Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIOL2010 - Flow of Genetic Information > DNA Repair > Flashcards

DNA Repair Flashcards

1
Q

different categories of DNA damage?

A

replication errors
spontaneous damage
environmental damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what do mutations lead to?

A

cancer & heritable disease
restored DNA
senescence/apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is DNA damage fixed?

A

direct reversal
base excision repair
nucleotide excision repair
mismatch repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how many mismatches per cell division?

A

100 mismatches per cell division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how many lesions per cell per day?

A

10^5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

lesion definition?

A

modification to DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

mutation definition?

A

misincorporation of nucleotides during replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does DNA repair affect no of lesions per cell per day?

A

Reduces 1,000 fold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

transition mutations?

A 
A  G (purines)
C  T (pyrimidines)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

transversion mutations?

A

A C or T

G C or T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

replication errors?

A

mismatches
tautomerisation
strand slippage
intercalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

spontaneous and environmental damage?

A 
hydrolysis (depurination/deamination)
oxidation 
alkylation 
bulkyl adduct formation
radiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

error rate of typical DNA polymerase?

A

1 in 10^5 nucleotides

1 in 10^7 after DNA repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the wobble pairs?

A

A-C especially in lower pHs, maybe in nucleus

G-T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

are the wobble pairs isomorphic?

A

no, they don’t overlay. Allows some enzymes to recognise that they aren’t the correct base pair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is tautomerisation?

A

alternate hydrogen positioning.

usual keto form of T can be in the alternative enol form, can allow it to pair with G

imino A can also pair with C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what can enol T pair with?

A

G

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what can imino A pair with?

A

C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is strand slippage?

A

newly synthesised strand can slip out slightly and cause an extra nucleotide to be incorporated

or for deletion - template strand slips

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where is strand slippage prevalent?

A

in trinucleotide repeats and Huntington’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is intercalation?

A

causes insertions.
intercalation is exhibited by flat/aromatic compounds which can sit between base pairs.
disrupt the replication machinery and can lead to insertion mutations (e.g. frameshift)

22
Q

example of intercalation substance?

A

ethidium bromide found in dyes and cigarette smoke

23
Q

what is an insertion due to transposons?

A

elements which come from viruses can catalyse their removal and insertion into different regions of genes

24
Q

what is a transposon?

A

cut and paste

25
Q

what is a retrotransposon?

A

copy and paste

26
Q

what can chemical modifications lead to?

A 
mismatches
structural alterations to double helix
single/double stranded breaks
blockage/stalling of machinery 
influence gene expression by altering chromatin architecture
27
Q

what percentage of genetic mutations are caused by simple replication errors?

A

66%

28
Q

what is depurination?

A

spontaneous hydrolysiss of the glycosidic bond between a purine and the formation of an ABASIC site

20 times more likely to happen with purines

increased susceptibility to strand breaks

29
Q

what is deamination?

A

converts C to U by hydrolysis

adenine –> hypoxanthine
guanine –> xanthine
5-methylcytosine –> T

30
Q

why does DNA contain T, but RNA contains U?

A

to detect cytosine deamination

31
Q

what is base oxidation by reactive oxygen species?

A

guanine can often be attacked at 8 position and add oxygen.

leads to bond formation with A

32
Q

what is base oxidation by reactive nitrogen species?

A

adenine –> hypoxanthine which pairs with C

33
Q

what is base alkylation?

A

transfer of methyl, ethyl or alkyl groups to nitrogen or oxygen of base

often used in chemotherapy

G pairs with T
forms 3-methyl A

34
Q

what does 3-methyl A do?

A

blocks polymerase from processing

35
Q

what is base adduct formation?

A

modifies N7 of guanine and causes GC to TA transversions

36
Q

example of base adduct chemical?

A

alfatoxin B

37
Q

what makes aflatoxin B reactive?

A

metabolism by cytochrome P450 in liver

38
Q

what is base dimerisation?

A

caused by UV exposure and causes dimerisation of pyrimidines next to each other
Cs and Ts

really distort the DNA so easily fixed

39
Q

Ames test?

A

examines the mutagenic potential of a compound

contains defective histidine gene but requires histidine to live
mix with mutagen
frameshift mutations will reactivate histidine gene and colonies will grow

40
Q

mechanisms for repairing replication errors and DNA damage?

A 
direct reversal 
base excision repair 
nucleotide excision repair 
mismatch repair 
double strand break repair 
translesion synthesis
41
Q

direct reversal?

A

acts directly on modification (alkylation/UV)

human example
removes a methyl group using MGMT. Irreversible reaction once methyl is transferred (suicidal enzyme).

Methylated form of MGMTis a transcription activator, upregulates synthesis of other repair proteins

42
Q

base excision repair?

A

removes specific small non helix distorting base lesions. (deamination/oxidation/alkylation)

removes base.

DNA glycosylase generates an abasic site. AP endonuclease leaves a hydroxyl group.

ligase/DNA pol I seal the gap

e.g. uracil DNA glycosylase

43
Q

MutM?

A

removes 8-oxo-G from the GC lesion

44
Q

MutY?

A

removes A opposite 8-oxo-G following DNA replication

45
Q

MutT?

A

breaks down 8-oxo-dGMP and ppi before DNA synthesis

46
Q

nucleotide excision repair?

A

cleaves backbone either side, removes oligonucleotide (bulkyl, helix distorting lesions)

endonuclease/helicase then DNA poly I/ligase

UvrABCD recognise and remove pyrimidine dimers

UvrA recognises lesion
UvrB opens and binds DNA
UvrC creates incisions either side of lesion
UvrD excises the oligonucleotide

can see a big difference in the DNA surface when there is a TT dimer

47
Q

difference in nucleotide excision repair in humans?

A

single stranded segment is longer

can get recruited to an RNA polymerase which is stalled at the site of a lesion

48
Q

mismatch repair?

A

error reducing process of 1000 fold

repairs main GT, GG, AC and CC mismatches

removes a long stretch of nucleotides

MutSLH recognises distortion. straight after replication, daughter strand isn’t methylated yet so this means it can find the mismatch and replace the unmethylated DNA

MutH nicks the daughter strand, MutS recognises the distortion. MutL is the communicator between the two

exonuclease, UvrD (helicase) and DNA polymerase

49
Q

double strand break repair?

A

before the two sister chromosomes have been generated, NHEJ protects and processes the broken ends and joins them together but usually results in small deletions and is mutagenic

50
Q

translesion polymerases?

A

non processive, template dependent polymerases that synthesis acrss a blockage, introduce nucleotides independent of base pairing

some enzymes fix certain lesions - open active site so allows any nucleotide to be added

51
Q

p53 protein?

A

transcription factor that regulates the expression of genes involved in growth arrest, DNA repair and apoptosis

50% of cancers have a defective p53

52
Q

Xeroderma Pigmentosum?

A

Increased sensitivity to UV light

1000 fold increased risk of skin cancer

BIOL2010 - Flow of Genetic Information (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions