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POM 1a - Molecular Biology Of The Cell > Cell Replication > Flashcards

Cell Replication Flashcards

1
Q

What is the cell cycle?

A

Sequence of events where a cell duplicates its contents and divides in two

  • duplication
  • division
  • co-ordination
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2
Q

What causes cells to divide at different rates?

A

Embryonic vs adult cells

Complexity of system

Necessity for renewal

State of differentiation

Tumour cells?

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3
Q

What are the stages of the cell cycle?

A

G0

G1

S

G2

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4
Q

What is G0?

A

Quiescent phase —> cells go there in absence of stimulus

Cells not dormant —> non-dividing

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5
Q

What cell cycle checkpoints are there?

A

G1 —> damaged DNA, unfavourable extracellular environment
- nutrients
- growth factors

S —> damaged or incompletely replicated DNA

G2 —> damaged or incompletely replicated DNA

M —> chromosome improperly attached to mitosis spindle

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6
Q

How do cells leave G0?

A

Response to extracellular growth factors\

Growth factor binds to GF receptor on cell-surface
—> initiates intracellular signal pathway
—> increase in protein synthesis + decrease on protein degradation —> cell growth

MAP kinases involved

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7
Q

What is c-Myc?

A

Transcription factor that promotes G0 to transition to G1 by stimulating the expression of cell cycle genes

Oncogene expressed in many tumours

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8
Q

What are cyclin dependent kinases?

A

Entities part of key signalling events in the cell cycle
—>Phosphorylation + dephosphorylation at serine, threonine and tyrosine residues

Allow for tight control of the cell cycle

Present in all proliferating cells but only active when cyclin is bound

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9
Q

Where do cyclins get their name from?

A

Their concentration within the cell fluctuate
—> production + degradation

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10
Q

What events need to happen for a cell to move from G0 to G1?

A

Growth factor bonds to its receptor —> causes c-Myc expression
—> Induces expression of cyclin D —> binds to Cdk 4/6
—> moves cell into G1

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11
Q

What is a protein kinase cascade?

A

Frequently the protein regulated by a kinase is another kinase

Leads to —> signal amplification
—> diversification
—> opportunity fo regulation

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12
Q

What is the Cyclin-dependent kinases relevance to the cell cycle?

A

Present in all proliferating cells throughout the cycle

Activity regulated by:
—> interaction with cyclins
—> phosphorylation

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13
Q

What is the cyclins relevance in the cell cycle?

A

Transiently expressed at specific points ion the cell cycle

Regulated at level of expression

Synthesised, then degraded

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14
Q

Stages of Cdk activation

A
  1. Inactive Cdk
  2. Cyclin binds to Cdk —> cyclin:Cdk complex still inactive
  3. Protein kinases phosphorylate Cdk at various sites
  4. Activating protein phosphatase removes the inhibitory phosphate —> activates the complex
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15
Q

How does positive feedback work in Cdk activation?

A

Once M-Cdk activated —> phosphorylatesCdc25 phosphatase
(now active) —> activates production of more M-Cdk

Helps drive cell from G2 to M phase rapidly

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16
Q

How are cyclins turned off?

A

By ubiqutination

Ubiquitin molecules are stuck onto proteins that the cell wants to degrade by proteasome cell machinery

17
Q

How is direction and timing given to the cell cycle?

A

Cdk become sequentially active and stimulate synthesis of genes required for next phase

Cyclins susceptible to degradation —> hence cyclical activation

18
Q

What is retinoblastoma?

A

Protein that is a molecular break

Tumour suppressor
—> if missing or inactive —> issues with cell cycle progression

Abundant in all uncleared cells

19
Q

What does retinoblastoma do?

A

Active Rb sequesters a TF in an inactive form
—> TF cannot turn on genes needed for cell cycle progression
—> can’t bind to DNA and induce transcription (e.g DNA polymerase)

20
Q

What do mitogens do?

A

Activation of intracellular signalling through mitogens leads to production of G1-Cdk and G1/S-Cdk complexes
—> phosphorylate Rb inducing its inactivation
—> release TF
—> target genes such as DNA polymerase now
activated

21
Q

What is p53?

A

Arrests cells with damaged DNA in G1

Regularly being turned over which is why stabilisation is needed

22
Q

How does p53 work?

A

Recognises breaks in double stranded DNA

Induces the p21 gene which inhibit cyclin:Cdk complexes by binding them and sequestering them

23
Q

Oncogene: EGFR/HER2

A

Mutationally activated or over expressed in breast cancers

Herceptin antibody for the treatment of HER2+ metastatic breast cancers

24
Q

Oncogene: Ras

A

Mutationally activated in many cancers

25
Q

Oncogene: Cyclin D1

A

Overexpressed in 50% of breast cancers

26
Q

Oncogene: C-Myc

A

Overexpressed in many tumours

27
Q

What tumour suppressors are relèvent to the cell cycle?

A

Rb —> loss of function mutations in 80% of small cell lung cancer

p53 —> loss of function mutation in over 50% of all human cancers

POM 1a - Molecular Biology Of The Cell (18 decks)

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