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MCBG > DNA Repair and Cell Cycle > Flashcards

DNA Repair and Cell Cycle Flashcards

1
Q

What happens in cell division of prokaryotes?

A
  • The process going from one mother cell to two draughtier cells.
  • The genetic information is replicated first
  • The cell will grow and the DNA will move to opposite sides of the cell - Cell will undergo binary fission.

Pg 2

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2
Q

What does the cell cycle contain in somatic cells and germline cells?

A

Somatic cells - the cell cycle includes the cell division mitosis (from one cell to two identical daughter cell)
- needed for growth, healing and replacement.

Germline cells - The cell cycle has a specialised cell division -meiosis (from one cell to 4 non-identical sex cells).

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3
Q

What is the two divisions involved in division (M) stage of the cell cycle?

A
  1. Nuclear division (mitosis)

2. Cellular division (cytokinesis)

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4
Q

What are the different phases in cell cycle and which ones are in interphase?

A
  1. G1 phase (10-12hr)
    - Cell content duplication
  2. S phase (6-8hr)
    - DNA replication
  3. G2 phase (3-4hr)
    - Double check and repair
  4. M Phase (<1hr)
    - Mitosis (or meiosis)

G1, S, G2 are in interphase

Pg 9

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5
Q

What occurs in the G0 phase?

A

Stationary phase or quiescence.

  • It is a temporary or permanent phase, cells in G0 can go back into the cell cycle.
  • Growth factor are needed for the cell to go back into the cycle and to G1.
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6
Q

What are the different ways in which the cell cycle is controlled? And what happens when there is loss of control?

A
  • Checkpoint control - where the cell checks if the things are alright before going into the next phase
  • By CDK(cyclin dependant kinase)/cyclins
  • Loss of control can lead to cancer.

Pg 12

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7
Q

What are the two levels that DNA integrity is important at?

A
  • Important at nucleotide and gene level

- Important at chromosome level (chromosomes are lasted from one generation to the next).

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8
Q

Shat are the different types of damage that can affect the DNA?

A
  • Single strand damage
  • Double strand damage

Pg 15

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9
Q

What do DNA repair mechanisms do?

A
  1. Recognise damage to the DNA and repair it.
    - If DNA is not checked by the DNA repair mechanism, this could lead to mutation and permanent change
  2. If the DNA mechanism makes a mistake this can lead to mutations and can lead to cancer.

Pg 17

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10
Q

What are exogenous sources of DNA damage?

A
  • ionising radiation
  • UV
  • alkylating agents
  • mutagenic chemicals
  • anti-cancer drugs
  • free radicals

Pg 21-25

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11
Q

What endogenous sources if DNA damage?

A
  • Free radicals

- replication errors

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12
Q

What is DNA replication stress?

A
  • Inefficient DNA replication that leads to DNA replication fork slowing, stalling and or breakage.

Pg 29

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13
Q

What is miscorporation and proofreading?

A
  • Mis-incooorating is when the DNA polymerase add in the wrong base.
  • DNA polymerase has the ability to recognised it has done something wrong and goes back and changes it, this is proofreading.
  • DNA polymerase has 3’ to 5’ exonuclease activity and can back and take out the mis-incorporated.

Pg 30

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14
Q

What are the two ways to cause DNA replication stress?

A
  • Replication machinery defects. pg 29 &31
  • Replication fork progression hinderance (anything that hinders the replication fork going forward).pg 33
  • Defects in response pathways pg 41
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15
Q

What does fork slippage do?

A
  1. Newly synthesised strand can loop out and one nucleotide is added to the new strand. P
  2. Template strand loop out and one nucleotide is omitted on the new strand.
  3. Repetitive areas of 3 bases adding 3 extra bases (new strand) or loss of three bases in the template cans leads to loss of the three bases.

Pg 36-37

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16
Q

What occurs in the genes that causes Huntington’s disease?

A
  • Trinucleotide repeat disorders.
  • CAG repeats in HTT gene leading to polyglutimine repeats in the Huntington protein.
  • Notmal 6-39 repeats leading to healthy neurone
  • Disease 35-121 repeats leads to neurone degeneration
17
Q

What occurs in Huntington’s disease?

A
  • Normal function of Huntington protein still unknown
  • Mutant Huntingtin protein aggregates in neurons affecting mainly basal ganglia
  • Progressive, late onset disease
18
Q

What is DNA damage response (DNA)?

A

The cellular processes that sense, signal and repair DNA damage.

19
Q

What happens in DNA damage response?

A
  1. DNA damage and replication stress cause a signals which can be read and sensed.
  2. Then Sensed by sensors then goes to transducers and the effectors (which are all proteins)
  3. The effectors can include:
    - Senescence (permanent cell cycle arrest
    - Cell cycle transition (cell cycle stops)
    - Apoptosis
    - Transcription leading to DNA repair.

Pg 46-47

20
Q

What are the three outcomes of DNA damage response ?

A
  • Senescence
  • Proliferation
  • Apoptosis
21
Q

What happens if the DNA damage is too high or persist? What is the ideal scenario?

A
  1. Senescence: Permanent cell cycle arrest
    - Last resort.
  2. Apoptosis
    - To repair the DNA damage and maintain function
    - Through proliferation , after DNA repair and cell cycle control.

Pg 49-50

22
Q

What occurs in cell cycle control and what are the three checkpoints?

A
  • Slow down of the cell cycle (temporary arrest) to allow for DNA repair.
  1. G1 checkpoint
    - is it environmentally favourable before going into S phase
  2. G2. Checkpoint
    - Is all the DNA replicated
    - Is all the damaged DNA repaired
    - Before going into mitosis
  3. Checkpoint in mitosis
    - are all the chromosomes properly attached to the mitotic spindle?
    - Before pulling duplicated chromosomes apart (anaphase).
23
Q

What occurs in Base excision repair?

A
  1. If the wrong base is added, it is detected and removed.
  2. This leaves a base-less nucleotide, the nucleotide is removed leaving a small hole in the backbone.
  3. The hole is filled with the right base by DNA polymerase and the gap is sealed by ligase.

Pg 53-54

24
Q

What is nucleotide excision repair?

A
  1. A mutation occurs (UV radiation producing a thymine dimmer).
  2. Once it is detected the surrounding DNA opens up to form a bubble.
  3. Enzymes cut the damaged region of the bubble out.
  4. DNA polymerase replaces the cut out (excised) DNA and ligase seas the backbone.

Pg 55-56

25
Q

What is mismatch repair?

A
  1. mismatch detected in the newly synthesised DNA.
  2. the new DNA strand is cut and the mispaired nucleotide and its neighbours are removed by exonuclease activity.
  3. The missing patch is replaced by correct nucleotides by DNA polymerase.
  4. DNA ligase seals the gap in the DNA backbone.

Pg 57-58

26
Q

What are the features of a single stand break?

A
  • Relatively simple
  • Many different mechanisms
  • Integrity of the DNA molecule intact
  • ‘Damage’ removed on one strand only
  • Homology of other strand used to repair
  • Not error-free, but not error-prone either
27
Q

What are the features of a Double strand break?

A
  • Complex
  • Integrity of the molecule is lost
  • most likely error prone
  • Use of homology my be possible
28
Q

What are the two different types of double strand break repair?

A
  1. Non-homologous end joining
    - double strand break is recognised and protected as it is susceptible to further damage .
    - Complex formed and damaged end is removed
    - Broken ends are liagated
    - Error prone
  2. Homologous directed repair
    - Use of homologous pair to repair damage

Pg 62 - 65

29
Q

What can lead to cancer?

A

Loss of control of the cell cycle

30
Q

What is the Multi-step cancer model?

A
  • Mutation accumulation: multiple mutations need to be picked up before the cell becomes cancerous.

Normal - Premalignant - maglinant

69-70

31
Q

What can cause and what prevents carcinogenesis?

A
  • DNA replication stress stimulates carcinogenesis (mutations).
  • DNA repair defects stimulates carcinogenesis.
  • DNA damage response prevent carcinogenesis
32
Q

What are the different DNA repair defects?

A
  • DDR defect
  • Mutated gene
  • Syndrome
  • Cancer predisposition
33
Q

What is tumour heterogeneity?

A

Different people have different tumours.

  • Tumours are not all the same

Pg 79

34
Q

What occurs in Cancer evolution?

A
  • Mutations in DNA repair factors are common in cancer.
Normal
- early driver mutations 
- mutation accumulation 
Malignant 
- Clonal expansion(different clones within a tissue).
Heterogenous tumour

Pg 80

35
Q

What are the two different pathways caused by chemotherapy on a heterogenous tumour?

A
  1. Differential sensitivity (similar to antibiotic resistance)
  2. Chemotherapy induced mutagenesis
    - Chemical from treatment induce mutations

Pg 81-82

36
Q

What is the synthetic lethality strategies?

A
  • Give a trite end to knock out one gene.
  • So that the gene that has the cancer mutation can be specifically targeted.

Pg 83-85

MCBG (6 decks)

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