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QUIZ 6 > DNA Damage, Repair, and Recombination > Flashcards

DNA Damage, Repair, and Recombination Flashcards

1
Q

meiotic recombination allows _

A

gene diversity

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2
Q

mitotic recombination allows _

A

mutations repair in somatic cells

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3
Q

site specific recombinations

A

used by viruses and transposons to integrate into host, only at specific sites

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4
Q

phage recombination is an example of _

A

site specific recombination

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5
Q

transposons

A

regions of DNA that can duplicate and jump from one position in the genome into another

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6
Q

homologous recombination

A

occurs between two DNA molecules that share sequence homology

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7
Q

V(D)J recombination in antibodies is _

A

site specific recombination

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8
Q

damage

A

affects the structure of DNA molecule (usually chemical)

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9
Q

mutation

A

affects the transmission of information in DNA (usually occurs after replication of damaged DNA)

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10
Q

multisite mutations

A

cause gross chromosome abnormalities and affect large regions of DNA; arise during meiosis

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11
Q

types of multisite mutations

A

inversions, duplications, deletions, insertions, substitutions

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12
Q

point mutations

A

affect only 1 or 2 nucleotides and arise during DNA replication

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13
Q

point mutations require _

A

an error during DNA replication and failure to correct the error

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14
Q

types of point mutations

A

inversions, duplications, deletions, substitutions, insertions

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15
Q

types of substitutions

A

transitions or transversions

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16
Q

transitions

A

purine to purine (A to G) or pyrimidine to pyrimidine (T to C)

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17
Q

types of substitutions within coding regions

A

missense, nonsense, and frameshift

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18
Q

What is the first defense against point mutations?

A

3’ to 5’ exonuclease activity of the DNA polymerases

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19
Q

types of damage that cause mutations

A

base tautomerization, pyrimidine dimer, hydroxylation, deamination, base loss, strand breaks, and methylation/alkylation

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20
Q

base tautomerization

A

an adenine tautomer (double bond at C6) can now bond to cytosine –> will now cause G-C base pair after replication instead of the normal A-T

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21
Q

dimerization

A

thymine dimers caused by UV damage

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22
Q

hydroxylation

A

mediated by free radicals; 8-oxodeoxyguanosine can base pair with A or C

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23
Q

spontaneous deamination

A

adenosine to hypoxanthine, guanine to xanthine, and cytosine to uracil

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24
Q

Why is spontaneous deamination possible?

A

3 of the 4 bases have exocyclic amino groups

25
Q

hypoxanthine

A

deamination of adenosine; base pairs with cytosine

26
Q

base loss

A

depurination, depyrimidination; results in abasic site (removes deoxy ribose + phosphate)

27
Q

types of chemical mutagens

A

chemicals that accelerate deamination reaction, base analogues, alkylation agents, intercalation agents

28
Q

nitrous acid & derivatives

A

chemicals that accelerate deamination reaction

29
Q

alkylating agents

A

dimethyl sulfate (DMS methylates guanine) and ethylmethane sulfate (EMS ethylates guanine)

30
Q

base analogues

A

5-bromouracil will be treated as a thymine (can base pair with A but also G)

31
Q

Ames assay

A

take mutant E. coli –> plate them without histidine –> add substance of interest –> if it induces growth of the bacteria, it is a mutagen

32
Q

recombination repair/homologous recombination occurs in _

A

S and G2 phase when there is a spare copy (template strand to correct damage)

33
Q

homologous recombination is used to repair _

A

double stranded breaks

34
Q

non-homologous end joining happens when _

A

there is no template available, usually G1 phase

35
Q

non-homologous end joining is used to repair _

A

double stranded breaks

36
Q

NHEJ process

A

double stranded breaks are repaired by ligating ends together

37
Q

mismatch repair must be able to _

A

distinguish parent from daughter strand

38
Q

How does mismatch repair identify the daughter strand?

A

adenines are methylated during replication so there will be a methylated adenine on the parent strand but no methylation on the daughter strand

39
Q

mismatch repair process

A

mutH nicks the unmethylated strand –> uvrD (helicase) and exonuclease remove the strand back to mismatch –> pol III fills gap and ligase fixes nick

40
Q

mutH

A

binds the hemimethylated A

41
Q

mutS

A

binds the mismatch

42
Q

mutL

A

brings mutS and mutH together

43
Q

base excision repair is used to correct _

A

single strand break or single-base damage

44
Q

base excision repair recognizes _

A

deaminated bases

45
Q

base-excision repair steps

A

DNA glycosylase removes damaged base –> AP endonuclease cuts the backbone of the abasic site –> DNA polymerase I adds new bases –> DNA ligase seals nick

46
Q

Why do cells use thymine in DNA rather than uracil?

A

if DNA was U and C rather than C and T, you would not know if the U was supposed to be there or if it was just a deaminated C

47
Q

nucleotide excision repair is used to correct _

A

bulky lesions and crosslinks

48
Q

nucleotide-excision repair process

A

enzymes recognize kink –> nick the DNA –> remove damaged strand –> DNA polymerization –> ligation

49
Q

nucleotide excision repair is more active in _

A

transcribed DNA because repair factors are associated with RNA polymerase

50
Q

SOS response in bacteria

A

lexA repressor is bound to SOS genes, turning off the repair system –> damage encountered –> recA removes lexA –> SOS genes transcribed

51
Q

translesion DNA synthesis occurs when _

A

there is damage to both strands and there is no sister strand to copy from

52
Q

translesion DNA synthesis process

A

damaged bases prevent NHEJ –> allows replication to continue over the damaged base, inserting a random base –> must accept the mutation and just ignore the damaged base

53
Q

TLS is activated by _

A

SOS response

54
Q

exceptions to mutations in the repair system being lethal

A

Lynch syndrome, xeroderma pigmentosum, BRCA cancers

55
Q

Lynch syndrome

A

missing enzymes needed to for the mismatch repair (MutS and MutL)

56
Q

xeroderma pigmentosum

A

person is unable to repair pyrimidine dimers (no nucleotide excision repair)

57
Q

BRCA1

A

associates with RNA polymerase to help repair double stranded breaks in DNA, mismatch repair, and recombination repair

58
Q

accelerated aging diseases from deficiencies in DNA repairs

A

Bloom syndrome, cockayne’s syndrome, Fanconi’s anemia, Werner syndrome

QUIZ 6 (11 decks)

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