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Which of the following mechanisms are used by cells to overcome or circumvent damage from non-ionizing radiation? More than one answer may be correct.

Phytolase expression in response to UV light. Nucleotide excision repair Base excision repair Methyl directed mismatch repair Translesion DNA synthesis and SOS repair

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Jean Keeling
Jean KeelingLv2
28 Dec 2018

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Related questions

Please help with some epgenetics! I got partial credite for the answers I put but I'm not sure which ones I got wrong!

1) Match the repair pathway to the type of damage it most commonly repairs.

a. Non-homologous end joining

b. Nucleotide excision repair

c. Mismatch repair

d. homologous recombination

e. photolyse

Choices: double strand breaks, UV-induced photodamage, replication error, spontaneous depurination, 5-methyl cytosine

My answer: a. 5-methyl cytosine, b. UV-induced photodamage, c. replication error, d. double strand breaks, e. spontaneous depurination

2) Match the human diseas to the repair patheay that is deficient that disease. Answers may be used more than once.

a. Hereditary polypsis colorectal cancer

b. Xeroderma pigmentosum

c. Ataxia telangiectasia

d. Fanconi Anemia

Choices: mismatch repair, nucleotide excision repair, double strand break repair, base excision repair, photolyse

My answer: a. mismatch repair, b. nucleotide excision repair, c. mismatch repair, d. double strand break repair

3) ____ (a) is a histone chaperone that is recruited by the PCNA and binds to newly synthesized _____(b).

______ (c) is a histone chaperone that acts during the replication-independent assembly pathway, when _____ (d) is incorporated into chromatin.

______(e) is a thrid chaperone that is recruited to replication forks by the replicative helicase.

My answers: a. CAF1, b. H3 and H4, c. H3.3, d. nucleosomes, e. ASF

Match each statement with one of the choices (A-E)

A.) Uracil N-glycosidase B.) AP repair C.) SOS repair D.)Nucleotide excision repair E.) Proof-reading

21.) Deficits in this system account for the UV-sensitivity ofaptients with Xeroderma pigmentosum.

22.) When this "repairs" DNA damage that reuslts from aparticular deamination, it creates an AP site which must besubsequntly repaired by the AP repair system

23.) This inducible, post-replication" repair system is errorprone because it allows DNA polymerase to "bypass" or read-throughthe replication blocks that occur wherever DNA damage precludes thepossibility of normal base-pairing.

24.) This repairs the damage that results from spontaneousdepurination of DNA

25.) In wild type E.coli, most of the replication errors thatresult from tautomeric shifts are repaired by this

I think 21 is D, 22 is A, and 24 is B, but I'm not completelysure. Please help!!

What are the advantages of recombination? What are the disadvantages? Under what kinds of ecological conditions (stable environment, high predation rates, exposure to rapidly evolving parasites, etc.) would you expect to favor one, or the other?

Suppose you found a region of a genome in a vertebrate that was quite large (say, 10 million base pairs) that had an extremely low recombination rate. Suggest a reason why it might be advantageous to not recombine the genes in that genomic region.

How do prokaryotes distinguish the newly synthesized strand from the old template strand? Why don’t eukaryotes use the same mechanism?

What is methylation used for in prokaryotes? In eukaryotes?

What happens if mismatch repair occurs shortly after replication? How does it know which mismatched, normal base is incorrect? What happens if mismatch repair occurs long after replication has occurred?

Why does uracil DNA glycosylase have so an easier task to perform than thymine DNA glycosylase?

Describe the steps that occur following uracil DNA glycosylase activity. What needs to happen; what enzymes are involved?

What do x-rays do to DNA? What does UV radiation do? What do microwaves do?

Is there a safe minimum dose of radiation?

Why is telomerase turned off in human somatic cells? Is it turned off in mouse somatic cells? Would you expect it to be turned off in elephants? Would you expect elephants to have high cancer rates compared to mice?

Where is telomerase necessary? Is it on the leading, or lagging strand, or both? Why don’t bacteria need telomerase?

Why is microsatellite instability used by physicians to measure problems with mismatch repair?

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