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Cell biology > Week 12: Cell cycle > Flashcards

Week 12: Cell cycle Flashcards

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1
Q

2 basic functions of the cell cycle

A
  1. Accurately duplicate the DNA of the chromosomes
  2. Precisely segregate the sister chromatids into 2 daughter cells
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2
Q

cell cycle control system

A

comprised of regulatory proteins that govern progression through the cell cycle

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3
Q

2 phases of the cell cycle and what is in them?

A
  1. S phase: chromosome duplication
  2. M phase: separation of sister chromatids within one cell
    - Mitotic spindles (MT based): molecular muscles that pull chromatids apart
    - Cytokinesis: division of the cytoplasm
    - Contractile ring: actin/myosin based
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4
Q

what does M phase consist of?

A
  • nuclear (mitosis)
  • cytoplasmic (cytokinesis) division
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5
Q

what does interphase contain? (3)

A
  • G1: cell growth and monitoring
  • S phase: chromosome duplication
  • G2: cell growth and monitoring
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6
Q

how can DNA content of proliferating cells be determined?

A

by flow cytometry
- look at different content of DNA by labeling cells with fluorescent dyes
- each drop of medium contains 1 cell

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7
Q

what do the first and second peaks show in flow cytometry?

A
  1. can assume the DNA is normal in the first peak
    - Unreplicated complement of DNa (G1)
  2. the second peak shows the duplication for M phase
    - Fully replicated complement of DNa (G2 and M)
  3. there are low amounts of cells in between the two peaks
    - Intermediate amount of DNA (S)
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8
Q

cyclin dependent kinases (Cdks)

A

phosphorylate substrates which control major cell cycle events ⇒ binds to cyclin as a heterodimer (active form)
- Activity of Cdks oscillates throughout the cell cycle ⇒ makes sure they are only active at the appropriate time

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9
Q

cyclins

A

bind Cdks and act as their major regulators ⇒ required for activation
- Cdks are active only when a cyclin Cdk complex is formed
- Cyclical changes in cyclin levels control Cdk activity

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10
Q

how does cyclin change over the cel cycle?

A

cyclins undergo a cycle of synthesis and degradation over the cell cycle, while levels of Cdks remain constant

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11
Q

G1/S-cyclins

A

help trigger cell division commitment

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12
Q

S-cyclins

A

trigger chromosome duplication and early mitotic events

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13
Q

M-cyclins

A

trigger entry into early mitosis
- Gradually increases amounts in G2 phase and peaks in M phase before it goes down in the middle of M phase
- Means that the complex (M-Cdk) activity should go up and down during certain phases of the cell cycle

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14
Q

each cyclin-Cdk complex phosphorylates what/

A

a different set of target proteins

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15
Q

cyclins not only activate Cdks but also ___

A

direct Cdks to their target proteins

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16
Q

G1-Cdk related to which cyclin?

A

cyclin D

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17
Q

G1/S-Cdk related to which cyclin?

A

Cyclin E

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18
Q

S-Cdk related to which cyclin?

A

cyclin A

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19
Q

M-Cdk related to which cyclin?

A

cyclin B

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20
Q

inactive state of Cdks

A

the active site is blocked by the T-loop

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21
Q

partial activation of Cdks

A

cyclin binding causes the T-loop to move out of the active site
- Not active yet because the protein conformation has been changed but there is no phosphate group

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22
Q

full activation of Cdks

A

Cdk-activating kinase (CAK) phosphorylates a Thr residue near active sites
- The T loop site has been phosphorylated to make it fully active

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23
Q

what does phosphorylation at the active site do to cyclin-idk activity inhibitory phosphates?

A

it inhibits them
- Inhibitory phosphorylation is dominant ⇒ if you have both phosphate groups added then it is inactivated vs only 1

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24
Q

Wee 1 kinase

A

cyclin-Cdk activity is turned off by this ⇒ adds the inhibitory phosphate (1 phosphate group is already present for activation)

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25
Q

Cdc25 phosphatase

A

cyclin-Cdk is activated by this ⇒ “good” enzyme for activating (removes the 2nd phosphate group)

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26
Q

Cdk inhibitor proteins (CKIs)

A

binding interferes with the active site and or the ATP binding site of Cdk
- Ex of CKIs: p21, p27
- inactivates the cyclin-Cdk complex

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27
Q

level

A

refers to amount of proteins

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28
Q

what is the relationship between M-Cdk levels and Cdk1 activity

A

Increases gradually and then drops
A- ctivity levels are different because they peak at M phase, but these are sharper
- Suggests that there is a feedback system => If you have small amounts of active molecule they feed in to form a positive feedback loop making more and more of the active molecules

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29
Q

what does “activity” not refer to?

A

the amount of protein present

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30
Q

what does activation of M-Cdk trigger?

A

entry into mitosis
- M-Cdk accumulates during G2 and M phase due to increased synthesis of M-cyclin

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31
Q

what does CAK do?

A

adds activating phosphate and Wee1 adds inhibitory phosphate ⇒ M-Cdk is initially inactive

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32
Q

when Cdc25 is added, what does it do?

A

remove the inhibitory phosphate to make fully active M-CDK
- This is an active kinase which will phosphorylate key enzymes to feed back into the system
- The active M-Cdk inhibits Wee1 and phosphorylates CAK to become active

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33
Q

positive feedback loop

A

rapidly promote the complete and irreversible activation of M-CDK

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34
Q

synthesis of M-cyclin during G2 increase what? rapid degeneration does what? When?

A

increase the level Cdk/cyclin B ⇒ entry into mitosis
- rapid degradation of cyclin at anaphase inactivates Cdk1 ⇒ exits from mitosis
Note: this is called metaphase anaphase transition => From an active controlled degradation of cyclin

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35
Q

Anaphase-promoting complex/cyclosome (APC/C)

A

controls the metaphase to anaphase transition
- APC is a ubiquitin ligase, which transfers poly-ubiquitin to target proteins, promoting their degradation in proteasomes
- M-Cdk phosphorylates APC
- M-Cdk should only be activated once throughout the cycle and then shut down until the next cell cycle

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36
Q

Cdc20

A

binds to APC to activate it during mid-mitosis

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37
Q

Cdh1

A

binds to APC to activate it during late mitosis

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38
Q

2 targets of APC

A
  1. Cyclin B (M-cyclin) ⇒ inactivation of M-Cdk
  2. Securin ⇒ activation of separase
    - both have the same activity and form a complex with APC to activate it which inactivates M-Cdk
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39
Q

Phosphorylated APC binds to Cdc20 to what?

A

inactivate M-Cdk
- M-Cdk both activates APC/C and gets inactivated by APC/C

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40
Q

Phosphorylated Cdh-1 cannot bind to what?

A

APC
- M-Cdk can phosphorylate Cdh-1 which cannot bind to APC and inhibits the complex
- once M-Cdk is inactivated by Cdc20-APC complex will allow Cdh1-APC complex to become active which will further inactivate M-Cdk

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41
Q

what is the sequential activation of APC/C? (6)

A
  • M-Cdk phosphorylates APC/C enhancing its binding to Cdc20
  • APC/C-Cdc20 triggers anaphase
  • APC/C-Cdc20 inactivates M-Cdk
  • APC/C-Cdc20 is thereby inactivated in anaphase
  • In anaphase, Cdk inactivation allow Cdh1 dephosphorylation, which stimulates formation of APC/C-Cdh1 => Cdh1 phosphorylation by Cdks inhibits its binding to the APC/C
  • APC/C-Cdh1 remains active until Cdh1 is phosphorylated by G1/S and S-Cdks at the beginning of the next cell cycle
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42
Q

functions of active M-Cdk (4)

A
  1. Assembly of mitotic spindles
  2. Control microtubule associated proteins
  3. Chromosome condensation
  4. Nuclear envelope breakdown
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43
Q

M phase subphases (5 + 1 extra)

A
  1. prophase
  2. prometaphase
  3. metaphase
  4. anaphase
  5. telophase
  6. cytokinesis (not technically M phase)
44
Q

prophase events

A
  • chromosomes have condensed and 2 sister chromatids hold together
  • Centrosomes move apart to initiate formation of 2 spindle poles
45
Q

why are sister chromatids condensed?

A

for sister chromatids to be separated without breakage they must be compacted and resolved into distinct units ⇒ DNA strands cannot be broken

46
Q

chromosome condensation

A

chromosomes are dramatically compacted

47
Q

sister chromatid resolution

A

2 sister chromatids are resolved into distinct separable units

48
Q

condensin

A

in the central core of the chromosome
- Condensin forms a ring like structure which encircles DNa loops within each sister chromatid

49
Q

what does condensing need?

A

Needs ATP activity and when active it circles around the DNa and makes a higher order
- Requires phosphorylation of 1 subunit

50
Q

what phosphorylates condensing?

A

M-Cdk phosphorylates condensin subunits to stimulate condensin activity

51
Q

mitotic spindle

A

dynamic and dense microtubule (MT) array includes MAPs and MT-dependent motors (kinesins and dyneins)

52
Q

what do mitotic spindles contain?

A
  1. kinetochore MTs
  2. Non-kinetochore MTs
  3. Astral MTs
53
Q

kinetochore MTs

A

connected to kinetochore (red) which binds ⇒ comes from centrosome

54
Q

Non-kinetochore MTs

A

dynamic interconnected meshwork not bound to the kinetochore coming from the centrosome but is segmented
- Eventually become interconnected through motor proteins

55
Q

Astral MTs

A

radiated out from centrosomes and bind to the internal part of the cell membrane at the cellular cortex ⇒ sometimes the + end goes to the opposite side
- These control the position of the centrosome

56
Q

kinesins

A

plus end directed (most are + end)

57
Q

dyneins

A

minus end directed
- motors attach cell cortex to astral MTs and pull centrosomes ⇒ controls the position of the centrosomes

58
Q

Kinesin 5

A

attach to non kinetochore MTs and push MTs to lengthen the spindle (look like an X)
- Form 2 together and each side associated with different tubules
- Each part wants to go to the plus end, but since they are connected each fragment will move the opposite ways to extend the microtubules

59
Q

kinesin 12

A

(exception) minus end directed motors attach to non-kinetochores MTs and pull MTs shortening the spindle

60
Q

the centrosome side is always + or -?

A

always -

61
Q

Chromokinesins (Kinesin4 and 10)

A

associate with chromosome arms and push the chromosome away from the centrosome

62
Q

prometaphase

A

nuclear envelope breaks down and chromosomes attach to kinetochore MTs ⇒ cannot have the envelope so the microtubules can meet the chromosomes

63
Q

nuclear lamina

A

control shape and stability of nuclear envelope

64
Q

what do nuclear lamina do in interphase?

A

In interphase nucleus, nuclear lamins polymerize into a 2 dimensional lattice

65
Q

at pro metaphase what phosphorylates lamina?

A

M-Cdks
- dephosphorylation occurs between prophase and telophase
- Phosphorylated lamins depolymerize ⇒ disassemble the nuclear lamina
- Nuclear envelope breaks down into small vesicles

66
Q

kinetochore

A

large protein complex assembling onto the centromere
- attach chromosomes to the mitotic spindles ⇒ + ends of kinetochore MTs
- MTs are attached on both sides ⇒ both sides of the kinetochore need to be connected with these

67
Q

centromere

A

the domain on the chromosome where kinetochores bind
- This is where the chromosomes are attaching at metaphase
- these events are random because the dynamic microtubules must meet at the chromosome from each side

68
Q

Ndc80

A

a large protein complex binds from the sides of the centromeric nucleosome which makes the + end of the microtubules free to polymerize and depolymerize
- the complex slides along the microtubules as it treadmills

69
Q

how are correct attachments detected?

A

The kinetochore senses a correct attachment through tension
- Incorrect attachment results in low tension
- Correct bipolar attachment results in a high level of tension
- When you have a small gap between the two chromosomes from tension that is what signals it is correctly been done

70
Q

aurora B kinase

A

connects the inner kinetochore to the outer kinetochore where it kinase domain is so it can phosphorylate target proteins
- tethered to the inner kinetochore and phosphorylates MT attachment site including Ndc80
- This reduces the affinity of MT binding

71
Q

bi polar attachment (high tension) components (4)

A
  • aurora-B unable to reach the outer kinetochore
  • MT attachment site not phosphorylated (Ndc80)
  • Increases the affinity of MT binding
  • Stable attachment
72
Q

difference between unphosphorylated and phosphorylated Ndc80?

A

unphosphorylated Ndc80 has a stronger affinity to the MT so it won’t release them
- it uses a spring and by pulling on the spring you can measure the distance in how much the spring extends

73
Q

metaphase

A

Chromosomes are aligned at the equator ⇒ metaphase plate and they come to the middle and stabilize
- state is dynamic but you don’t see it

74
Q

where do kinetochore Mts polymerize?

A

they are polymerizing at the plus end (kinetochore side) and depolymerizing at the minus end (spindle side)

75
Q

dynamic equilibrium

A

a net addition of tubulin subunits equal to a net loss of tubulin subunits ⇒ treadmilling (MT length constant)
- The rates are equal so length doesn’t change

76
Q

anaphase

A

sister chromatids abruptly and synchronously separate and move toward opposite poles

77
Q

why is it important to start anaphase? When?

A
  • the cell is in danger ⇒ too many chromosomes
  • Cells need to make sure they don’t start anaphase until all chromosomes are attached to MT’s or they end up with doubles of genes
78
Q

cohesion

A

ring holds sister chromatids together until anaphase
- when APC gets activated it breaks this glue

79
Q

securin

A

binds to and inhibits a protease called separase
- This happens before anaphase

80
Q

separase

A

cleaves cohesin which frees the sister chromatids
- The tension will then pull the two apart

81
Q

spindle assembly checkpoint (metaphase checkpoint)

A

ensures that cells do not enter anaphase until all chromosomes are properly attached to the spindles

82
Q

what does improperly attached kinetochores do?

A

sends out a diffusible signal that blocks Cdc20-APC/C activation
- Unattached kinetochores catalyze conformational changes in Mad2

83
Q

Mad2

A

gets recruited to unattached kinetochores and binds and inhibits Cdc20-APC/C
- Mad2 is involved with blocking APC which is what signals for anaphase to occur ⇒ we don’t know mechanism yet

84
Q

2 ways to separate chromosomes

A
  1. Shrink microtubules
  2. Pulling the centrosomes to the poles of the cell
    - anaphase A and B are not completely sequential ⇒ often overlap in some cells (cells do both)
85
Q

anaphase A

A

plus ends of kinetochore MTs depolymerize, pulling the attached chromatid toward the pole

86
Q

what role do Ndc80 complexes play in anaphase A?

A

hold on to the disassembling MTs

87
Q

anaphase B

A

dynein motors on the cell cortex attach to astral MTs and pull spindle poles while kinesin-5 on non-kinetochore MTs pushing spindle poles at the same time

88
Q

telophase

A
  • Daughter chromosomes arrive at the spindle poles and decondense, the mitotic spindles disassemble
  • Nuclear envelope reassembles
    → cells wrap up what they have done already in mitosis (reversal of beginning of mitosis)
89
Q

how does exit from mitosis work?

A

APC/C causes Degradation of securin ⇒ activate separase (anaphase event) and Degradation of M-cyclin ⇒ inactivate M-Cdk (telophase event)
- M-Cdk gets inactivated

90
Q

what happens when M-Cdk gets inactivated when exiting mitosis?

A

Set of phosphatases are activated to reverse phosphorylation of M-Cdk substrates => Reversion of mitotic program
- Chromosomes disassemble
- Spindles disassemble
- Lamin proteins are dephosphorylated ⇒ reform the nuclear envelope

91
Q

cytokinesis

A

Cytoplasm is divided in two ⇒ this is done by the contractile ring structure and cleavage furrow occurs on the cell surface
- no longer mitosis phase

92
Q

contractile ring

A

assembles during anaphase and is composed of actin and myosin filaments to pinch the cytoplasm into 2
- Structure underlying the cytokinesis process
- Located just beneath the plasma membrane of the cleavage furrow and the actin myosin bundles contract to pull the membrane inward

93
Q

midbody

A

the plasma membrane of the cleavage narrows ⇒ there are some structures in between the separating cells
- Daughter cells remain connected by the midbody
- Midbody contains remnants of the central spindle midzone surrounded by dense matrix material

94
Q

what may residual middy components function to do?

A

mark orientation of next spindles
- we don’t know completely what is in the midbody
- There may be translation going on ⇒ very new
- Some kind of spindle midzone

95
Q

3 models of determining the placement of the contractile ring

A
  1. Astral stimulation model
  2. Central spindle stimulation model
  3. Astral relaxation model
96
Q

Astral stimulation model

A

astral MTs carry signals to the cell cortex which specify the site of furrow formation
- 2 signals will meet int he middle which forms a certain position for cleavage contractile ring

97
Q

Central spindle stimulation model

A

spindle midzone generates signals which allows the contractile ring to form here
- This model may likely be the correct model

98
Q

Astral relaxation model

A

astral MTs promote the relaxation of actin myosin bundles except at site encircling the midzone of the spindle
- These send a negative/inhibitory signals not to assemble the contractile ring in the region

99
Q

RhoA

A

a small GTPase that triggers assembly and contraction of contractile ring
- actin and myosin must both be activated

100
Q

RhoGEF (Ect2)

A

is localized in the cell cortex at the future site of cell division
- Stimulates Rhoa activation to occur at the cleavage site

101
Q

RhoA-GTP

A

activates formins and multiple protein kinases (such as Rock)

102
Q

RhoA activates which 2 molecules?

A
  1. formis
  2. rock
103
Q

formis

A

nucleates the growth of actin filaments ⇒ controlled by RhoA

104
Q

rock

A

group of kinases stimulating myosin 2 filament formation and motor activity

105
Q

centralspindlin

A

concentrated at the beginning of cytokinesis at the overlapping plus ends of antiparallel microtubules upstream of RhoGEF
- starts in the middle of the cell and goes out toward the ends somehow

106
Q

what does centralspindlin bind to?

A

binds to the RhoA-GEF (Ect2) at the spindle midzone
- These form a complex at the spindle midzone
These complexes at the midzone will migrate to the cortex underneath the plasma membrane

107
Q

what does the centralspindlin and RhoA-GEF complex activate?

A

RhoA

Cell biology (12 decks)

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