Cell Cycle Flashcards

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1
Q

3 major functional aspects of the cell cycle

A
  1. cell growth - chromosome replication
  2. chromosome segregation
  3. cell division
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2
Q

how is the cell cycle controlled?

A

by a series of biochemical switches

regulatory proteins and checkpoints

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3
Q

chromosomal events

A

s phase – chromosomes are duplicated DNA synthesis phase

m phase – chromosome segregation

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4
Q

phases of cell division

A
prophase
metaphase
anaphase
telophase
cytokinesis
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5
Q

GAP phases of cell cycle

A

cells have gap phases to allow more time for growth

includes G1 and G2 phases

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6
Q

G1 phase

A

between M and S

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7
Q

g2 phase

A

between S and M

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8
Q

the 4 phases of the cell cycle

A

g1
s
g2
m

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9
Q

interphase

A

g1
s
g2

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10
Q

how long is M phase?

A

1 hour

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11
Q

prophase

A

chromosomes are condensed into rigid sister chromatids

attach to mitotic spindle

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12
Q

metaphase

A

sister chromatids line up at equator

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13
Q

anaphase

A

sister chromatids are pulled apart to poles of spindles

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14
Q

telophase

A

spindle disassembles

chromosomes packed into separate nuclei

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15
Q

what are the 3 checkpoints of the cell cycle

A

start
g2/m
meta to anaphase

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16
Q

START checkpoint

A

if cell passes this point it is committed to the cell cycle

before start – if poor environment cell will not pass
after start – cell will continue even if in poor conditions

also called the restriction point

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17
Q

G2/M checkpoint

A

is dna replicated?
is the environment favorable?

will trigger chromosome alignment on spindle in metaphase

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18
Q

meta- to ana- phase checkpoint

A

are all chromosomes attached to spindle?

passage will trigger chromatid separation and cytokinese

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19
Q

the cell cycle control system uses a series of switches made of ____ that turn on various steps.

A

cdks
cyclin dependent kinases

they phosphorylate proteins downstream to activate them

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20
Q

Cdk _____ changes during the cell cycle but Cdk ____ does not change.

A

activity changes

level/amount of cdks does not change

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21
Q

Cdks are dependent on the prescence of _____ .

A

cyclins

must be bound to cyclin to be active

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22
Q

inactive Cdks

A

a protein called T loop blocks the cave site (active site)

cyclin binds, T loop moves, and cdk can be phosphorylated

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23
Q

cyclins

A

cyclin presence changes thru the cycle since if they present Cdk will be active - if missing cdks will be inactive

activate Cdks and can direct them to their targets

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24
Q

4 classes of cyclins

A
  1. g1/s cyclin
  2. s cyclins
  3. m cyclins
  4. g1 cyclins
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25
Q

g1/s cyclins

A

start cell cycle by activating cdks in late g1

  • -trigger progression thru start
  • -cyclin level drops in s phase
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26
Q

s cyclins

A

duplicate dna by activating cdks after progression thru start

  • -stim chromosome duplication
  • -s cyclins levels remain high until mitosis begins
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27
Q

m cyclins

A

activate cdks that stim entry into mitosis at g2/m checkpoint

are removed mid mitosis

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28
Q

g1 cyclins

A

govern activity of g1/s cyclins

aka control progression thru start

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29
Q

4 Cdks

A

g1/s - Cdk
s - Cdk
m - Cdk
g1 - cdk

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30
Q

cyclin levels after mitosis

A

fall

and must fall in order to finish cycle

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31
Q

CAKs

A

Cdk activating kinase

cause phosphorylation of cyclin-Cdk complex

when cyclin binds Cdk and displaces t loop - phosphorylation of Cdk is caused by CAK

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32
Q

CKIs

A

Cdk inhibitory proteins

inhibit cyclin-Cdk complexes

bind to both to inactivate

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33
Q

primary use of CKIs

A

for control of g1/s-Cdk and s-Cdk in early cell cycle

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34
Q

INK4A

A

CKI involved in g1 phase

  • family hereditary melanoma
  • -mutation in this gene = loss of activity = loss of inhibition

aka no control over cell cycle

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35
Q

p53

A

tumor suppressor that influences a lot of other genes

responsible for regulating p21

p21 is a CKI that stops cell division

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36
Q

Wee1 kinase

A

Cdk inhibitor

by phosphorylating the roof of the cave site

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37
Q

Cdc25

A

a phosphatase that dephosphorylates the roof to increase Cdk activity

to oppose/undo Wee1 kinase activity

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38
Q

proteolysis of _____ to turn on S-Cdks

A

CKIs

removal of cki = removal of inhibitory factors

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39
Q

how is proteolysis of CKIs achieved?

A

by tagging them w/ ubuiqitin and proteasomes will kill them

40
Q

SCF

A

a ubiquitin adder
adds it to phosphorylated CDI

adds in g1
to help activate/restore S-cdks complex activity

41
Q

SCF activity depends on ?

A

F-Box subunit

which helps scf recognize it’s targets

42
Q

progression from metaphase to anaphase is triggered not by protein ______ but by _____ .

A

not by phosphorylation

but by protein destruction

43
Q

APC/C

A

anaphase promoting complex/cyclosome

regulator of mvt from metaphase to anaphase

44
Q

APC/C factors

A
  • -a ubiquitin ligase enzyme
  • -catalyzes addition of ubiq. to proteins
  • -S and M cyclins are major targets
45
Q

APC/C activation

A

activated by binding to cdc20

46
Q

APC/C affects 2 major proteins

A

cohesin

securin

47
Q

cohesin

A
  1. glues sister chromatids together along length
  2. large protein
  3. a structural maintenance protein
  4. forms rings around sisters
48
Q

securin

A

protects cohesin protein links that hold sisters together

how? by inhibiting the separase enzyme

APC/C will ubiq. securin and it will be destroyed allowing separase to activate

49
Q

separase

A

an enzyme that cleaves cohesin

resulting in the separation of sister chromatids

50
Q

what is the role of PRE-RC in duplicating chromosomes once?

A

PRE-RC = pre replicative complex

assembles at origins of dna replication

during mitosis no new pre-rc are made thus dna is only duplicated once

51
Q

assembly of PRE-RC is inhibited by ?

A

Cdk activity

52
Q

DNA at the end of S phase

A

it is a tangled mess and must be organized into sisters to avoid breaks

done thru a 2 step process by condensin

53
Q

condensin

A

a 2 step process to condense chromatids

  1. condense chromosomes
  2. resolution = sister chromatids becoming distinct separate units
54
Q

what is condensin?

A
  • -5 subunit protein complex
  • -2 smc and 2 non-smc units
  • -uses ATP to promote compaction and resolution
55
Q

order of mitosis

A
  1. condensation of chromosomes
  2. assembly of mitotic spindle
  3. breakdown of nuclear envelope
  4. attachment of chromatids to spindle
56
Q

3 types of microtubules

A

kinetochore
Interpolar
astral

57
Q

kinetochore microtubules

A

attach plus end to kinetochores on chromatids

minus end attached to spindle pole

have associated motor proteins for pulling

58
Q

Interpolar microtubules

A

hold the two spindle poles together

attach to Interpolar microtubules from the other pole

plus end interacts w/ other plus end

59
Q

astral microtubules

A

connect the spindle to cell cortex

radiate out
helping to position pole in cell

60
Q

astral and Interpolar motor proteins

A

their motor proteins work to push chromosomes towards their respective poles

61
Q

kinetochores

A

large protein structures on chromosomes located at the centromeres

62
Q

origination of microtubules

A

MTOC - microtubule organizing center or centrosome

minus end always stays attached to the centrosome

centrosome is also the site of the spindle poles

63
Q

assembly and function of mitotic spindles depend on ?

A

motor proteins
dynein - mvt toward minus end
kinesin - mvt toward plus

64
Q

4 major motor proteins involved in spindle function

A

kinesin-5
kinesin-14
kinesin-4,10
dynein

65
Q

kinesin-5

A

interacts w/ plus end of anti-parallel microtubules

mvt forces centrosomes apart

the 2 motor domains walk towards the plus end of each mt to push centrosomes apart

66
Q

if no kinesin-5?

A

spindles will collapse

67
Q

kinesin-14

A

minus oriented
1 motor domain
walks towards the minus end - pulling the poles together - towards center

68
Q

kinesin-5 and -14 action

A

oppose each other to stabilize the poles

69
Q

chromokinesins

A

also called kinesin-4,10

70
Q

kinesin-4,10

A

plus directed
1 motor domain
head domain attached to chromosomes

mvt towards plus end pushes chromosomes away from pole

71
Q

dynein

A

minus end directed motor

link astral mts to actin skeleton

mvt pulls the spindle poles away from each other

72
Q

3 forces of chromosomal mvt

A
  1. depolymerization
  2. microtubule flux
  3. polar ejection
73
Q

kinetochore attachment

A

anchoring proteins - Ndc80
links kinetochore to microtubules

microtubules depolymerize at open plus end which pulls chromosomes towards the centrosome

74
Q

kinetochore must be properly attached - sister chromatids must attach to opposite poles. a stable attachment is detected by ?

A

kinetochore tension

75
Q

force 1 - depolymerization

A

pulls the kinetochores to centrosome

happens at the open plus end of microtubules

76
Q

force 2 - microtubule flux

A

microtubules are moving towards poles while being dismantled at minus end

Interpolar mts add at plus, lose at minus = escalator effect

77
Q

force 3 - polar ejection

A

kinesin-4,10 motors on chromosomes interact w/ mts and transport chromosomes

results in a push pull effect - where the chromosome ends trail behind the kinetochore that is being pulled

78
Q

anaphase A vs. anaphase B

A

a - chromosomes move apart by mts depolymerization

b - separation of poles by kinesin-5

79
Q

3 classes of extracellular signaling molecules to regulate cell size/number

A

mitogens
growth factors
survival factors

80
Q

mitogens

A

binds to receptors on cells to activate the Ras-map kinase pathway

resulting in increased gene regulatory proteins - including Myc

81
Q

Myc

A

a regulatory protein that promotes entry into cell cycle by increasing expression of g1 cyclins

82
Q

cells in culture will divide on _____ dependence of ____ levels.

A

density

mitogens

83
Q

G1-Cdk-cyclin activates a group of ?

A

gene regulatory factors called E2F proteins

84
Q

E2F proteins

A

bind to promoters of g1/s cyclin and s cyclin genes

to promote DNA synthesis

85
Q

growth factors

A

stimulate cell growth

86
Q

survival factors

A

suppress apoptosis

87
Q

E2F protein is inhibited by ?

A

interaction w/ Rb protein

it shuts down entry into s phase

88
Q

what stops Rb?

A

active g1-cdk phosphorylates Rb to stop it from inhibiting E2F

89
Q

what if Rb protein does not work?

A

no control over cell cycle

cancer

=retinoblastoma

90
Q

Retinoblastoma

A
  • -no Rb protein
  • -Rb is tumor suppressor and prevents over proliferation of cells

must lose BOTH copies for retina tumors to develop

91
Q

DNA damage activates ?

A

ATM and ATR protein kinases

92
Q

ATM and ATR associate w/ sites of damage to

A

DNA

will phosphorylate Chk1 and Chk2

93
Q

Chk1 and Chk2 targets

A

target p53 proteins to stimulate p21 transcription

p21 is a CKI which will stop cell cycle to allow DNA time to fix itself

94
Q

AT disease

A

ataxia telangiectasia
mutation in AT gene - ATM protein

radiation sensitive which damages DNA

mutation in ATM protein so cell cycle is not stopped - DNA not fixed

95
Q

AT symptoms

A

ataxia - poor coordination
telangiectasia - small dilated BVs

autosomal recessive