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POM > Cell Replication > Flashcards

Cell Replication Flashcards

1
Q

3 components of the cell cycle

A

Duplication
Division
Co-ordination

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2
Q

5 factors that affect cell division

A

Cell maturity
Complexity of system
Necessity for renewal
State of differentiation
Tumourigenesis

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3
Q

Cell maturity

A

Embryonic cells divide at a faster rate than adult cells ; most mammalian mature cells can divide every 24 hours

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4
Q

Complexity of system

A

Higher system complexity the LOWER THE RATE of expected division ; yeast cells take 1.5-3 hours

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5
Q

Necessity for renewal

A

Cells with high turnover like intestinal epithelial cells divide at a faster rate than hepatocytes (once every year)

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6
Q

State of differentiation

A

Neurons and cardiac monocytes are terminally differentiated so will never divide

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7
Q

How are terminally mature cells repopulated

A

By stem cells and progenitor cells

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8
Q

Tumourigenesis

A

Loss of all control elements governing cell cycle ; tumours have uncontrollable fast rate of division

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9
Q

Interphase

A

G1 S G2

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10
Q

M phase

A

Mitosis + cytokinesis (cytoplasmic splitting)

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11
Q

G phases

A

Gap phases - prepping for S (by growing in size + synthesising proteins) OR prepping for M (by growing in size and checking/repairing DNA)

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12
Q

S phase

A

Synthesis phase

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13
Q

G0

A

Quiescent - takes urself out of cell cycle ; terminally mature cells - if cells need to quiesce (rest) they can enter G0

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14
Q

How does G0 work?

A

Cell must have necessary resources to endure replication of 3.2 B base pairs/double in size ; so if no stimuli present most differentiated cells go into G0 phase

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15
Q

What about cells in G0 phase

A

They are simply non-dividing ; neurons/skeletal muscle/hepatocytes

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16
Q

Monitoring of external environment includes

A

Ample nutrients + ample growth factors

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17
Q

Checkpoints in cell cycle

A

3 checkpoints - G1 checkpoint to enter S phase ; is environment favourable?
G2 checkpoint to enter M - has DNA replicated correctly/not damaged
M checkpoint - are all chromosomes properly attached to mitotic spindle

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18
Q

Pause process?

A

IF CELL HAS TO UNDERGO DNA REPAIR
Cell pauses at checkpoint to allow DNA repair to occur ; if DNA beyond repair cell leaves cell cycle + undergoes apoptosis

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19
Q

Why do cells enter G0 phase?

A

Differentiation - specialised cell types do not divide until needed for tissue repair etc
Senescence - may lost its ability to divide but still remain metabolically active ; can result from aging/cellular stress/DNA damage/oncogenes signals
Cell quiescence - resting cells to conserve energy (until activated for growth/repair)
Terminal maturity - neurons/muscle/mature RBCs - PERMANENTLY post-mitotic in G0
External signals - lack of growth factors/nutrients signals from neighbouring cells
DNA damage - time needed for repair mechanisms
Cell stress - protective mechanism in oxidative stress/heat shock/inflammatory signals etc

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20
Q

How do cells leave the G0 phase?

A

Through extra cellular stimuli (growth factors binding to receptor on cell surface membrane) which starts an intracellular signalling cascade
Growth factor binds to receptor which leads to intracellular signalling pathway causing protein synthesis to increase or protein degradation to decrease (either way leads to CELL GROWTH)

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21
Q

Signal cascade also known as

A

Signal amplification ; cascades can modulate various other cascades in parallel - signal integration/modulation by other pathways - causes cell to enter cell cycle from G0

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22
Q

c-Myc

A

Is a type of growth factor called a transcription factor which expresses a particular gene ; promotes transition of cell out of G0 into G1
ONCOGENE - over expressed in many tumours (cell will be going into replication when conditions are not favourable)

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23
Q

Why are serine threonine and tyrosine all sites of phosphorylation?

A

They all contain hydroxyl groups in their side chains so can be phosphorylated by kinases (just like glucose)

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24
Q

Idk levels during cell cycle?

A

Really do not fluctuate

25
Q

How do cdks work?

A

Only active when a cyclin is bound to it (but cdks are present in all proliferating cells)

26
Q

Cyclin fluctuations?

A

Their greatest concentration matches the optimum levels of cdc during the mitotic phase (cyclin conc simply rises during interphase)

27
Q

Cdk activity during interphase

A

Practically non-existent

28
Q

Cyclin concentration?

A

Fluctuates - it is cyclic as it is produced and then degraded after mitosis to be produced again

29
Q

Growth factor drives what pathway?

A

Tyrosine kinase signalling pathway

30
Q

At the end of that pathway?

A

Transcription factor c-Myc is present which turns on Cyclin D gene that cdk needs to drive the cell into S phase

31
Q

cdk + phosphorylation….

A

Drives the cell into S phase

32
Q

How does a kinase usually turn on?

A

It is phosphorylated ; that kinase can phosphorylate other kinases leading to an amplified intracellular response ; POTENTIAL FOR REGULATION

33
Q

Phosphatases job?

A

Removal of the phosphates from those kinases will turn them off

34
Q

Cyclins are —- expressed

A

Transiently

35
Q

Sequential phosphorylation/dephosphorylation Cdks-4

A

Cyclin dependent kinase chilling by itself
Cyclin comes along but the acc cdk has an inhibitory and activating phosphate (which is getting phosphorylated)
Only will phosphorylate when an activating protein phosphatase comes along and removes that inhibitory phosphate

36
Q

What also drives the cell cycle forward?

A

Positive feedback ; once you have your active Cdk which is phosphorylating it will phosphorylate many things such as the inactive phosphatase making it active (MASSIVE POSITIVE FEEDBACK)

37
Q

What else can positive feedback do?

A

Active Cdk can also activate inhibitory kinase and inhibit the whole process

38
Q

What is the term for constant degradation/turning signal systems on and off?

A

Progressive induction

39
Q

Ubiquitination

A

Process by which many proteins are removed from the body ; a tag for a proteasome to degrade the protein its attached to (in this case the cyclin) - GENE INDUCTION

40
Q

What is ubiquitination coupled with?

A

Proteosomal degradation

41
Q

Exit out of different phases of cell cycle

A

Controlled by degradation of cyclins

42
Q

Retinoblastoma

A

Gene product that acts as a molecular brake ; this is a tumour suppressor that is missing/inactive during tumour genesis

43
Q

Mechanism of Rb

A

Active Rb sequesters a Transcription factor (in the E2F family) inactive so the TFs cannot turn on genes needed for cell cycle progression like DNA Polymerase or Thymidine kinase for S phase

44
Q

How is this molecular brake released?

A

Activation of cyclin dependent kinases phosphorylates Rb which induce its inactivation causing a conformational change and for it to release TF which will bind to correct place in genome and turn on genes for DNA synthesis

45
Q

Another tumour suppressor is

46
Q

p53 life cycle?

A

Constantly produced and degraded/turned over - process of ubiquitination

47
Q

Mechanism of p53

A

x-rays cause DNA damage which leads to activation of protein kinases that phosphorylate p53 stabilising + activating it ; it is a TF that will bind upstream of p21 gene (needed when a cell is making DNA)

48
Q

Oncogenes

A

Overexpressed resulting in tumour formation

49
Q

EGF4/HER2

A

Over expressed in breast cancers ; Herceptin antibody for treatment of HER2 metastatic breast cancer

50
Q

Ras

A

Mutationally activated in many cancers

51
Q

Cyclin D1

A

Over expressed in 50% of breast cancer

52
Q

C-Myc

A

Overexpressed in many tumours

53
Q

Order of cyclin expression

A

C-myc promotes cyclin-D which upregulates cyclin E which upregulates cyclin A which upregulates cyclin B

54
Q

When is cyclin D present

55
Q

When is cyclin E present

A

End of G1 going into S

56
Q

Cyclin A

A

Middle of S going and stays till mitosis

57
Q

When is cyclin B present

A

Start of mitosis till anaphase

58
Q

What does p53 do

A

STOPS cell cycle from continuing

59
Q

What is c-myc

A

Transcription factor which stimulates the expression of cell cycle genes (genes that synthesise cyclins)

POM (12 decks)

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