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genetics > chapter 11 part 2 > Flashcards

chapter 11 part 2 Flashcards

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Biology 101 flashcards
1
Q

mutagens

A

agents that cause DNA damage

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2
Q

induced mutations

A

produced by mutagens in an experimental setting to study types of damage caused, mutation process, or repair responses

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3
Q

chemical mutagens can be classified by their modes of action on DNA as:

A
  1. nucleotide base analogs
  2. deaminating agents
  3. alkylating agents
  4. oxidizing agents
  5. hydroxylating agents
  6. intercalating agents
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4
Q

intercalating agents

A

molecules that fit between DNA base pairs and distort the DNA duplex

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5
Q

what does distortion from intercalating agents lead to

A

DNA nicking that is no efficiently repaired
- results in added or lost nucleotides

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6
Q

DNA stains that are intercalating agents

A
  • ethidium bromide
  • acridine orange
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7
Q

photoproducts

A

aberrant structures with additional bonds involving nucleotides

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8
Q

what are photoproducts caused by

A

UV irradiation

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9
Q

pyrimidine dimers

A

produced by formation of one or two additional covalent bonds between adjacent pyrimidine nucleotides

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10
Q

2 common types of photoproducts

A
  1. thymine dimer
  2. 6-4 photoproduct
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11
Q

thymine dimer

A

formed between 5 and 6 carbons of adjacent thymines

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12
Q

6-4 photoproduct

A

formed by bond between carbon 6 on one thymine and carbon 4 on other

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13
Q

types of radiation higher than UV

A

X-rays, gamma rays, radioactive materials

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14
Q

most serious damage from radiation

A

single-stranded or double-stranded breaks in DNA

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15
Q

what can ss or ds breaks block

A

DNA replication

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16
Q

how do organisms preserve the fidelity of DNA

A

using multiple repair systems

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17
Q

how to multiple repair systems fix problems

A

directly repair DNA or allow organism to circumvent the problems

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18
Q

most direct way to repair DNA

A

proofreading activity of DNA polymerase
- 3’ to 5’ exonuclease activity

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19
Q

do humans have photo reactive repair?

A

no

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20
Q

is photo reactive repair direct?

A

yes

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21
Q

direct repair of UV-induced photoproducts
- photo reactive reapir

A

enzyme photolyase uses energy from visible light to break bonds between pyrimidine dimers

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22
Q

what is photolyase encoded by

A

E. coli phr (photo reactive repair) gene

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23
Q

how is DNA damage by alkylating agents repaired

A

by enzymes that remove the added chemical groups to restore the nucleotide to its normal form

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24
Q

what is the direct repair of damage by alkylating agents performed by

A

class of enzymes called alkyltransferases

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25
Q

alkyltransferases

A
  • remove alkyl groups (methyl/ethyl)
  • can reverse effects of EMS and NG
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26
Q

ex. of alkyltransferases

A
  • O6-methylguanine is converted back to guanine by enzyme O6-methylguanine methyltransferase
  • enzyme permanently inactivated after one such reaction
27
Q

nucleotide base excision repair (BER)

A

multistep process that may repair damage to a nitrogenous base or replace an incorrect base

28
Q

DNA glycosylases

A

series of enzymes that recognize specifically modified/incorrect bases and remove modified purine bases
- leaves an AP site

29
Q

AP site

A

apurinic/apyrimidic site - no base

30
Q

nucleotide base excision repair

A
  • DNA glycosylases recognize incorrect base, remove it, and leave AP site
  • AP endonuclease creates single-stranded nick near AP site
  • nick translation - DNA polymerases initiate removal/replacement of nucleotides including AP site
  • DNA ligase seals sugar-phosphate backbone
31
Q

nucleotide excision repair (NER)

A

used to repair UV-induced damage to DNA

32
Q

what is nucleotide excision repair also known as

A

ultraviolet repair

33
Q

nucleotide excision repair basic process

A
  1. enzymes recognize and bind to damaged region
  2. segment of nucleotides is removed from the damaged strand
  3. DNA polymerase fills in gap
  4. DNA ligase seals the sugar-phosphate backbone
34
Q

UV repair (NER)

A
  1. UVR A and B proteins bind to DNA strand opposite photoproduct
  2. UVR C joins UVR B to form UVR BC complex
  3. UVR C cleaves damaged DNA strand about 4-5 nucleotides to 3’ and 5’ sides of the photoproduct
  4. UVR D (a helicase) helps remove DNA fragment containing photoproduct
  5. DNA polymerase fills gap and DNA ligase seals backbone
35
Q

xeroderma pigmentosa

A

human hereditary cancer-prone condition that is caused by the mutation of any seven different genes involved in NER

36
Q

symptoms of xeroderma pigmentosa

A
  • extreme UV sensitivity
  • develop UV-induced pre-cancerous and cancerous lesions
37
Q

mismatch repair

A

detects and repairs mismatched nucleotides that escape DNA polymerase

38
Q

how do repair enzymes distinguish between the original, correct nucleotide and the new, mismatched nucleotide

A

using presence of methylation on original strand
- E. coli: methylation common on adenine of 5’GATC3’

39
Q

mismatch repair process

A
  1. MuhH binds to hemimethylated DNA region
  2. MutS locates/binds to DNA mismatch and then forms a complex with MutL
  3. MutS/MutL complex binds to MutH
  4. MutH protein breaks phosphodiester bond on 5’ side of guanine on unmethylated daughter strand
  5. exonuclease enzymes digest nucleotides from nick
  6. DNA polymerase fills gap on daughter strand
  7. DNA ligase completes the repair
  8. Dam methylate methylates the adenine of the GATC sequence on the daughter strand
40
Q

what do DNA damage signaling systems to

A
  • recognize presence of
    DNA lesions
  • initiate repair response
41
Q

ATM

A

plays pivotal role in communicating DNA damage to activate transcription of p53 gene

42
Q

what does ATM activate

A

p53 repair pathway

43
Q

p53 repair pathway

A

controls cell responses to mutation

44
Q

how does p53 repair pathway control cell responses to mutation

A
  • pauses cell cycle at G1-to-S transition to allow time for repair
  • initiates apoptosis
45
Q

p53 levels are ______ in healthy cells

A

low

46
Q

p53 levels ________ as ATM levels __________

A

increase, increase

47
Q

how does p53 initiate G1 arrest

A

by inducing synthesis of p21

48
Q

p21

A

inhibits formation of cyclin-CDK complexes

49
Q

what do completed repairs do to the p53 levels

A
  • reduce them
  • allows cell cycle to proceed
50
Q

what does the synthesis of p21 allow

A

time to repair damaged DNA

51
Q

p53 activates transcription of the ______ gene

A

BAX

52
Q

BAX gene

A

encodes a slowly acting inhibitor of BCL2

53
Q

what does BCL2 repress

A

apoptosis

54
Q

activity of BCL2 protein in healthy cells

A

mains repression of apoptosis

55
Q

activity of BCL2 protein in damaged cells

A

if p53-induced pause is too long, then apoptotic pathway is induced when BCL2 inhibited

56
Q

SOS repair system is activated in response to what?

A

heavily damaged DNA in E. coli cells

57
Q

how is SOS repair accomplished

A

by activation of translesion DNA polymerases

58
Q

another name for translesion DNA polymerases

A

bypass polymerases (Pol V)

59
Q

translesion polymerases

A

error-prone polymerases that have no proofreading ability and can replicate across lesions that would stall DNA pol III

60
Q

SOS repair in E. coli

A
  • when pol III stalls at damaged DNA, RecA proteins coat the template strand ahead of the lesion (already bound by SSB protein) to form a DNA-RecA-SSB complex
  • RecA also activates transcription of pol V
  • Pol V displaces pol III, synthesizes short stretch of new DNA across lesion, and is then replaced by pol III which resumes normal replication
61
Q

what happens when both strands of DNA are broken

A

neither can act as a template for repair

62
Q

how can double-stranded breaks happen

A

exposure to X-rays and certain types of oxygen radicals

63
Q

what can double-stranded breaks cause

A
  • chromosome instability
  • incomplete replication
  • cell death
  • increase risk of cancer
  • chromosome structure mutations
64
Q

2 mechanisms for carrying out double-stranded break repair

A
  1. non-homologous end joining
  2. synthesis-dependent strand annealing

genetics (37 decks)

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