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Med 105 > DNA repair mechanisms > Flashcards

DNA repair mechanisms Flashcards

1
Q

what are gene mutations classified into

A

Hereditary (germline mutations) and Acquired (or somatic) mutations

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2
Q

what are the DNA repair mechanisms

A
  • Proofreading (during replication)
  • Mismatch repair (during replication)
  • DNA damage repair mechanisms
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3
Q

what are the types of DNA damage repair mechanisms

A

i. Direct reversal
ii. Excision repair (base or nucleotide)
iii. Double-stranded break repair

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4
Q

what mammalian DNA polymerases are capable of DNA proofreading

A

delta and epsilon

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5
Q

give 7 differences between exonuclease and endonuclease

A
  • Endonuclease separates the nucleotides into two or more fragment, Exonuclease removes the nucleotides one by one from the fragment
  • Endo-nuclease cuts the nucleotide bases from the middle, exo from 5’ or 3’ end
  • endo doesnt req 5’ or 3’ end, exo does
  • endo- lag phase, exo- absent
  • endo- sequence specific, exo- not
  • endo- releases oligonucleotides, exo- nucleotides
  • endo- DNA repair, blocking pathogen entry, exo- repair, proofreading, stabilization, no pathogen blocking
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6
Q

when does mismatch repair happen

A

right after new DNA has been made

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7
Q

what is the general function of mismatch repair

A

remove and replace mis-paired bases (ones that were not fixed during proofreading)

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8
Q

what else can mismatch repair detect

A

detect and correct small insertions and deletions that happen when the polymerases “slips,” losing its footing on the template

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9
Q

how does mismatch repair work

A

1) protein complex recognizes and binds to the mispaired base
2) A second complex cuts the DNA near the mismatch, and more enzymes chop out the incorrect nucleotide and a surrounding patch of DNA
3) A DNA polymerase then replaces the missing section with correct nucleotides, and an enzyme called a DNA ligase seals the gap

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10
Q

how can original and newly made strands be told apart in bacteria

A

by a feature called methylation state (old DNA has methyl on some of its bases while new doesn’t)

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11
Q

what recognizes the wrong match and connects

A

MutS

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12
Q

what binds to MutS to form a complex

A

MutL

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13
Q

what does MutH do

A

recognizes the GATC sequence which is methylation

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14
Q

how do MutH and the MutS-L complex

A

by looping

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15
Q

what happens after MutS-L complex merges with MutH

A

DNA exonuclease cuts from the methylated GATC sequence to the wrong base

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16
Q

________________ resynthesizes and binds the DNA ligase nucleotides

A

DNA polymerase III

17
Q

how does O-6-methylguanine happens and how can it be repaired

A

addition of a methyl group to the structure of guanine by alkylating agents and can be reversed with enzymes

18
Q

what enzyme repairs O-6-methylguanine

A

O-6-methylguanine-DNA methyltransferase (MGMT)

19
Q

what is the major type of damage induced by UV light

A

formation of pyrimidine dimers

20
Q

how do pyrimidine dimers form

A

joined by the formation of a cyclobutane ring resulting from saturation of the double bonds between carbons 5 and 6

21
Q

what does formation of a pryrimidine dimer cause

A

distorts the structure of the DNA chain and blocks transcription or replication

22
Q

what is a mechanism of repairing UV-induced pyrimidine dimers and why

A

photoreactivation (photolyase) because energy derived from visible light is utilized to break the cyclobutane ring structure

23
Q

how do DNA photolyases work

A

DNA photolyase recognized kink in DNA and bind to site. when excited by Blue Light, photolyases change confirmation breaking a part dimer

24
Q

what species has photoreactivation repair and which doesnt

A

e.coli, yeast and some plants and animals.

humans lack this mechanism

25
Q

what enzymes play a key role in base excision repair

A

glycosylases

26
Q

what does deamination of cytosine cause and how is this problem fixed

A

converts a cytosine base into uracil, and pairing uracil with guanine
the problem is fixed by DNA glycolyase which removes the base

27
Q

what is nucleotide excision repair used for

A

corrects types of damage that distort the DNA double

helix and UV damage

28
Q

how else does UV radiation affect DNA

A

can make cytosine and thymine bases react with neighboring bases that are also Cs or Ts, forming bonds that distort the double helix

29
Q

what is the most common linkage fixed by Nucleotide excision repair

A

thymine dimer

30
Q

what enzymes are used in Nucleotide excision repair

A

Excision endonuclease, OR UV-specific endonuclease

31
Q

what does high energy radiation cause

A

doublestranded breaks in DNA (splitting a chromosome in two)

32
Q

Two pathways involved in the repair of double-stranded DNA breaks are

A

Non-homologous end joining (NHEJ)

Homologous recombination pathways (HRP)

33
Q

how does Non-homologous end joining (NHEJ work

A

two broken ends of the chromosome are simply glued back together by DNA ligase

34
Q

why is Non-homologous end joining (NHEJ) unfavorable

A

This repair mechanism is “messy” and typically involves the loss, or sometimes addition, of a few nucleotides at the cut site but its better than the alternative

35
Q

how does Homologous recombination work

A

Information from the homologous chromosome that matches the damaged one (or from a sister chromatid, if the DNA has been copied) is used to repair the break

36
Q

Homologous recombination is “cleaner” than ______________ and does not usually cause mutations

A

non-homologous

37
Q

what is Hereditary nonpolyposis colorectal cancer (Lynch syndrome)

A

by mutations in genes encoding certain mismatch repair proteins

38
Q

what causes xeroderma pigmentosum

A

by mutations affecting the nucleotide excision repair pathway, thymine dimers and other forms of UV damage can’t be repaired

39
Q

what is Distichiasis

A

double eyelashes, is a rare condition where you have two rows of eyelashes

Med 105 (16 decks)

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