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MIMS > Cell Cycle > Flashcards

Cell Cycle Flashcards

1
Q

What 2 things must cells be able to do

A

Multiple and differentiate

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2
Q

What did Virchow say

When

A

“Omnis cellula e cellular”

1858

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3
Q

What is used to mark when observing DNA

A

Histones

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4
Q

Cancer is a disease of hyperplasia

True or false

A

True

Therefore many treatments inhibit cell division

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5
Q

Other than cancer, what diseases affect the cell cycle

A

Some Viruses cause hyperplasia and even cancer

Cylcomodulins allow pathogenic bacteria to control the host cell cycle

Rare genetic diseases eg microcephaly can be caused by cell cycle mutations

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6
Q

What are the phases of the cell cycle

A

M -> G1 -> S -> G2

⬆️ ⬇️ ⬆️⬅️⬅️⬅️⬅️⬅️⬅️

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7
Q

What is S phase

A

Synthesis phase (DNA replication)

Making a perfect copy of the genome

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8
Q

What is M phase

A

Mitosis and cytokenesis

Nuclear division - splitting DNA between 2 daughter cells

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9
Q

What is cytokinesis

A

Cytoplasmic division

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10
Q

What happens in the gap phases

A

Critics for maintaining cell size

Cell growth

Also where cell responds to cues

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11
Q

What is G0 phase

When is it

A

Prolonged exit from cell cycle

Early G1 phase

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12
Q

Which cycle phase must cancers overcome to induce hyperplasia

A

G0

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13
Q

When do cells only go through half the cycle

A

Never - it is an all or nothing process

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14
Q

What keeps the cell cycle as an all or nothing process

A

Check points - you can proceed unless the previous phase is complete

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15
Q

What are the cell cycle checkpoints

A

Spindle assembly checkpoint (SAC)
START (G1/S checkpoint) - commit to entire cycle
G2/M checkpoint - is replication complete

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16
Q

How do you build a molecular switch

A

Enzyme is only active when bound to a cofactor which then inhibits the inhibitor of the enzyme creating a bistable switch

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17
Q

What is the graph of Cofactors concentration vs enzyme activity if the enzyme requires the cofactors to be active

A

Hyperbolic relationship - increases until enzyme is saturated then plateau

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18
Q

What is the graph of a bistable switch

A

Cofactors concentration vs enzyme activity

Shallow positive gradient (off), then v steep gradient, then shallow (on)

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19
Q

Explain bistable switch phases

A

Off- when inhibitor concentration is high and cofactor concentration is low - inhibitor is winning so enzyme is “off”

Steep- after a critical point when enough enzyme is activated to inhibit the inhibitor - positive feedback loop - rapid enzyme activation

On- all enzymes are on

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20
Q

What do bistable switches ensure

A

You can only go one way and the phase is completed in full

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21
Q

What is the master regulator in the cell cycle

A

Cyclin Dependent Kinase (CDK)

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22
Q

What do kinases do

A

Transfer phosphates usually from ATP to a substrate

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23
Q

How does CDK act on its own

A

It doesn’t it is inactive by itself

It must be activated by binding to different cyclins in different phases of the cell cycle

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24
Q

Which cyclin is present in G1

What does it activate

A

Cyclin E

CDK2

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25
Q

Describe how the cyclins change in concentration throughout the cell cycle

A

Cyclin E is high in G1
Cyclin A begins to rise after the START checkpoint and remains high throughout S and G2. Cyclin A then drops at G2/M checkpoint, falling to 0 by the middle of M phase
Cyclin B begins to rise at the end of S phase, rises throughout G2 and plateaus in the first half of M phase and drops to 0 after the SAC checkpoint

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26
Q

What does cyclin A activate

A

CDK2

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27
Q

What does cyclin B activate

A

CDK1

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28
Q

When do cyclin D levels rise

What does it activate

A

G1

CDK4/6

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29
Q

Which cyclin and CDK is necessary for replication of genome (S phase)

A

Cyclin A

CDK2

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30
Q

Which cyclin and CDK is necessary for mitosis

A

Cyclin B

CDK 1

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31
Q

How are cyclin levels regulated

A

Cyclin transcription is tightly controlled within the cell cycle

Cyclin levels are tightly controlled by ubiquitin mediated degradation

Inhibitory phosphorylation

CDK inhibitor proteins

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32
Q

What are the transcription factors that regulate cyclin transcription

A

E2F transcription factors
(1-5)
1,2,3 are activators
4,5 are repressors

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33
Q

What are the co repressors of the E2F transcription factors

A

Rb family (repress activator E2F)

p107 and p130 exacerbate repressor E2F proteins

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34
Q

What was the first cloned tumour suppressor protein

A

Rb

All cases of retinoblastoma are caused by Rb mutations

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35
Q

What does Rb do in G0 phase

A

Binds to E2F proteins and inactivates them

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36
Q

How do repressor E2F proteins work

Give an example and how it can be exacerbated

A

They are bound to DNA and inhibit cyclin transcription

Eg E2F4 inhibits cyclin E gene transcription
This is augmented by p107 binding to E2F4
Turn off these genes so cell cycle can’t start

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37
Q

How do you start the cell cycle

A

Mitogens activate cyclin D-CDK4, this deactivates p107 and Rb to inhibit the repressors

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38
Q

What does the phosphorylation of Rb by cyclin D-CDK4 do

What about phosphorylation of p107

A

Releases Rb from E2F1, allowing E2F1 to bind to the target promoters

No longer bound to E2F4, so doesn’t help inhibition

Now cyclin E can be transcribed

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39
Q

How does ubiquitin degrade substrates

A

A chain of ubiquitin bound to a substrate is a signal to the proteasome to destroy the substrate

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40
Q

What binds ubiquitin to a substrate

A

Ubiquitin ligases

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41
Q

Name an important ubiquitin ligase in the cell cycle

A

Cyclosome (APC/C)
Or
Anaphase promoting complex

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42
Q

When is APC/C active

A

When bound to an activator

Either Cdc20 or Cdh1

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43
Q

What does APC/C - cdc20 degrade

A

Cyclin B

Securin

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44
Q

What does the APC/C - cdh1 complex degrade

A

Cyclin A

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45
Q

When is APC-cdc20 active

A

After mitosis

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46
Q

When is APC-cdh1 active

A

After G0

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47
Q

How do cyclins affect APC-cdh1

What does this result in

A

Cyclin E- CDK2 and cyclin A-CDK2 both inhibit APC-cdh1

Bistable switch

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48
Q

How do cyclins affect APC-cdc20

A

Cyclin B - CDK1 activate APC-cdc20

It activates its own inhibitor

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49
Q

What causes inhibitory phosphorylation of cyclin CDK complexes

Why is this called this

A

Wee1 kinase

Without Wee1 there is not enough inactive cyclin CDK so cells go through the cycle too quickly and end up being v small

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50
Q

What acts antagonistically to Wee1

A

Cdc25 phosphatase

Which activates cyclin-CDK complexes

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51
Q

When are CDK inhibitor proteins active

A

In G0 and G1 if you want to be quiescent and you want CDK to be fully inhibited

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52
Q

What transition must be overcome to cause hyperplasia

A

G0 to G1 transition

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53
Q

What is a mitogen

Give an example
What does this example bind to

A

A (usually)extracellular signal that tells a cell to divide

Eg EGF binds to EGFR (a tyrosine kinase receptor)

54
Q

What molecule is almost always involved in starting the cell cycle after the mitogen binds to a receptor

What does this activate

A

RAS
(Active RAS is bound to GTP, it is inactive when bound to GDP)

MAPK

55
Q

What is the important thing that MAPK activates for the cell cycle

A

Transcription eg Transcription of MYC

56
Q

What does Myc do for the cell cycle

A

It is a transcription factor that leads to Cyclin D - CDK4 expression

Also inhibits inhibitors (p16 INK4a) of Cyclin D CDK4

57
Q

How common is EGFR mutated in MSC lung carcinomas

What does this mutation do

A

20%

Makes it independent of mitogen

58
Q

How common are Ras mutations in human tumours

A

20-25% of all human tumours

59
Q

How often is Myc altered in cancer

A

4% of all cancers

60
Q

Do you get multiple mutations in different parts of the cascade leading to entry to the cell cycle in cancer ?

A

No

Only one part will be mutated, there is no benefit of having more

61
Q

How do cancer viruses cause cancer

A

Inhibiting Rb

62
Q

How does HPV inhibit Rb

What about Adenovirus

What about SV40

KSHV

A

E7 is expressed which inhibits Rb

E1A is expressed

T-antigen

vCyclin

63
Q

What does cCyclin do

A

Expressed due to KSHV

vCyclin is v similar to Cyclin D2, which binds to CDK6, driving the cell into cell cycle

64
Q

What do you call signals that tell cells to stop dividing

Give an example

A

Antimitogens

TGF-β

65
Q

How does TGF-β work

A

Activates SMADS

66
Q

How do SMADS prevent cell cycle progression

A

They are a co repressor of p107-E2F4 complex - add extra layer of repression

Also Activate p15 INK4b which inhibits Cyclin D-CDK4

67
Q

How are anti mitogens involved in cancer

Give an example

A

SMADS are deleted

SMAD4 is mutated/ deleted in 55% of pancreatic cancers

68
Q

Talk about the Belgian blue cow

A

They have mutations in the anti-mitogen myostatin which stops proliferation of myoblasts so end up 2x amount of muscle cells

69
Q

What are the problems with DNA replication

A

Accuracy and rate

70
Q

How do cells over come the rate of replication problem

A

Multiple origins
Human cells have roughly 50,000 origins
So replication can occur multiple times in S phase

71
Q

What is the problem that arises from having multiple origins

A

They must all fire in a coordinated manner

72
Q

How do we coordinate the cell cycle

A

Replication initiation is a 2 step process

Step 1: licensing
Step 2: activation of helicase and recruitment of polymerases

73
Q

What is licensing

When does this happen

A

Helicase loading - separating 2 strands

G1 phase

74
Q

Is the cell ready to enter the cell cycle after licensing?

A

No

Licensing leads to an inactive complex

75
Q

When does step 2 of replication initiation occur

A

S phase

76
Q

What stops the 2 steps of replication initiation happening simultaneously

A

They are mutually exclusive

77
Q

Why are step 1 and step 2 of replication initiation mutually exclusive

A

Cyclin A -CDK2 is required for step 2
APC-cdh1 is active in step 1
The high [APC- cdh1] rapidly degrades Cyclin A-CDK2 so step 2 cannot be initiated
Also inhibits Geminin which is needed for step 2

Equally, cyclin A - CDK2 inhibits APC-cdh1, and absence of APC - cdh1 allows geminin to to accumulate and thus helicase loading is inhibited. This prevents the previous step occurring at the same time a

78
Q

What does geminin prevent

A

Loading of helicase

CDK2 also inhibits this

79
Q

What do you want from the 2 daughter chromosomes during mitosis

A

You want the 2 different chromosomes together at either side of the cell

80
Q

How do cells ensure the 2 sisters don’t end up together in mitosis

A

2 sisters are bound together and align in the centre so they can be pulled apart to opposite sides of the cell

81
Q

How is DNA supercoiling resolved during mitosis

What is this called

A

The action of topoisomerases which rotate the chromosome, leading to the sisters becoming intertwined

Topological linkage

82
Q

What is a type 1 topoisomerase

A

Causes ssDNA nicks

83
Q

What is Type 2 topoisomerase

A

Causes dsDNA breaks

84
Q

Other that topoisomerase enzymes, what enzyme class can resolve intertwines in DNA

A

NONE

Only topoisomerases can

85
Q

Other than topologically, how does replication result in sister chromosomes being held together

A

Cohesion of the sisters by cohesin

86
Q

describe the structure of cohesin

A

A ring formed by 2 dimers bound at the top by each dimer’s head and a gap at the opposite end, which is closed by a protein called Scc1

87
Q

What does cohesin do

A

Wraps around 2 daughters after replication in S phase

88
Q

Where is the last place cohesin is lost from sister chromosomes

A

The centromere

89
Q

How are sisters aligned in the middle of the cell

A

Mitotic spindles

90
Q

What are spindles made of

A

Tubulin which make up polymers called microtubules

91
Q

Other than for spindles what are mircotubules needed for

A

The structure of the cell

92
Q

What is the kinetochore

A

The point of attachment of microtubules to the chromosome

93
Q

What is the centromere

A

The region of the chromosome that assembles the kinetochore

94
Q

What is the centrosome

A

The microtubule organising centre

95
Q

What are astral microtubules

A

Emanate away from spindle to the cell vortex to position the spindle in the middle of the cell

96
Q

How do spindles arrange the chromosomes in the centre of the cell

A

Microtubules released from the centrosome on one side bind to the chromosome, but only when spindles from both sides bind will tension be generated

The tension will be equal in each microtubule when the bound chromosome is in the centre of the cell

97
Q

What happens if the microtubules bind incorrectly to the kinetochore

A

Low tension

If only one microtubule binds, there will be low tension
If two microtubules from the same side bind to 2 kinetochores on the same chromosome, there will be low tension.

This is how Two centrosomes ensure the chromosomes are aligned in the centre of the cell

98
Q

Which molecule is involved in splitting the sisters after they’re aligned in the cell

What does it do

A

APC-cdc20

Degrades cyclin B and securin

99
Q

What does securin do

A

Secured the cohesin ring by binding to and inhibiting separase

100
Q

What does separase do

When is it active

What can happen now

A

Cleaves cohesin ring by cleaving scc1 gate

When APC-cdc20 is present as it degrades cyclin B (which phosphorylates and inhibits separase) and securin (which inhibits separase)

Spindles can pull sisters apart

101
Q

What does chromatin mean

What about mitosen

A

Stainable

Thread

102
Q

What are the phases of mitosis

A

Prophase➡️ prometaphase ➡️ metaphase ➡️ anaphase ➡️ telophase ➡️ cytokinesis

103
Q

What happens in the first phase of prophase

A

Chromosomes condense in the nucleus

Centrosomes separate in the cytoplasm

104
Q

What happens in prometaphase

A

Nuclear envelope breakdown and kinetochores start to attach to microtubules

105
Q

What happens in metaphase

A

Chromosomes align in the centre in the centre of the spindle

After this APC - cdc20 is turned in

106
Q

What happens in anaphase

A

Sister chromosomes synchronously separate

107
Q

What happens in telophase

A

Two nuclear envelopes reassemble

108
Q

What is the final stage of mitosis

What happens here

A

Cytokinesis

Division of the cytoplasm

109
Q

Which cyclin / CDK is needed for centrosome duplication

A

Cyclin E - CDK2

110
Q

Which cyclin / CDK is needed for genome duplication

A

Cyclin A

CDK2

111
Q

What are the 2 important events that cyclin E - CDK2 initiate

A 
Centrosome duplication 
Genome duplication (via activation of Cyclin A -CDK2
112
Q

Where is cyclin B-CDK1 found initially

Why

A

Cytoplasm

It controls the movement of centrosomes to opposite ends of the cell
And
Controls cell rounding

113
Q

What is cell rounding

A

Changing the shape of the cell - if the cell is attached to another cell it must detach, go through mitosis, then reattach

114
Q

How does cyclin B CDK1 enter the nucleus

What does it do once it’s in there

Why is this a badly phrased question

A

By breaking down the nuclear membrane

Inhibits spindle elongation and activates APC -cdc20

Cyclin B CDK1 breaks down the nuclear membrane so there is no nucleus so it can’t be inside the nucleus

115
Q

5 things Cyclin B - CDK1 does to prepare for mitosis

A 
Centrosome movement
Cell rounding
Nuclear membrane breakdown
Inhibits spindle elongation 
Activates APC-cdc20
116
Q

Why is cyclin B CDK1’s inhibition of spindle elongation important

A

Prevents spindle pulling apart too early and stops anaphase happening too early

117
Q

What is the SAC

A

Spindle assembly checkpoint

Checks all chromosomes are attached to the mitotic spindle before anaphase can occur

118
Q

What checkpoint ensures replication is complete

How

A

G2/M

Use of check point kinases

119
Q

Which check point kinases are used at the G2/M checkpoint

A

ATM and ATR which then activate check 1 and check 2 (both kinases)

120
Q

What do checkpoint kinases do specifically

What does this do ultimately

A

Inhibit activation of Cyclin B-CDK1 by inhibiting cdc25 phosphatase and activating Wee1 kinase

Prevents progression into mitosis

121
Q

What tells the The cell not to activate APC yet as kinetochores are not fully attached

A

SAC - a signal from the unattached kinetochores - the MCC (mitotic checkpoint complex)

This sequesters and inhibits the APC by inhibiting cdc20 subunit

cdc20 is released when all kinetochores are attached and anaphase is allowed

122
Q

How many cancer mutations are caused by random mutations during replication according to which 2017 study

A

66%

Tomasetti and Vogelstein

123
Q

Most solid cancers are aneuploid. True or false?

A

True

124
Q

How do cancers become aneuploid

A

They have more than 2 centrosomes, giving a random distribution of chromosomes

125
Q

How do you get multiple (>2) centrosomes

A

Mutations in cyclin D-CDK4 pathway (eg of Rb) leads to too much cyclin E and too many centrosomes (as cyclin E leads to centrosome duplication)

126
Q

How was nitrogen mustard discovered to be a treatment for cancer

A

In WWII when it was used as mustard gas

Victims were seen to have no RBCs so nitrogen mustard must inhibit replication (RBCs are rapidly dividing)

127
Q

Where do taxane drugs come from

A

The Pacific yew tree

128
Q

Why may chemotherapy lead to further cancerous evolution

A

Selection pressure

And

Anything that messes with the cell cycle will result in mutations, which cancers thrive off, and chemotherapy tackles cancer by inhibiting DNA replication or mitosis (both parts of the cell cycle)

129
Q

What kind of cancer drug are Astra Zeneca interested in

What kind of mutant does this attack

A

PARP inhibitors

BRCA

130
Q

Easy way to remember to remember the phases of mitosis

A 
Please (prophase)
Pass (prometaphase)
Me (metaphase)
A (anaphase)
Taco (telophase)
Chief (cytokinesis)

MIMS (12 decks)

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