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BB10005 COPY > Cell cycle, quiescence and senescence in eukaryotes > Flashcards

Cell cycle, quiescence and senescence in eukaryotes Flashcards

1
Q

What is free living cell growth regulated by?

A

Environmental cues such as nutrient supply.

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2
Q

What is cell growth and proliferation controlled by in multicellular animals?

A

Extracellular signals.

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3
Q

What is necrosis?

A

Unplanned death.

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4
Q

What is the cell division cycle?

A

The reproductive cycle of the individual eukaryotic cell.

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5
Q

What did Lee Hartwell discover?

A

Checkpoints.

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6
Q

What does necrosis occur in response to?

A

Damage or infection and can cause further damage to surrounding cells and tissues.

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7
Q

What did Tim Hunt discover?

A

Cyclin.

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8
Q

What did Paul Nurse prove?

A

That MPF was cyclic + Cdk, and he also isolated human Cdk.

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9
Q

What are four main phases of the cell division cycle?

A

Mitosis, growth/gap 1 and 2 and the synthesis phase.

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10
Q

What are the checkpoints in the cell cycle?

A

G1, S, G2, M.

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11
Q

What happens in the G1 checkpoint?

A

Checks for DNA damage and unfavourable extracellular environments.

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12
Q

What happens in the S checkpoint?

A

Checks for incomplete replication.

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13
Q

What happens in the G2 checkpoint?

A

Checks for insufficient cell growth.

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14
Q

What happens in the M checkpoint?

A

Chromosome incorrectly attached to mitotic spindle.

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15
Q

What are the checkpoints regulated by?

A

Cyclin/Cdk complexes.

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16
Q

What is Cdk?

A

Cyclin-dependent kinases.

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17
Q

How is the cycle taken from G2 to M?

A

M-phase promoting factor is activated from M-cyclin and M-Cdk working together with their regulators.

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18
Q

What causes a peak in Cdk activity?

A

A steady accumulation of cyclin followed by rapid destruction.

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19
Q

How is cyclin inactivated?

A

An inhibitory kinase (Wee1) phosphorylates cyclin.

20
Q

What does activating phosphatase do?

A

It removes the inhibitory phosphates.

21
Q

What happens after the activating phosphatase has removed the inhibitory phosphatases?

A

Active cyclin/Cdk phosphorylates Cdc25 (the activating phosphatase) - this is positive feedback.

22
Q

What is the anaphase-promoting complex and what does it do?

A

It adds chains of ubiquitin molecules to cyclin proteins - tagging them for rapid destruction at proteosomes.

23
Q

What happens if DNA is damaged at the G1/S checkpoint?

A

Protein kinases that phosphorylate p53 are activated. p53 binds to the regulatory region of the p21 gene and causes p21 protein to be formed - which is a Cdk inhibitor protein, causing S-Cdk cells to be inactivated.

24
Q

What is the purpose of p53?

A

It allows time for the cell to repair damaged DNA or undergo apoptosis.

25
Q

How may cancer form?

A

The p53 gene is mutated in at least 50% of human cancers - loss of its activity accelerates the accumulation of mutations required for uncontrolled proliferation of cancer cells - its molecular role as a transcription factor allows it to function genetically as a tumour suppressor.

26
Q

What is G0?

A

When cells leave the cell cycle - undergoing apoptosis or entering a modified state called G0.

27
Q

What differences occur in different cells in the cell cycle?

A

The time spent in G1.

28
Q

What are Quiescent cells?

A

Cells that have withdrawn from G0 but have the capacity to re-enter the cell cycle when appropriate.

29
Q

What allows quiescent cells to exist?

A

The regulation of the G1/S phase checkpoint by retinoblastoma (Rb) protein.

30
Q

What are Retinoblastoma sequester transcription factors important for?

A

Initiating DNA replication and nucleotide metabolism at the start of S phase.

31
Q

How is the Rb transcription regulator activated?

A

Mitogen binds to a receptor that activated G1-Cdk and G1/S-Cdk which phosphorylates Rb which promotes the release of transcription factors that promote the initiation of S phase - transcription, translation and resulting cell proliferation.

32
Q

What do mitogen signals promote?

A

Cyclin synthesis and KIP degradation.

33
Q

What are examples of terminally differentiated cells?

A

Neurons, keratinocytes in the skin, goblet (secretory) and enterocytes (absorptive), gut epithelial cells.

34
Q

What does it mean that cancer cells are immortalised or transformed?

A

They evade senescence and can continue dividing.

35
Q

What is cellular/replicative senescence?

A

When cells lose the capacity to divide - this is a post-mitotic state.

36
Q

What are contributing factors to cellular/replicative senescence?

A

The accumulation of KIP/CIPs with successive divisions and the shortening of telomeres.

37
Q

What is cell number a balance between?

A

Cell proliferation and apoptosis.

38
Q

What is the aim of apoptosis?

A

Remove unwanted cells in an organised way, such as webbing between digits during animal development.

39
Q

What happens if there is excess neurons?

A

Cell death will match the number of nerve cells to the number of target cells.

40
Q

What are telomeres?

A

Repetitive sequences at the ends of chromosomes.

41
Q

What are the two biological problems that telomeres create?

A

Free chromosome ends could stimulate the DNA-damage response pathway and the ends of chromosomes cannot be replicated by normal DNA replication.

42
Q

How can some cells overcome senescence?

A

Activating telomerase reverse transcriptase or acquiring mutations that release blocks on the cell cycle, such as mutations in p53 or Rb.

43
Q

Why does the last part of the 3’ end of the chromosome get shorter through every replication?

A

An RNA primer is needed to replicate DNA strands, but a primer cannot be placed beyond the very end of the chromosome.

44
Q

What happens when the 3’ end (telomeres) gets shorter below a certain threshold?

A

The exposed DNA is recognised as a DNA double-strand break (DSB) by the DNA damage response (DDR) machinery. This triggers the DNA damage checkpoint and this is the basis of replicative senescence.

45
Q

How can the ends of chromosomes be extended?

A

Telomerase.

46
Q

How does telomerase work?

A

It adds additional repeats to the telomerase template strand, and the lagging strand is completed by DNA polymerase.

47
Q

What does telomerase reverse transcriptase do?

A

It makes DNA from RNA.

BB10005 COPY (23 decks)

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