Cellular Reproduction: The Cell Cycle (3) Flashcards Preview

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Flashcards in Cellular Reproduction: The Cell Cycle (3) Deck (40)
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1
Q

cell cycle

A

time from one division to the next division

2
Q

how is the cell cycle divided?

A

2 phases: M phase & interphase

3
Q

interphase

A

cell growth & metabolism

4
Q

what causes the variation in duration of interphase?

A

depends on cell type

5
Q

what are the categories that we did cells into in the cell cycle?

A
  1. cells that don’t cycle but enter a permanent arrest stage, once differentiated remain in that state until they die (ex: neurons, muscle cells, RBCs)
  2. Cells that normally don’t divide but can be induced (ex: liver, lymphocytes)
  3. Cells that divide regularly (ex: epithelial cells)
6
Q

why do RBCs lack a nucleus?

A

no longer necessary since they will no longer be dividing

7
Q

what controls cell division?

A

cytoplasmic factors

8
Q

what was the experiment to find what controls the cell cycle?

A

fused mitotic & interphase cells

interphase cells in G1 had premature condensed c’some & attempted M phase (the non mitotic cell)

concluded that there is a factor in the mitotic cell that directs cells to undergo mitosis

9
Q

what controls the cell cycle at the G2/M transition?

A

maturation promoting factor

entry into mitosis requires this PRO complex

10
Q

what is MPF?

A

complex of 2 PROs:
cyclin b: regulates cdK1 activity, levels rise & fall through the cell cycle
Cdk1: kinase added a phosphate tot other PROs, modifying the target’s PROs activity (cyclin dependent kinase)

11
Q

when is there first an increase in cyclin b?

A

G2

12
Q

when does cyclin b peak? and when does it drop?

A

M phase & at the end of M phase

13
Q

what is the role of MPF?

A

phosphorylates & activates PROs of mitosis

14
Q

when are cyclins not produced?

A

G0

15
Q

What are some MPF functions?

A

activates lamin PROs, causing the nuclear envelope to break (dissociates PRO from membrane)

alters DNA bound PROs (histones) causing DNA to condense. During Prophase enabling c’some to travel to poles

activates PROs of the mitotic spindle in pro prometaphase

16
Q

Wee1 PRO & what happens when the mutant lacks it

A

inhibitor of MPF

results in early cell division (enters too early), smaller daughter cells than what they should be

17
Q

Cdc25 PRO & what happens when the mutant lacks it

A

activates MPF

division fails too occur, large cell

18
Q

how does cdc25 activate cdk?

A

Removes phosphate form Tyr15 activating cdk

19
Q

what inhibits MPF activity?

A

wee1 adds phosphate to Try 15

20
Q

CAK

A

cyclin activating kinase

adds P to Thr161, when removed mitosis is terminated

activates Cdk1

21
Q

What happens when P is removed from Thr161?

A

cyclin detaches & degraded, ends mitosis

22
Q

what activates Cdk1?

A

CAK adds P on Thr161

once removed mitosis ends

23
Q

what inactivates Cdk1?

A

wee1 phosphate on Tyr15

24
Q

how is cyclin action turned off?

A

activation of ubiquitin ligase

25
Q

ubiquitin ligase

A

terminates MPF activity

Attaches ubiquitin to cyclin tagging it for destruction by causing proteolysis

26
Q

What does MPF phosphorylate?

A

lamin
histones
microtubules
ubiquitin ligase

27
Q

When are cyclins & cdk1 low?

A

G1

28
Q

proteasome

A

proteolysis of cyclin terminating MPF activity

29
Q

What is necessary to work at G0 to have successful mitosis?

A

if wee1 isn’t working the cells go on too soon & end up small

30
Q

What are the MPF checkpoints & end do they occur?

A

Metaphase checkpoint:
o M phase
o Chromosomes aligned?

Start or restriction checkpoint:
o End of G1
o Cell decides whether to continue or not Cell big enough? Envr okay? DNA okay?

G2 checkpoint:
o G2
o DNA intact post replication?
Will not attempt division if DNA is damaged

MPF checkpoint:
o End of G2
o DNA replicated? Cell big enough? Does it have enough stuff?

31
Q

What is the result of the DNA damage checkpoint in G1 not functioning properly?

A

Ataxia-telangiectasia (AT)

PROs involved in DNA repair fail indivs with AT

prone to cancer: 
     Ionizing radiation (ATM PRO) - breaks DNA 
     Ultraviolet radiation (ATR PRO)
32
Q

What are the steps in the checkpoint if there is DNA damage?

A
  1. ATM detects break in DNA in G1
  2. ATM phosphorylates Chk2 activating it
  3. Chk2 phosphorylates p53
  4. Phosphorylated p53 activates gene p21 (gene is synthesized)
  5. P21 PRO binds to Cdk (inhibition)
    cell prevented from entering S phase until DNA is repaired
33
Q

ATM PRO role

A

detects break in DNA in G1

34
Q

Chk2

A

kinase

phosphorylates p53 in cell damage checkpoint

35
Q

p53 role

A

when phosphorylated, turns on p21 gene causing its synthesis

36
Q

p21

A

gene synthesized when there is damage in DNA, PRO inhibits Cdk

37
Q

50% of human tumor cells have mutations in which gene?

A

p53

38
Q

what are the 3 components of a checkpoint?

A
  1. Sensor –> is DNA damaged? (ex: ATM/ATR PROs)
  2. Transducer: create a signal, enables the cell to work in a multi-step fashion, diff controls systems interact (ex: Cdc25, p53, MPF PROs)
  3. Effector: change key enzyme action/PRO (ex: P21, phosphorylated lamins, histones, ubiquitin etc.)
39
Q

What is the effector in then DNA damage checkpoint?

A

P21

40
Q

What are the checkpoints in the cell cycle?

A
  1. Progression from G2 to M by the MPF
  2. Checkpoints for DNA damage in G2 + G1 (before & after rep) –> cell cycle halts allowing time for repair
  3. Spindle checkpoint in M phase