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MSI Unit I > 1-7 DNA Repair > Flashcards

1-7 DNA Repair Flashcards

1
Q

What are the different types of DNA damage?

A

Deamination, Depurination, Alkylation, Pyrimidine Dimer, Mismatch, Inserted Ribonucleotide, Base oxidation, bulky adduct, Single strand break, double strand break,

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2
Q

Deamination

A

cytosine to uracil. after replication will cause an AT pair instead of a CG pair in daughter

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3
Q

depurination

A

removal of purine from dna molecule

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4
Q

alkylation.

repaired by?

A

of guanine, makes it bind to thymine. duaghter strands will become A-T not C-G.

repaired by MGMT (direct reversal)

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5
Q

pyrimidine dimer

A

cross-linking between adjacent thymines by UV. distorts helix and blocks replication.

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6
Q

mismatch

A

incorrectly paired bases

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7
Q

inserted ribonucleotide

A

nucleotide in the sequence is a ribonucleotide instead of deoxyribonucleotide

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8
Q

base oxidation

A

extra hydroxl group bonded to a base

oxidized G pairs with A and causes CG to AT transverse mutation.

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9
Q

bulky adduct

A

large organic molecule is bonded to a nucleotide

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10
Q

single strand break

A

one strand of DNA molecule broken

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11
Q

double strand break

A

both strands broken

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12
Q

BER

steps

removes?

strands?

A

Base excision repair - Important for removing damaged bases that could cause mustations or mispairings or breaks in DNA during replication (repairs deamination, depurination, base oxidation, and single strand breaks.

  • Initated by DNA glycoslyases that recognize altered/incorrect bases.
  • glycosylase will remove the base, created an abasic (apurinic/apyrimidinic) site.
  • AP endonuclease cleaves phosphodiester bond at 5’
  • dTTP synthesized.
  • Sealed with DNA ligase

endonuclease cleavage at one strand

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13
Q

NER

removes? enzymes?

strands?

A

Nucleotide excision repair - repair pyrimidine dimers and bulky adducts. Involves enzymes XPA through XPG.

Involves endonuclease cleavage a both strands.

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14
Q

MGMT

A

in non placental mammals

-directly repairs alkylation damage by scanning molecule

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15
Q

Defective BER is linked to?

A

cancer, neurological disorders

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16
Q

Defective NER leads to?

A

diseases such as xeroderma pigmentosum - caused by one or more enzymes of excision pathway deficiency.

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17
Q

RER

What enzyme used?

A

used to excise incorrectly placed ribonucleotides in the DNA molecule using RNase H2.

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18
Q

Most common type of DNA damage?

A

transient contamination of DNA with rNTP’s.

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19
Q

RER deficiency leads to?

A

Mutations arising from short deletions.

=Aicardi-Goutieres Syndrome

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20
Q

Mismatch Repair

A

repairs 99% of errors occuring during replication.

  • complex of mismatch repair proteins scans newly replicated DNA for mismatches
  • removes section of strand containing incorrect base
  • resynthesizes missing strand
21
Q

How does the DNA mismatch repair complex know where to look?

A

newly synthesized DNA contains gaps that have not been sealed yet - guiding the repair apparatus as to where to look for mismatches

22
Q

mutation of any of the 6 genes that code for mismatch repair leads to

A

predisposition to certain cancers including the most common form of heredity colon cancer (hereditary non-polyposis colon cancer) (HNPCC)

23
Q

Direct reversal

A

reverses alkylation. involves methyl guanine methyl transferase (MGMT). MGMT covalently transfers the alkyl group to it’s active cysteine cyte.

  • inactivates MGMT
  • restores guanine to normal
24
Q

double strand break repair (??)

A

fixes ds breaks via homologous recom and non-homo end joining (NHEJ). Occurs when nick in DNA occurs prior to replication, leading to a long continuous strand ds, and then a blunted strand. ds

25
Q

describe non homologous end joining (?)

A

in NHEJ, the two broken ends of DNA are joined via DNA ligase

  • more error prone pathway but necessary when no template available
  • favored by higher eukaryotes (humans)
26
Q

Describe homologous recombination (?)

A

HR more accurate - uses a homo sequence (identical) as template to repair double strand breaks. Often used with dsb are created during replication

27
Q

what is the DNA Damage Response?

major regulators?

A

DDR - pathway that involves signals, sensors, transducers, and effectors to accomplish cell cycle transitions, dna rep, dna repair, apoptosis.
-major regulators are the PI3K related Kinases (PIKKs) including ATM and ATR.

28
Q

ATM

A

functions in response to rare DSBs.

29
Q

ATR

A

activated during every S phase to

  • regulate rep origin firing
  • repair damaged forks
  • prevent premature mitosis onset
30
Q

Xeroderma Pigmentosum

A

defective NER (specifically because of XPA through XPG)

31
Q

Hereditary Non-Polyposis Colon Cancer (HNPCC)

A

Due to mutations in any of the mismatch repair(MMR) genes. Develops the mutator phenotype (mutations accumulate in cells more frequently).

32
Q

Aicardi–Goutières Syndrome (AGS) -

A

Mutations in the RNase H2 subunits, hindering RER. Due to short deletions. Rare neuroinflammatory disorder

33
Q

Ataxia Telangiectasia

A

Due to homozygously inheriting mutations in the ataxia telangiectasia mutated (ATM) gene. Predisposes the individual to cancers and neurodegenerative diseases.

34
Q

exo vs endo nucleases

A

endo - cut like scissors within DNA
exo - chew from outside.
5’-‘3 exo start at 5’
3-5’ exo start at 3’ end

35
Q

what is a mutation?

A

permanent, heritable alterations in the base sequences of DNA

36
Q

in BER, the lesion is removed by

A

dna glycosylase

37
Q

distamycin

A

DNA groove binder. interacts with A-T in minor groove. Terminal end of molecule attracts the drug

38
Q

Actinomycin

A

DNA intercalators - blocks chain elongation

39
Q

cisplatin

A

dna crosslinking agent. anti-cancer for testicular and ovarian. crosslinks cause helix unwinding which prevent additional transcription/replication. eventual cell death

40
Q

in NER, endonuclease makes nicks on either side of the lesion, which is then removed to make a gap which is filled by ____ to make the final phosphodiester bond.

A

DNA polymerase

41
Q

What happens if the cell cycle checkpoint is reached, and DNA damage is not repaired.

A

DNA damage response (DDR) pathway is initiated. ATM is recruited to activate p53, which leads the cell to senescence or apoptosis.

42
Q

Xeroderma pigmentosum patients lack one or more enzymes required for:

A

excision repair

43
Q

The proofreading activity of DNA polymerase involves:

A

A. 3’–>5’ exonuclease function

44
Q

Ultraviolet light produces thymine dimers in DNA strands. Excision repair requires all of the enzymes listed EXCEPT:
A. primase

B. DNA polymerase

C. DNA ligase

D. nuclease

A

A. Primase

45
Q

HNPCC? caused by?

A

hereditary non-polypsis colon cancer - caused by mutation in any of the 6 mismatch repair genes

ussually only one allele inherited, doesnt appear until second allele mutates
autosomal dominant?

46
Q

NER vs BER endonuclease activity

A

NER - both strands

BER - one strand

47
Q

xeroderma pigmentosum

A

family of diseases caused mutations/deficiencies in one or more of the excision pathway enzymes

XPC, RPA, TFIIH, XPG, ERCC1-XPF

autosomal recessive

sensitive to UV light. damage not reversed

48
Q

ataxia telangiectasia

A

caused by defect in DNA repair gene ATM

autosomal recessive

MSI Unit I (52 decks)

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