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SCRA > 16. ageing biology 2 > Flashcards

16. ageing biology 2 Flashcards

1
Q

name three types of DNA repair mechanisms

A
  • nucleotide excision repair
  • base excision repair
  • homologous recombination
  • non-homologous end joining
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2
Q

what is nucleotide excision repair used for and describe the process

A

bulky adducts

>removal of a short single strand DNA segment, DNA polymerase uses other strand as template, ligation by DNA ligase

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3
Q

what is base excision repair used for and describe the process

A

ssDNA breaks and small base damage
>DNA glycosylases which recognises and removes damaged base, AP site cleaved by exonucleases, DNA polymerase uses other strand as template, ligation by DNA ligase

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4
Q

what is homologous recombination used for and describe the process

A

interstrand cross links and double strand breaks

>nucleotide sequences are exhcnaged between two similar or identical DNA molecules

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5
Q

what is non-homologous end joining used for and describe the process

A

double strand breaks

>non-homologous end joining joins broken chromosome end in a manner that does not require sequence homology

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6
Q

what is mismatch repair used for and describe the process

A

mismatches

>nucleotide excision of mismatched base and a few surrounding bases, DNA polymerase fills in gap

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7
Q

what is used to overcome telomere shortening?

A

telomerase reverse transcriptase/RecQ

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8
Q

sometimes damage is not repaired, why might this happen?

A

UV induced cyclobutane pyrimidine dimers often ignored because they look like normal DNA

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9
Q

which DNA repair process can be coupled with transcription?

A

nucleotide excision

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10
Q

what may happen is DNA repair is faulty? and what disease is this seen in

A

cancer or stall in polymerase which kills cells - these are seen in progeroid syndromes

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11
Q

name a disease where faulty DNA repair leads to premature ageing? and what is this disease?

A

Cockayne syndrome

>a rare segmental progeroid syndrome

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12
Q

what are the symptoms of Cockayne syndrome ?

A

growth failure, microcephaly, sensitive to sun, eye disorders and premature ageing

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13
Q

what is the mean lifespan of Cockayne syndrome ?

A

12 years

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14
Q

what causes Cockayne syndrome ?

A

mainly due to defects in CSB gene
>transcription coupled excision repair protein
rest due to defects in CSA - involved in the same process
>also component in ubiquitin ligase complex (might ubiquitinate CSB)

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15
Q

what can people with Cockayne syndrome not repair? and what does this lead to?

A

oxidative induce damage to DNA bases in the strands of DNA that are being transcribed i.e. transcription coupled DNA repair
>blocks in transcription which leads to apoptosis

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16
Q

what has been seen to recuse premature ageing in Cockayne syndrome?

A

high fat diet in mice which activates sirt1

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17
Q

in general what accumulates as we age and what does this lead to?

A

DNA damage

can kill or senesce cells

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18
Q

what are senescent cells linked to? and what does this lead to?

A

inflammatory signals

chronic inflammation is associated with ageing and plays a causative role in age-related disorders such as cancer

19
Q

what does increased levels of p53 trigger?

A

a senescence response

20
Q

what happens to guanine when ROS attack it and what results from this?

A

it forms 8-oxo-guanine

>this can pair with cycteine and adenine

21
Q

what type of therapy can induce premature ageing?

A

chemotherapy and radiotherapy

22
Q

what does decreased HDAC1 function result in in the brain?

A

more double stranded DNA breaks

- neural death and neurodegeneration

23
Q

name two class III NAD+ dependent HDACs? and what is their secondary function?

A

SIRT1 and SIT6

>required for efficient double stranded DNA break repair

24
Q

what happens when people lack the enzyme SIRT6? and what do KO mice for this display?

A

they are not efficiently repairing oxidative damage

>several progeroid symptoms and early death

25
Q

what are some of SIRT6’s functions? and what are these linked to?

A

DNA repair, telomere maintenance, glycolysis and inflammation
>ageing

26
Q

what causes Huntington’s disease?

A

unstable expansion of CAG repeats within coding regions of the HD gene, which expresses huntingtin. this leads to neurodegeneration.

27
Q

what happens when oxidative damage is removed from huntingtin gene?

A

lead to further CAG repeat expansion as patients age

this will lead to further death of the neural population

28
Q

which might oxidative damage at a promoter in the brain lead to? and what other tissue has this been implicated in?

A

repression of genes involved in synapse plasticity, memory and inflammation in the ageing brain
the ageing muscle - random deregulation of genes

29
Q

what are down regulated in G0?

A

many repair mechanisms

>adult stem cells may be equipped to maintain genome integrity in different ways to somatic cells

30
Q

if mutations in these adult stem cells spread throughout the tissue what will this lead to?

A

tissue degeneration

31
Q

what poses a significant threat to stem cell survival and their longevity?

A

loss of DNA repair - this alters proliferation, quiescence and differentiation

32
Q

what might we be able to do in the future?

A

model mutation and see how this affect ageing

33
Q

what is telomerase?

A

a ribonucleoprotein complex = TERC (a RNA template for species specific telomeres) and TERT (telomerase reverse transcriptase subunit)

34
Q

what cells is telomerase restricted to?

A

germ line, stem and progenitor cells

35
Q

what happens with cells that do not have telomerase?

A

they can eventually enter replicative senescence

36
Q

if telomeres reach a critical length what happens?

A

this triggers a p53 DNA damage response

37
Q

which genes does p53 promote that lead to senescence?

A

p21 and p16

38
Q

what happens when telomerase is KO in mice?

A

telomeres shorten, organs start to deteriorate and they start to show symptoms of ageing

39
Q

what happens when telomerase is over expressed? and what else needs to be expressed to stop tumoiurigenesis?

A

mice had 26% longer lifespan

>tumour suppressers

40
Q

what might telomere length be a indicator of?

A

tissue age

41
Q

4 serum markers that indicate telomere dysfunction and DNA damage have been identified, what happens when we age?

A

levels of these increase in the blood

42
Q

what happens in terms of epigenetics when we age?

A

changes in chromatin packing and changes in how the chromatin interacts with laminin
>there are redistribution of chromatin modifiers as we age
>organisation of chromatin maybe so dysfunctional that you can push cell into senescence

43
Q

what happens when chromosome/genome maintenance mechanisms fail?

A

this can mimic ageing

SCRA (19 decks)

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