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BIO 201 > DNA Mutation and Repair > Flashcards

DNA Mutation and Repair Flashcards

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Biology 101 flashcards
1
Q

Any hereditary change in the DNA sequence

A

mutation

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2
Q

different from the “wild type”

A

mutant

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3
Q

agents that cause mutation

A

mutagen

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4
Q

Types of mutation based on the number of bases changed

A
  1. base substitution (point mutation and frameshift mutation)
  2. multiple/chromosomal mutation
  3. numerical chromosomal aberrations
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5
Q

change from purine to purine or pyrimidine to pyrimidine

A

transition point mutation

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6
Q

change from purine to pyrimidine or pyrimidine to purine

A

transversion point mutation

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7
Q

insertion of a base causes the RF to shift to the?

A

left

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8
Q

deletion of a base causes the RF to shift to the?

A

right

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9
Q

types of chromosomal mutation

A
  1. insertion
  2. duplication
  3. deletion
  4. inversion
  5. translocation
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10
Q

addition or loss of 1 or a few chromosomes

A

aneuploidy

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11
Q

duplication or addition of genomes

A

euploidy

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12
Q

change in base results to no change in the AA sequence

A

silent mutation or neutral mutation

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13
Q

change in base in the intronic regions

A

silent mutation or neutral mutation

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14
Q

change in base leads to a different AA

A

missense mutation

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15
Q

change in base leads to translation termination

A

nonsense mutation

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16
Q

types of mutagenesis

A
  1. spontaneous
  2. induced
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17
Q

Types of spontaneous mutations

A
  1. uncorrected mismatches
  2. tautomerization
  3. replication slippage
  4. spontaneous depurination
  5. spontaneous deamination
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18
Q

amine form of A pairs with

A

T

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19
Q

imine form of A pairs with

A

C

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20
Q

keto form of T pairs with

A

A

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21
Q

enol form of T pairs with

A

G

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22
Q

keto form of G pairs with

A

C

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23
Q

enol form of G pairs with

A

T

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24
Q

amino form of C pairs with

A

G

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25
Q

imine form of C pairs with

A

A

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26
Q

what can happen when the template DNA loops out during replication

A

base may fail to be complemented

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27
Q

what can happen when the new DNA loops out during replication?

A

base may be complemented twice

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28
Q

What happens during spontaneous depurination

A

the N-glycosidic bond between a purine base and the deoxyribose sugar is broken

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29
Q

what happens to C during spontaneous deamination

A

converts to U

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30
Q

T occurred after spontaneous deamination, what was the original form?

A

5mC (5-methylcytosine)

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31
Q

What are the six types of induced mutation?

A

chemical mutagens
1. base analogs
2. base-modifying agents
3. intercalating agents

physical mutagens
4. UV radiation at 260 nm
5. ionizing radiation
6. heat

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32
Q

Base analog of T

A

5-bromouracil

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33
Q

keto form of 5-bromouracil pairs with?

A

A

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34
Q

enol form of 5-bromouracil pairs with?

A

G

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35
Q

illustrate the effect of the introduction of a 5-bromouracil

A

see illustration
1. keto B pairs with A
2. shift of keto B to enol B
3. enol B pairs with G
4. shift of enol B to keto B
5. keto B pairs with A
and G is paired with C

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36
Q

base analog of A

A

2-aminopurine

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37
Q

3 modifying agents

A
  1. deaminating agent
  2. hydroxylating agent
  3. alkylating agent
38
Q

nitrous acid

A

deaminating agent

39
Q

sulfur dioxide

A

deaminating agent

40
Q

sodium bisulfite

A

deaminating agent

41
Q

hydroxylamine

A

hydroxylating agent

42
Q

what happens to G in the presence of nitrous acid?

A

G converts to X which pairs with C (no change in base pairs)

43
Q

what happens to C in the presence of nitrous acid?

A

C converts to U which pairs with A (C=G pairing –> T=A)

44
Q

what happens to A in the presence of nitrous acid

A

A converts to H which pairs with C (A=T pairing –> G=C)

45
Q

what happens to C in the presence of sodium dioxide

A

converted to U

46
Q

what happens to C in the presence of hydroxylamine

A

C converts to HAC which pairs with A (C=G pairing –> T=A)

47
Q

epoxides

A

alkylating agent

48
Q

tetraethyl lead

A

alkylating agent

49
Q

nitroso-derivatives

A

alkylating agent

50
Q

MMS/EMS

A

methyl-/ethylmethane sulfate - alkylating agent

51
Q

what happens to G in the presence of MMS

A

converts to O6mG which pairs with T (G=C –> A=T)

52
Q

ethidium bromide

A

intercalating agent

53
Q

acridine orange

A

intercalating agent

54
Q

2 mechanisms of intercalating agents

A
  1. intercalation can result in insertion in the DNA
  2. loss of intercalating agent can result in deletion
55
Q

4 possible effects of inducing UV radiation of 260 nm

A
  1. dimerization of pyrimidine bases
  2. formation of (6-4) lesions and (6-4) photoproducts
  3. shifting of C to imine tautomer
  4. interchain dimerization
56
Q

4 possible effects of inducing ionizing radiation

A
  1. formation of rare enol tautomers
  2. removal of C from the DNA
  3. shifting of C to imine tautomer
  4. production of ss/ds breaks
57
Q

induced mutation by heat?

A

water-induced cleavage of the ß-N-glycosidic bonds can cause removal of bases or can result in AP sites

58
Q

3 biological agents that can induce mutations

A
  1. transposable elements
  2. viruses
  3. bacteria
59
Q

suppression mutation within the same gene

A

intragenic suppression

60
Q

suppression mutation involving different genes

A

intergenic suppression

61
Q

what is suppressor mutation

A

an initial mutation is masked or compensated by a second mutation from a different site/location (can be either intragenic or intergenic)

62
Q

Importance of mutation in the germ cell.

A

Mutations in the germ cells are heritable, which means they can be transmitted to the next generations.

63
Q

Why do mutations occur in low frequency?

A

Mutations are rarely observed because the cell has effective repair systems against unwanted changes in the DNA. It may also be due to mutations happening in the somatic cells (not the germ cells) so the mutations are only observed in tissues or a group of cells, and are not inherited.

64
Q

Kinds of DNA repair mechanisms

A
  1. direct repair
  2. base excision repair (BER)
  3. nucleotide excision repair (NER)
  4. mismatch repair
  5. double strand base repair
  6. SOS response
65
Q

3 types of damages that are repaired directly

A
  1. nicks
  2. alkylation damage
  3. cyclobutyl damage
66
Q

enzyme: repairs nicks

A

DNA ligase

67
Q

adenosine deaminase (ADA) repairs?

A

alkylation damage in E. coli

68
Q

human MGMT repairs?

A

alkylation damage in humans

69
Q

enzyme: repairs cyclobutyl damage

A

photolyase (via photoreactivation)

70
Q

2 main enzymes involved in BER

A
  1. DNA glycosylase
  2. AP endonuclease
71
Q

function of DNA glycosylase in BER

A

removes damaged base

72
Q

function of AP endonuclease in BER

A

cuts DNA in the damaged region (incision)

73
Q

mechanism of BER

A
  1. recognition of damage
  2. excision
    - damage is removed by DNA glycosylase, forming a baseless site, and is excised by AP endonuclease
  3. resynthesis by DNA polymerase ß and DNA ligase
74
Q

NER enzymes in bacteria

A

uvrA
uvrB
uvrC

75
Q

mechanism of NER

A

recognition
- uvrA and uvrB trimer attaches
- uvr A is detaches
- uvrC attaches

excision
- uvrB and uvrC cuts the segment
- helicase II removes the single strand
- uvrB bridges the gap

resynthesis
- replacement and resynthesis of bases by DNA Pol I and DNA ligase

76
Q

2 major types of MMR

A
  1. long patch
  2. short patch
77
Q

3 major enzymes of MMR in prokaryotes

A

Mut S
Mut H
Mut L

78
Q

counterpart of Mut S in eukaryotes

A

hMSH2/hMSH6

79
Q

counterpart of Mut H in eukaryotes

A

none/unknown

80
Q

counterpart of Mut L in eukaryotes

A

hMLH1

81
Q

5 steps in the MMR system

A
  1. recognition of the mismatch by Mut S
  2. production of nicks where Mut H determines which strand contains the mismatch
  3. Mut L recruits Mut S and Mut H to form the key intermediate complex
  4. Mismatch is excised by exonuclease and DNA helicase
  5. resynthesis by DNA Pol I and DNA ligase
82
Q

2 types of DSBR

A
  1. homologous recombination
  2. non-homologous end-joining
83
Q

steps of NHEJ

A
  1. recognition and binding of Ku and DNA-PKcs proteins
  2. DNA-PKc activates XRCC4
  3. XRCC4 activates ligase IV
  4. DNA ligase IV seals breaks
84
Q

function of Ku in NHEJ

A

recognition of break and binding of DNA-PKcs

85
Q

function of DNA-PKcs in NHEJ

A

activates XRCC4

86
Q

function of XRCC4 in NHEJ

A

activates DNA ligase IV

87
Q

function of DNA ligase IV in NHEJ

A

seals breaks

88
Q

mutasome in SOS response

A

DNA Pol V (2 UmuD and 1 UmuC proteins)

89
Q

2 major proteins in SOS response

A
  1. RecA
  2. LexA
90
Q

function of RecA in SOS response

A

acts as co-protease (with ATPase and ssDNA binding)

91
Q

function of LexA in SOS response

A

repressor; autoregulatory protein

92
Q

mechanism of SOS response

A
  1. DNA damage produces ss gap
  2. RecA proteins bind to the ssDNA
  3. LexA is inactivated (via activated proteolysis)
  4. error-prone resynthesis/replication

BIO 201 (10 decks)

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