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MCM Test 2 > B2.033 DNA Repair Mechanisms > Flashcards

B2.033 DNA Repair Mechanisms Flashcards

1
Q

what is the difference between DNA damage and DNA mutations?

A

damage is routine

mutations come from unrepaired damage and become a permanent part of the genome

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2
Q

what is a somatic mutation?

A

only affects individual

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3
Q

what is a germline mutation?

A

mutation in cells that produces gametes, every cell of offspring will have mutation

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4
Q

what are the 3 steps of DNA lesion repair?

A
  1. recognize the lesion
  2. remove the lesion
  3. fill in the gap
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5
Q

how are lesions recognized?

A

marked by protein binding and/or chromatin modification

proteins that can recognize these markers surveil the genome (PARP1)

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6
Q

what are the two types of simple DNA lesion repair?

A
  1. base excision repair

2. mismatch repair

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7
Q

what is base excision repair?

A

damaged base recognized by DNA glycosylase that mediated base removal
nuclease, polymerase, ligase repair

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8
Q

what is mismatch repair?

A

mismatch and single nucleotide insertion/deletion
triggers single strange incision
nuclease, polymerase, ligase repair

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9
Q

what is HNPCC/Lynch Syndrome?

A

hereditary nonpolyposis colorectal cancer

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10
Q

characterize HNPCC

A

autosomal dominant
60-80% lifetime risk of CRC
elevated risks of other cancers
congenital absence of any 1/4 proteins involved in mismatch repair

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11
Q

what are two types of complex DNA lesion repair?

A
  1. nucleotide excision repair

2. interstrand cross-link (ICL)repair

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12
Q

how does nucleotide excision repair work?

A

recognized helix distorting lesions
20-30 nt region removed
polymerase, ligase repair

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13
Q

how does interstrand cross link (ICL) repair work?

A
  1. recognize stalled replication forks
  2. necessary factors recruited and activated
  3. homologous recombination repair
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14
Q

what is a nucleotide excision repair pathology?

A

xeroderma pigmentosum (XP)

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15
Q

what is an ICL pathology?

A

fanconi’s anemia

loss of any one of the proteins involved (homozygous in 1 of 13)

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16
Q

what are the types of double strand break repair? which is better?

A
  1. homologous recombination (this one rox)

2. non homologous end joining (this one sux)

17
Q

characterize homologous recombination repair of DSBs

A

error free
occurs in S and G2 phases of cell cycle
ssDNA invased undamaged homologous template
BRCA1, BRCA2/FANCD2 involved

18
Q

what syndromes result from defects in homologous recombination repair pathways?

A

chromosome instability syndromes

fanconi’s anemia

19
Q

characterize non-homologous end joining repair of DSBs

A
  1. KU protein binds ends
  2. recruits/activates protein kinase
  3. kinase recruits/activated end processing enzymes
  4. ends join and are filled in
    wrong ends join a lot bc NHEJ is trash
20
Q

what are 3 ways to become unable to repair lesions?

A

congenital deficiency
somatic mutation
epigenetic silencing of gene coding for repair protein

21
Q

why are cancer cells reliant upon functional DNA repair mechanisms?

A

even cancer cells can only tolerate so much DNA mutation before they cease to be able to function like a normal cell and die

22
Q

how are BRCA1 and BRCA2 involved in DNA repair?

A

involved in homologous repair
recognizes and prepares DNA ends for strand invasion
without these genes functioning, you get more trash NHEJ repair

23
Q

what does PARP1 do?

A

binds to nicks/breaks and chemically modifies nearby chromatin so that repair can be completes

24
Q

how do PARP1 inhibitors work?

A

prevent repair of DNA lesions, leading to dsDNA breaks

25
Q

why are BRCA1 and BRCA2 neg breat cancers particularly sensitive to PARP1 inhibitors?

A

PARP1 inhibitors lead to dsDNA breaks
cant repair these correctly without BRCA1,2
have to resort to NHEJ trash mechanism and then ur unstable and die

MCM Test 2 (26 decks)

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