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BMS247 Stem Cells > L10 + L11 - Cell Cycle > Flashcards

L10 + L11 - Cell Cycle Flashcards

1
Q

4 causes of cancer

A

Enviro - carcinogens
Viral infection
Inherited factors
Genetic instability

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2
Q

Normal cells will only proliferate when …

A

There are growth factors present

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3
Q

Absence of growth factors =

A

No proliferation

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4
Q

What can other signals cause to happen to grwoth factors

A

Overrule the stimulatory effects of growth factors and force a halt to prolife

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5
Q

EC signals can induce a post mitotic differentiated state

What is significant about this state

A

There is no proliferation

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6
Q

What is the cell cycle clock

A

Master governer

Network of interacting proteins that recieves signals from the outside and inside - integrates these signals and then decides on the fate of the cells

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7
Q

cell proliferation is controlled by

A

Cooperation of a veriety of proteins

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8
Q

What are growth factors

A

Small proteins

Travel through EC space to covery messages to other cells

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9
Q

What are growth facotrs also known as

A

Mitogens

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10
Q

Why are growth factors often known as mitogens

A

Indicating their ability to induce proliferation

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11
Q

Uncontrolled cell proliferation can lead to

A

The formation of a tumour;

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12
Q

How do cancer proteins inflcuence the cell cycle clock

A

Disruption of the normal control mechanisms leading to sustained proliferation

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13
Q

Alternative ways cancer cells induce prolierations

A

Auto produce growth facotrs
Signals stimulate surrounding cells to cause production of GF
Degreulation of GF receptors (leads to seemingly inc conc of GF)
Consitit act of GF downstream targes
Disruption of negative feedback which atteuates signalling

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14
Q

G1

A

first gap pahase
Key decision to prolif or remain quiescent
8-10

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15
Q

G0

A

Non growting

Withdrawl from cell cycle

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16
Q

Is G0 reversible

A

Can be either

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17
Q

What cells is G0 irreversible

A

Neurones of the brain

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18
Q

How can G0 be revered

A

Through stimulation with mitogens

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19
Q

S

A

Replication

6-8 hrs

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20
Q

What cells is S phase faster

A

Normally proliferative cell types - lymphocytes

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21
Q

G2

A

Cell growth continues

Replication of the centrososmes

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22
Q

When is the decision to proliferate made

A

In G1

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23
Q

What is the difference between cell growth and cell division

A

Growth = accumulation of cellular constituents

Division = actual splitting of the cells via mtiosis and cytokinesis

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24
Q

What methods has histoirically been used to study the cell cycle

A

Flow cytometry

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25
Q

Advantages of flow cytometry

A

Fast

Quantitative

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26
Q

Flow cytometry analsyses …

A

DNA conent - cells must be loaded with a flourescent dye which lables the DNA

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27
Q

Describe what would be seen in flow cytometry of a cell in G2 or M phase

A

Would have double the DNA

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28
Q

What other methods may be used to study the cell cycle

Stages of mitosis

A

Immunoflourescence and epiflourescence microscopy

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29
Q

During G1 there is a discrete window to ….

This occurs …

Known as …

A

consult the EC environment

Onset of G1 to just before G2

Restriction R point

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30
Q

If GF and serum are removed before the cells have competed 80-90% of G1

A

Cells fail to proceed and exit into G0

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31
Q

If serum and GF removed in the final hour of G1

A

Cells proceed to S, G2 and M phase

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32
Q

If a cell goes past the restriction point what must it do

A

Complete the rest of the cell cycle

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33
Q

Why is there a discrete window to consult the EC environement

A

Downregulation of R point machinery in G1

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34
Q

What experiements were performed by Rao and Johnson

A

Nuclear fusion experiements

Mixing nuclei in the same cytoplasm to see if they influenced each other

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35
Q

Mixing multiple nuclei in the same cytoplasm is also know as `

A

Heterokaryon

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36
Q

S and G1 nuclei fused

A

Gives 2 s phase

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37
Q

S and G2 nucelus

A

No effect

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38
Q

G1 and G2 nucelus

A

No effect

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39
Q

Interphase and mitotic nucelus

A

Two mitotic nucelus

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40
Q

What conclusion can be made from the heterokaryon expt regarding:

THE S PHASE NUCELUS

A

Contains a diffusible factor inducing replication

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41
Q

What conclusion can be made from the heterokaryon expt regarding

G2 NUC

A

G2 nucelus is resisitant to the S phase promoting factor

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42
Q

What conclusion can be made from the heterokaryon expt regarding

G1 AND G2 NUCE

A

they have no effect on each other

43
Q

What conclusion can be made from the heterokaryon expt regarding

Mitotic nuceli

A

Mitoitc nuceli release mitosis promoting factor that affects all interphase nuclei

44
Q

two core components of the cell cycle clock

A

Cyclins and CDKs

45
Q

CDKS are

A

Kinase which have multiple tatger

46
Q

What is the effect of cyclins on CDKs

A

Activate the catalytic activity (can increase by up to 400’000 fold)

Help with substrate recognition of the cyclin CDK complexes in the cells

47
Q

3 model systems for cell cycle study

A

yeast
Frog Eggs
Sea urchin embryos

48
Q

Adavantage of frog eggs

A

Biochemical analysis is easy due to the size

49
Q

Two cell cycles shown in Yeast

A

Fission and budding

50
Q

What different mutatns were created in yeast

A

Wee
Cdc
Temperature sensitve

51
Q

Describe the principles of a temperature sensitive mutation

A

At a permissive temperature the protein has wildtype function

52
Q

What substance was discovered in frog eggs

A

Maturation promoting factor - AKA - mitosis promoting factor

53
Q

What is MPF linked to

A

A protein with kinase activity which osciallates during the cell cycle

54
Q

What happens if you were to put sea urchin embryos in soapy water

A

They start dividing

55
Q

What was seen when proteins in the C urchin embryo were labelled with radioactive-methionine

A

Shows that one protein accumulates as cells get ready to divide
This then disappear when division occurs

56
Q

Injection of cyclin is suffience to ….

A

Induce maturation and activation of MPF

57
Q

What is the 2 major activites of MPF

A

Binding of cyclin to Cdc2 kinase

Phosphorylation of cdc2

58
Q

What two enzymes act to regulate activity of CDKS

A

Wee 1 kinase

Cdc25 phosphatase

59
Q

What cyclin/CDK pairing involved in

G1

A

CDk4 and CDK6 depend on the association with cyclin Ds

60
Q

What are the D type cyclins

A

D1 D2 and D3

61
Q

What cyclin/CDK pairing involved in

After the R point

A

E type cyclins associate with CDK2

Then phosphorylation of the substrates required for the entry into S phase

62
Q

What cyclin/CDK pairing involved in

S

A

A type cyclins replace E type cyclins in complex with CDK2 this causes S phase progression

Later in S phase A type cyclins associate with CDC2 AKA CDK1

63
Q

CDK1 AKA

A

CDC2

64
Q

What cyclin/CDK pairing involved in

G2 phase

A

B type cyclins replace the A type cyclins in complex with CDC2

65
Q

What cyclin/CDK pairing involved in

M phase

A

B type cyclins in CDC2 trigger the entry into mitosis

66
Q

What cyclin/CDK pairing involved in

G0 to G1

A

Mediated by cyclin C in complex with CDK3

67
Q

Describe the fluctuations of cyclin E during the cell cycle

A

Low levels throughout most of G1 then rapid increase after the R point

68
Q

Describe the fluctuations of cyclin A during the cell cycle

A

Levels increase when the cell enters S phase

69
Q

Descrube the fluctuations of cyclin B during the cell cyce

A

Levels increase in anticiptation of entry into M phase

70
Q

Why does cyclin level decrease at various points in the cell cycle

A

Through degradation in a ubuiquitin dependent manner

71
Q

What is the reason that the cell cycle can only proceed in one direction

A

The cycling levels of cyclins

72
Q

Why is D cyclin an exception

A

Exp at constant levels and regulated by EC signals

73
Q

What controls the expression of D type cyclins

A

Growth factors and integrin mediated ECM attachement

74
Q

D type cyclins convey ..

A

Messages from the EC environment to the cell cycle clock in the nucleus

75
Q

Where are D cyclins synthesised

A

In the cytoplasm and then transported to the nucelus

76
Q

Removal of growth factors leads to

A

Rapid collapse of cyclin D1 levels

77
Q

Describe the two possible fates of D type cyclin in G1 what is the effect that this would have on the cell cycle

A

If favourable environment then cyclin D enters the nucleus and the cell cycle goes on

If unfavourable environment then the cell cycle arrests in G1

78
Q

D type cyclins respond to

A

EC environment

79
Q

How do cyclins/CDKs help with the forward progression of the cell cycle

A

Activate in the next phase

Inhibit complexes involved in previous phases

80
Q

What are CKIs

A

CDK inhibitors

81
Q

What proteins inhibit D type cyclins

A

P16, P15, P18, P19

82
Q

Why write out the inhibitors of D cyclins as

P16 P15 P18 P19

A

Because superscripts then go

p16 - INK4A
P15 - INK4B
P18 - INK4C
P19 - INK4D

83
Q

What is the other group of CKIs that inhibit E-CDK2, A-CDK2, A-CDC2, B-CDC2

A

P57
P27
P21

84
Q

At the start of G1 what is the cyclin CDK pairing?

A

D-CDK4/6

85
Q

After the restriction point what happens to the cyclins and CDKs

A

Cyclin E is brought into a complex with CDK2 triggering S phase

86
Q

What complex is responsible for driving the cycle into S phase

A

E-CDK2

87
Q

What happens in S phase to the E-CDK2 complex

A

E cyclin replaced with A cyclin forming A-CDK2

CDK2 is then replaced with CDC2 forming A-CDC2

88
Q

What is the complex is G2 phase

A

B-CDC2

B cyclin replaces the A cyclin

89
Q

What cyclin/CDK complex is responsible for driving the cell into M phase

A

B-CDC2

90
Q

What is the role of TGF-B in the early stages of carcinomas

A

TGF-B arrests the growth of many stages of cancer

91
Q

What is the role of TGF-B in the later stages of carcinomas

A

Contributes to the invaseivness of tumours

92
Q

What is the molecular mechanisms implicating TGF-B in the control of the cell cycle clock (R point)

A

TGF-B increases the levels of P15(INK4B) leading to inhibition of D-CDK4/6 so cells unable to make it to the cell cycle

93
Q

What does TGF-B weakly induce?

What is the effect of this?

A

Increases the levels of P21(Cip1) cell cycles is then halted

94
Q

What provides a stronger stimulation of P21(Cip1)

Why is this important

A

Stronger induction through DNA damage

Ensures the cell cycle does not progress into S phase and copy damaged DNA

95
Q

Akt AKA

A

P-B

96
Q

What is the action of Akt on P21

A

Phosphorylation in the nucleus causing translation to cytoplasma

97
Q

What is the effect of Akt on P27

A

Phosphorylation in the cytosol blocking nuclear translocation

98
Q

How may Akt be related to human tumours

A

Akt activation correlates with cytoplasmic P27 and doesnt block cell growth

99
Q

What must happen to Akt (PK-B) for it to become active

What is the active version known as as a result of this

A

Must be first phosphorylated

Induces a confirmational change

Phospho-Akt

100
Q

What is the result on P71 and the cell cycle of there being low levels of phospho-Akt present/

A

Localisaiton of P27 is strongly nuclear

Is able to act to block progression of the cell cycle

101
Q

What is the effect of active PKB (Akt)

A

Activated through phosphorylation
P27 in the cytoplasm
Unable to block progression of the cell cycle

102
Q

Is outlook better for patient when P27 is localised only to the nucleus or the cytosol

A

Better outlook when P27 only in nucleus - able to have more of an effect on arresting the cell cycle

103
Q

Does P27 being located in the cytosol cause the cancer

A

NO

Correlation here and not causation …

BMS247 Stem Cells (14 decks)

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