will receive it—all extra nerve cells will not receive survival factors and undergo apoptosis

39
Q
  1. What is cancer?
A

= Uncontrolled cell division

40
Q
  1. What is metastasis?
A

= When cancer cells start to move-spreading throughout the body-becomes more malignant

41
Q
  1. Is a single mutation sufficient to give rise to cancer? Why?
A

No, it is caused by slow accumulation of numerous mutations

42
Q
  1. How could over-activity of a protein or gene contribute to cancer? Give an example of a protein that could contribute to cancer if over active.
A

Over-activity of the myc or ras protein would cause too much cell division to occur

43
Q
  1. How could elimination of a gene contribute to cancer? Give an example of a protein that could contribute to cancer if absent.
A
  1. Elimination of P53 gene:
    = could no longer stop cell division
  2. Elimination of Rb gene:
    = Wouldn’t stop E2F-DNA replication would continue to occur

Bio344-Cell and Molec (6 decks)

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