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MCM-1 > Test 3_DNA Damage and Repair > Flashcards

Test 3_DNA Damage and Repair Flashcards

1
Q

Spontaneous Lesion

A
  1. consist of depurination or deamination reactions
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2
Q

Depurination

A

Hydrolysis of a purine to release nucleic acid and a purine

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3
Q

Deamination

A

conversion of cytosine into uracil.

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4
Q

Bulky Lesions

A
  1. covalent linkages formed by reactive oxygen, sunlight, or carcinogens.
  2. bond forms between adjacent nucleotides
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5
Q

Copy Errors.

A

Occurs when DNA polymerase introduces the improper base

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6
Q

Mutagens

A

a physical or chemical agent that alters the structure or sequence of DNA

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7
Q

Base analog

A
  1. chemical mutagen.

2. Resembles purine/pyrimidines and is incorporated into DNA during replication

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8
Q

Intercalating Agents

A
  1. chemical mutagen
  2. inserts into doube helix and causes stretching on one side, leading DNA pol to add more nuecleotides to the other strand
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9
Q

Direct acting Agents

A
  1. chemical mutagen
  2. chemically reacts with DNA
    (base analogs/intercalating agents???)
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10
Q

Indirect Acting Agents

A
  1. chemical mutagen

2. requires metabolic conversino by P-450 to actively alter DNA.

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11
Q

UV Radiation

A
  1. physical mutagen
  2. changes energy level or electrons, allowing it to act irradically.

short wavelength=higher energy=more damage

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12
Q

UV-A radiation

A
  1. 320-400nm

2. cause ds breaks and oxidation

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13
Q

UV-B Radiation

A
  1. 280-320nm

2. forms pyrimidine dimers

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14
Q

UV-C Radiation

A
  1. 180-290nm

2. germicidal and ozone filters out the majority of it.

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15
Q

Rank the UV-A,B,C in order from highest to lowest energy.

A

C > B > A in terms of energy.

energy and wavelength are inversely related.

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16
Q

Rank the UV radiation from highest to lowest in terms of frequency.

A

A > B > C

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17
Q

What is ionizing radiation?

A

1.loss of an electron creating an unstable radical.

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18
Q

What are the types and subtypes of ionizing radiation?

A
  1. electromagnetic (x-ray, gamma ray)

2. particulate ( decay of radioactive material)

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19
Q

Where do beta particles come from?

A
  1. ionizing radiation

2. these are high speed energy electrons from a decaying particle

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20
Q

What are alpha particles?

A
  1. ionizing radiation chemical

2. helium nuclei from a decaying particle.

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21
Q

What types of damage are common with ionizing radiation?

A
  1. cross-linking
  2. ss/ds breaks
  3. base damage
22
Q

DNA repair

A

correction of accidental lesions made in DNA during replication or sustained from the environment

23
Q

Types of DNA repair?

A

can repair the damaged bases or repair the bases that were incorrectly paired during replication.

24
Q

Base excision repair is used when?

A

for small, spontaneous lesions

25
Q

What is the process of Base excision repair?

A
  1. 6+ DNA glycosylases look for damaged bases by “flipping out”
  2. base is removed by base-sugar cleavage.
  3. AP endonucleases locate missing base, remove phosphodiester backbone.
  4. DNA pol adds correct nucleotide.
  5. DNA ligase seals the nick.
26
Q

When is nucleotide excision repair used?

A

to repair large sections of DNA bulky lesions

27
Q

What is the process of Nucleotide excision repair?

A
  1. multienzyme complex scans ds, and cleaves backbone on both sides of mutation.
  2. DNA helicase required to remove damaged section
  3. DNA polymerase adds nucleotide sequence.
  4. DNA ligase seals nick.
28
Q

When is mismatch repair used?

A

This is a method AFTER dna replication, to resolve the errors of DNA pol.

29
Q

What is the process of mismatch repair?

A
  1. MutS and MutL bind the improper base, and control excision of DNA between the ss break and the mismatched sequence.
30
Q

What is the role of MutS?

A

recognizes and binds to mispaired nucleotides and allows further action of MutL

31
Q

What is the role of MutL?

A

eliminate a portion of newly synthesized DNA strand containing the mispaired base

32
Q

What methods are used for replicative repair?

A
  1. proofreading (3’–>5’)

2. back-up polymerase

33
Q

What is the role of back-up polymerases?

A
  1. DNA polymerase stalls when DNA is too severely damaged to replicate.
  2. release of back-up polymerase provides terrible accuracy of repairing DNA.
  3. DNA is repaired so transcription can still occur.
34
Q

Why can back-up polymerases be used if they have such poor accuracy with repairing DNA BEFORE it is transcribed?

A
  1. the DNA contains large cast regions of introns that do not code for specific proteins, therefore it is assumed these mutations will take time before a coding region is actually affected.
35
Q

What is post-replicative repair?

A
  1. transcription-coupled repair

2. double strand break repair.

36
Q

What is transcription coupled repair?

A
  1. RNA pol 2 stalls on template DNA strand pulling “TCR machinery” to site
  2. RNA is remodeled.
  3. The lesion is repaired
  4. RNA pol restarts active transcription of genes
37
Q

What makes up “TCR machinery”?

A
  1. CSB: locates stalled RNA; recruits TFIIH
  2. TFIIH: remodels RNA Pol
  3. XPG: cuts the DNA
38
Q

What causes ds breaks?

A
  1. radiation
  2. errors
  3. oxidation
39
Q

How are ds breaks fixed using nonhomologous end joining?

A
  1. Ku70/80 locates free ds ends, and pull them together.
  2. DNA-PK acts like kinase to activate the DNA ligase
    * *very inaccurate due to loss of nucleotide sequences but is fast and most commonly used in mammalian**
40
Q

How are ds breaks fixed using homologous recombination?

A
  1. Rad51 pairs and guides the 3’ overhanging ss to homologue on sister chromatid.
  2. Homologue template allows DNA synthesis to occur
  3. leads to formation of Holliday Junction.
  4. Junction is cleaved and 2 strands of DNA produced.
    * *high accuracy, more energy required**
41
Q

What is a Holliday Junction?

A
  1. the results of 2 ds DNA strands that are interwoven to form a 4-way intersection.
  2. Essentially 4 ds arms of DNA that join together.
42
Q

What are the DNA damage checkpoints?

A
  1. G1 to S phase
  2. Middle of S phase (error of synthesis/replication)
  3. S to M phases
43
Q

What is the ATM protein?

A
  1. kinase released with DNA damage that phosphorylates specific kinases to promote cell cycle arrest.
44
Q

When would you expect to see the highest amounts of ATM protein?

A
  1. G1 to S phase
  2. during S pahse
  3. S to M phase.
45
Q

What does ATM protein target specifically?

A
  1. p53
46
Q

What happens if p53 is phosphorylated?

A
  1. will ditch the Mdm2.

2. stimulate p21 xcription

47
Q

What is the role of p21, after it has been activated by p53?

A
  1. bind to G1/S Ckd or S-Cdks to inhibit them; prevent cell cycle progression.
  2. technically CKI=p21
48
Q

What is the role of Chk1 and Chk2 in the ATM/DNA damage pathway?

A
  1. block the activation of M-Cdk

2. transmit the signal from ATM/ATR protein to the p53 protein

49
Q

What happens if p53 is not phosphorylated?

A
  1. it remains bound to Mdm2 and will be targeted for ubiquitination.
  2. this will occur when there is no DNA damage in the cell, allowing cell cycle to occur
50
Q

What event in a normal, healthy individual will lead to p53 activation to promote cell cycle arrest and therefore apoptosis?

A
  1. telomere shortening.

MCM-1 (8 decks)

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