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Molecular Biology > White: Cell cycle 1&2 > Flashcards

White: Cell cycle 1&2 Flashcards

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1
Q

Chromosomal duplication and segregation occur in which phase(s) of the cell cycle

A

Duplication- S phase

Segregation- M phase

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2
Q

G1 phase occurs between

A

M and S

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3
Q

G2 phase occurs between

A

S and M

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4
Q

Checkpoint I

A

START- cell commits to cell cycle entry and chromosome duplication

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5
Q

Checkpoint II

A

G2/M- Chromosome alignment on spindle in metaphase

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6
Q

Checkpoint III

A

Metaphase-to-anaphase - Trigger sister chromatid separation and cytokinesis

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7
Q

Cdk function

A

Phosphorylate proteins downstream to activate them and regulate cell cycle events
The cell cycle is governed by Cdks

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8
Q

Cyclins function

A

Proteins that regulate Cdks
Cdks must be bound to cyclin to be active and have protein kinase activity
Direct Cdks to their specific target

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9
Q

What is the variation in cyclin and Cdk levels throughout the cycle, if any?

A

Cyclin levels vary according to point of time in cell cycle, Cdk levels are constant

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10
Q

G1/S cyclins function

A 
Start cell cycle
Activate Cdks in late G1
Help trigger progression through start
Commitment made to cell cycle entry
Levels drop in S phase
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11
Q

S cyclins functions

A

Bind Cdks after progression through start
Help stimulate chromosome duplication
S-cyclin levels remain high until mitosis

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12
Q

M cyclins functions

A

Activate Cdks that stimulate entry into mitosis at G2/M checkpoint
Removed at about the middle of mitosis

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13
Q

CAK function

A

Cdk activating kinase

Phosphorylates Cdks to activate them

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14
Q

Wee1 Kinase

A

Inhibits Cdk activity by phosphorylating the “roof site” on Cdks

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15
Q

Cdc25

A

Phosphotase that dephosphorylates “roof site” to increase Cdk activity

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16
Q

CKI proteins

A

Cdk inhibitory proteins

Binds to both Cdk and cyclin to inactivate

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17
Q

SCF-ubiquitin ligase

A

Adds ubiquitin to CKIs to target for destruction

This activates the S-Cdks

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18
Q

SCF activity depends on

A

F-box subunit

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19
Q

M-Cdk is activated how

A

Cdc25 protein phosphatase removes inhibitory phosphates from M-Cdk

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20
Q

Progression from metaphase to anaphase is triggered by

A

Protein destruction, NOT PROTEIN PHOSPHORYLATION

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21
Q

APC/C

A

Anaphase-promoting complex
Catalyzes addition of ubiquitin to protein securin (which inhibits separase from cleaving cohesin)
Causes ubiquination of M-cyclins and S-cyclins
Activated by binding to Cdc20

22
Q

Cohesin

A

Glues together sister chromatids along their length

23
Q

Securin

A

Protects cohesin protein linkages that hold sister chromatid pairs together by inhibiting separase (an enzyme that cleaves cohesin)

24
Q

PRE-RCs

A

Pre-replicative complexes
Assembly of PRE-RC is inhibited by Cdk activity
While S-Cdk and M-Cdk levels are high during S and M stage, NO PRE-RC is formed

25
Q

Condensin

A

At the end of S phase, forms ring-like structures and uses ATP to promote compaction and resolution of sister chromatids (untangle them so they can be separated)

26
Q

What triggers prophase, anaphase, prometaphase and metaphase

A

Increase of M-Cdk activity at G2/M

27
Q

Kinetochore microtubules

A

Attach each chromosome to spindle pole

28
Q

Interpolar microtubules

A

Hold two halves of spindle together

29
Q

Astral microtubules

A

Interact with cell cortex

30
Q

Dyneins

A

Minus-end directed motors
Link plus ends of astral microtubules to actin filaments at cell cortex
-By moving towards minus end of microtubule, the dynein motors pull the spindle poles away from eachother

31
Q

Kinesin-5

A

Two motor domains that interact with plus ends of anti-parallel microtubules
Moves these two anti-parallel microtubules past each other to force the spindle poles apart
If there is no Kinesin-5, the spindle collapses

32
Q

Kinesin-14

A

Minus-end directed motor, pulls poles together

33
Q

Kinesin-4,10

A

Chromokinesins- plus-end directed motors

Push attached chromosomes away from the pole

34
Q

Kinetochore

A

Responsible for attachment of spindle to chromosomes
There is an exposed open end for addition and removal of tubulin subunits from microtubules attached to kinetochore
Removal of tubulin subunits leads to force pulling kinetochore/chromosomes to pole of cell

35
Q

3 Forces in chromosome movement

A

Depolymerization
Microtubule flux
Polar ejection force

36
Q

Depolymerization

A

Depolymerization of the plus end of the microtubule drives the pulling of the kinetochore towards the pole

37
Q

Microtubule flux

A

Tubulin added at plus end while being removed at minus end

-Occurs on interpolar microtubules

38
Q

Polar ejection force

A

Kinesin-4,10 motors on chromosomes interact with microtubules and transport chromosomes from poles
Results in push-pull phenomenon

39
Q

Anaphase A

A

Chromosomes move apart

-Due to spindle microtubule depolymerization at kinetochore

40
Q

Anaphase B

A

Separation of spindle poles themselves

-By kinesin-5 motor proteins (also dynein pulls pole apart)

41
Q

Mitogens

A

Stimulate cell division by triggering G1/S-Cdk activity

42
Q

Survival factos

A

Suppress form of programmed cell dealth (apoptosis)

43
Q

Mitogen Cell-cycle entry into S-phase

A

Mitogen binds receptor
Ras causes activation of MAP kinase cascade
Increase of gene regulatory proteins including Myc
Myc promotes entry into cell cycle by increasing expression of G1 cyclins
G1-Cdk-Cyclin activates gene regulatory factors called E2F proteins
E2F binds promotors of G1/S cyclin and S cyclin genes (leads to DNA transcription)

44
Q

Rb protein

A

Tumor supressor protein
E2F protein is inhibited by interacting with Rb protein
Shuts down entry into S-phase
Active G1-Cdk phosphorylates Rb to reduce binding to E2F

45
Q

What happens if Rb protein is inactive

A

No control going into cell cycle so cancer can occur (retinoblastoma)

46
Q

ATM and ATR protein kinases

A

Activated by DNA damage

Phosphorylate Chk1 and Chk2 proteins

47
Q

Chk1/2 proteins

A

Major target is p53 protein, which stimulates transcription of p21

48
Q

p21 CKI

A

Binds to G1/S-Cdk and S-Cdk to inhibit activity (no cell division- damaged DNA must be repaired)

49
Q

What if ATM/ATR proteins are not working

A

This can cause Ataxia telangiectasia and other cancers

50
Q

Ras is mutated in __% of cancers, p53 is mutated in __% of cancers

A

Ras mutated in 30% of cancers

p53 mutated in 50% of cancers

51
Q

PI-3 kinase pathway

A

Most important growth signaling pathway
PI-3 kinase adds ATP to inositol phospholipids
Activates TOR, which activates many factors for cell growth

Molecular Biology (25 decks)

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