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CMBL > Cell Division I and II > Flashcards

Cell Division I and II Flashcards

1
Q

what are the 3 discrete stages that cells reproduce?

A
  • interphase
  • mitosis
  • cytokinesis
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2
Q

what is the longest stage in the cell cycle?

A

G1

**she asked a question about sampling 100 cells and what phase they would be found in

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3
Q

what occurs in G1 phase?

A

-prep for DNA synthesis
-active RNA and protein synthesis
-intracellular structures are duplicated
GROWTH

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4
Q

G 0 phase

A
  • nondividing, differentiated stage
  • Most human cells are in G0
  • special examples liver (quiescent cells can be called out) and neurons
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5
Q

Synthesis of nuclear DNA occurs in ___ phase

A

S

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6
Q

which cell cycle phase ends with the formation of sister chromatids?

A

S phase

-takes about 6 hours

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7
Q

G2 phase

A
  • Cell volume increases

- Synthesis of organelles and proteins necessary for spindle formation/division

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8
Q

M phase

A
  • Duplicated chromosomes are distributed equally into a pair of daughter nuclei
  • Prophase, prometaphase, metaphase, anaphase, telophase
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9
Q

Replication of DNA can be assessed by measuring the synthesis of new DNA. What molecule is used to assess new DNA??

A
  • Metabolic labeling with 3H-thymidine

- Cells actively synthesizing DNA will accumulate radioactivity

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10
Q

Bromodeoxyuridine (BrdU)

A

-artificial thymidine analog used to identify S-phase

cells

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11
Q

CFSE

A

succinimidyl ester of carboxyfluorescein diacetate

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12
Q

FACs can measure the fluorescence of cells incubated with CFSE. Describe what we see from generation to generation

A

As cells divide, their fluorescently labeled cytoplasmic proteins are divided equally between the two daughter cells. Each daughter cell has half the fluorescence of the previous generation, which can be measured by flow cytometry

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13
Q

once can also assess cellular DNA content by flow cytometry. Describe how this graph works. What is on the x axis? what is on the yaxis

A

x-axis: relative amount of DNA per cell
y-axis: the number of cells

-Used to determine the lengths
of G1, S, and G2 + M phases

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14
Q

Quiescent (G0)

A

– cells that temporarily or reversibly stop dividing

-example liver cells

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15
Q

Senescent –

A

cells that permanently stop dividing due
to age or accumulated DNA damage
-examples: neurons

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16
Q

what are the 3 major checkpoints of the cell cycle?

A
  • G1: (Restriction Point/Start) : commits cell to entering the cell-cycle and chromosome duplication
  • G2 /M Checkpoint: triggers early mitotic events that lead to chromosome alignment on the spindle in metaphase
  • Metaphase-to-Anaphase transition: stimulates sister chromatid separation, leading to the completion of mitosis and cytokinesis
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17
Q

T/F: Cyclins depend on the fluctuating levels of CDK to regulate their activity

A

False! CDK levels are relatively constant, but CDK activity is regulated by the fluctuating [ ] of cyclins

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18
Q

cyclin D complexes with which CDKs to perform which function?

A
  • CDK-4 and CDK-6

- progress past the restriction point of G1 /S

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19
Q

cyclins E and A complex with which CDK to perform which function??

A
  • CDK2

- initiate DNA synthesis in early S phase

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20
Q

cyclin B complex with which CDK to perform which function?

A
  • CDK 1

- transition from G2 to mitosis

21
Q

what is the function of CAK?

A

phosphorylate CDK to active state

-phosphorylates at the T loop

22
Q

what enzyme is responsible for the 2nd inhibitory phorphorylation of CDK1?

A

-Wee1 kinase

23
Q

what enzyme is the phophatase that is able to free CDK-1 to do its job?

A

cdc25 phosphatase

24
Q

what is p27 and what is its relationship to cyclin-Cdk?

A
  • p27 is a CKI

- CKI binding causes rearrangement in the CDK active site rendering it inactive

25
Q

when/where do CKIs primarily regulate cell cycle progression?

A

-at G1/S and at S CDKs early on in the cell cycle

26
Q

Who is APC/C?

A

-anaphase-promoting complex or cyclosome

27
Q

what does APC/C do?

A
  • ubiquitinates (tags for destruction) securin, s-cyclin, and m-cyclin
  • initiates the separation of sister chromatids by destroying securin
28
Q

what are the two steps required for chromosome duplication?

A

step 1: pre-replication complex (occurs late mitosis and early G1)
step-2: pre-initiation complex (occurs at onset of S)

29
Q

where is DNA synthesis allowed to occur?

A

-at origins containing a pre-RC

30
Q

what triggers the formation of the preinitiation complex initiating DNA synthesis??

A

-S-CDK activation

31
Q

what stimulates pre-RC assembly?

A

-APC/C and Cdk inactivation

32
Q

What are two major regulatory steps in mitosis?

A
  • increase in M-CDK activity at G2/M checkpoint

- metaphase to anaphase transition when APC/C triggers the destruction of securin and cyclins

33
Q

what are the two categories of cancer-critical mutations?

A
  1. ) overactivity mutation (gain of function) DOMINANT oncogene
  2. ) underactivity mutation (loss of function) (recessive) tumor suppressor gene
34
Q

ras proto-oncogenes: what is the normal function of Ras?

A

-monomeric GTPases involved in signal transduction pathway from growth factor receptor to nucleus

35
Q

what happens in ras oncogenes?

A

-point mutation to make overactive

36
Q

what are the 3 ras mutants we learned about and where are their mutations?

A

-K-Ras: Arg at 12
-N-Ras: Arg at 61
H-Ras:val at 12

normal ras: gly at 12 and gln at 61

37
Q

what specifically explains why mutated Ras remains active?

A

-mutated Ras cannot hydrolyze its bound GTP

38
Q

take me through the Ras pathway

A

Ras –> Raf –> Mek –> Erk –> transcription factors –> genes turned on

39
Q

what is the clinical presentation in someone who has nonhereditary retinoblastoma?

A

-unilateral RB

40
Q

what is the clinical presentation in someone who has hereditary retinoblastoma

A

-bliateral RB

41
Q

what is the normal function of Rb?

A
  • controls entry into S phase

- nonphosphorylated version binds to transcription factors to STOP them

42
Q

who is responsible for phophorylating Rb so cell can continue into S phase?

A

-cyclin D-CDK 4/6 complex

43
Q

where in the cell cycle does p53 regulate?

A

G1

44
Q

what happens to activated p53 levels if DNA is damaged or repair intermediates accumulate?

A

-p53 levels will rise

45
Q

If DNA cannot be readily repaired, what will p53 do?

A
  • turn on Bax gene, repress Bcl2 gene

- Bax homodimers activate process of cell destruction

46
Q

Li-Fraumeni Syndrome

A
  • autosomal dominant

- predisposition to cancer due to mutation in TP53 gene

47
Q

how does HPV lead to cancer?

A

-viral protein E6 binds to p53

viral protein E7 binds to Rb

48
Q

what is a surrogate marker of HPV-positive cancers?

A

-p16

49
Q

describe the concept of synthetic lethality

A

-two genes are synthetically lethal if loss of function of BOTH leads to cell death. The idea is if tumors have a known loss of function of a gene with a buddy that can lead to synthetic lethality than we can target its buddy gene, kill the cell, and save normal cells

CMBL (22 decks)

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