Chapter 35 DNA Repair and Recombination
Matching Questions
Use the following to answer questions 1–10:
Choose the correct answer from the list below. Not all of the answers will be used.
a) uracil
b) DNA ligase
c) Huntington disease
d) Ames
e) xeroderma pigmentosum
f) tumor-suppressor genes
g) trinucleotide repeats
h) skin carcinoma
i) mutagen
j) direct repair
k) indirect repair
l) photolyase
1.
_______________ is(are) often found to cause alternative structures in DNA replication.
2.
A(n) _______________ chemically changes the nature of a base in DNA.
Ans: i
Section: 35.1
3.
_______________ is(are) typically involved in DNA repair.
Ans: f
Section: 35.2
4.
_______________ is(are) involved in joining DNA molecules together.
Ans: b
Section: 35.2
5.
_______________ is(are) caused by expanded trinucleotide repeats.
Ans: c
Section: 35.1
6.
_______________ is the process for correcting for base-pair mismatches without excising bases.
Ans: j
Section: 35.2
7.
The enzyme that uses light energy to form an excited state to cleave the dimer into individual
bases is _______________.
Ans: l
Section: 35.2
Ans: g
Section: 35.1
Chapter 35 DNA Repair and Recombination
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8.
_______________ is an enzyme that cleaves a glycosidic bond to release a damaged base.
9.
_______________ is a rare skin disease caused by the inability to correct for UV damage to skin
DNA.
Ans: e
Section: 35.2
10.
An assay used to determine carcinogenic potential is the _______________ test.
Ans: d
Section: 35.2
Fill–in-the-Blank Questions
11.
Proteins that contain a string of glutamines are likely to be involved in _____ disease.
Ans: Huntington’s Section: 35.1
12.
E. coli DNA polymerase III removes mismatched nucleotides from the _____.
Ans: 3 end of DNA Section: 35.1
13.
Hydroxyl radicals cause DNA damage by _____.
Ans: reacting with guanine Section: 35.1
14.
_____ is the enzyme that converts polycyclic aromatic hydrocarbons into a reactive epoxide that
alkylates the N-7 of guanine.
Ans: Cytochrome P450 Section: 35.1
15.
Light-driven DNA damage results in _____.
Ans: thymine dimers Section: 35.1
16.
Replication errors are often corrected by proofreading and _____.
Ans: mismatch repair Section: 35.2
17.
A photoreactivating enzyme is called _____.
Ans: DNA photolyase. Section: 35.2
18.
X-rays cause damage to DNA by inducing _____.
Ans: single- and double-stranded DNA breaks Section: 35.2
19.
The human genetic skin disease that is caused by a mutation in components of the human
nucleotide-excision-repair pathway is called _____.
Ans: xeroderma pigmentosum Section: 35.2
20.
_____ are intermediates in recombination pathways composed of four polynucleotide chains in a
cross-like structure.
Ans: Holliday junctions Section: 35.3; Figure 35.15
Ans: a
Section: 35.2
Chapter 35 DNA Repair and Recombination
3
Multiple-Choice Questions
21.
Damage to DNA may result in
A)
cell death.
B)
cell transformation.
C)
changes in inherited sequences.
D)
blockage of DNA replication.
E)
All of the above.
22.
_________________ is an ATPase needed for DNA repair by recombination.
A)
Polymerase III
B)
RecA
C)
RecB
D)
RAD51
E)
None of the above.
Ans: D Section: 35.3
23.
The three-strand structure involved in strand invasion is
A)
the D-loop.
B)
recombinase DNA.
C)
an RNA triplet.
D)
non-Watson–Crick pairing.
E)
RecA
Ans: A Section: 35.3
24.
The process whereby two daughter molecules of DNA are formed by the exchange of genetic
material between two parent molecules is known as
A)
chemical modification.
B)
recombination.
C)
alkylation.
D)
dimerization.
E)
None of the above.
Ans: B Section: 35.3
25.
In E. coli, mismatch repair involves
A)
recognition of mismatched pair by MutS.
B)
removal of a mismatched nucleotide by DNA polymerase III.
C)
cleavage of the backbone by MutH.
D)
A and C
E)
A, B, and C
Ans: D Section: 35.2
26.
Huntington disease is caused by
A)
pyrimidine dimers.
B)
trinucleotide expansion.
C)
suppressor mutants.
D)
All of the above.
E)
None of the above.
Ans: B Section: 35.1
Ans: E Section: Introduction
Chapter 35 DNA Repair and Recombination
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27.
Aflatoxin B1 is an example of a(n)
A)
intercalating chemical.
B)
alkylating agent.
C)
base analog.
D)
All of the above.
E)
None of the above.
28.
Photolyase functions to
A)
repair pyrimidine dimers.
B)
remove damaged bases.
C)
ligate single-strand breaks.
D)
All of the above.
E)
None of the above.
Ans: A Section: 35.2
29.
An important feature of the Ames test is:
A)
the inclusion of mammalian liver enzymes.
B)
a linear response curve.
C)
that the bacteria used are unable to grow in the absence of arginine.
D)
A and B
E)
A, B, and C
Ans: D Section: 35.2
30.
Exposure to aflatoxin B1 can lead to
A)
the expansion of repeats of three nucleotides.
B)
DNA damage by alkylation.
C)
the defective repair of DNA.
D)
the recombination of DNA.
E)
None of the above.
Ans: B Section: 35.1
31.
Why does the deamination of cytosine to uracil not cause a problem in the next round of DNA
replication?
A)
Although uracil cannot form the third hydrogen bond to guanine, it is recognized by DNA
polymerase as a mismatch and the error is corrected on the next round of replication.
B)
The AP endonuclease nicks the backbone and removes the uracil and replaces it with
another cytosine.
C)
The repair machinery recognizes uracil in DNA as a mistake and replaces it with
cytosine.
D)
The uracil undergoes spontaneous depurination and is replaced with a cytosine.
E)
Deamination of cytosine rarely occurs within the coding region and so causes few
mutations.
Ans: C Section: 35.2
Ans: B Section: 35.1
Chapter 35 DNA Repair and Recombination
5
32.
There are 1080 depurination repair events required per cell per hour and the human genome
contains about 6 109 base pairs. What is the spontaneous rate of depurination?
A)
1.08 10-8 depurinations per purine per minute
B)
1.8 10-7 depurninations per purine per minute
C)
4.8 10-9 depurinations per purine per minute
D)
2 10-9 depurinations per purine per minute
E)
3 10-9 depurinations per purine per minute
33.
The Ames test is a simple and sensitive test for detecting chemical mutagens. What
characteristic of the strain of Salmonella used in the Ames test makes them appropriate for
“detecting chemical mutagens”?
A)
A high proportion of the Salmonella reverse the original mutation.
B)
The addition of the chemical mutagen allows reversal of a mutation for DNA synthesis.
C)
The addition of the chemical mutagen allows reversal of a mutation for histidine
synthesis.
D)
Reversal of the original mutation requires liver homogenates; thus, no spontaneous
reversals.
E)
This strain of bacteria is susceptible to very low levels of mutagens and amplifies very
small signals.
Ans: C Section: 35.3
34.
If you are not genetically predisposed to xeroderma pigmentosum, is it okay to go ahead and get
a summer suntan?
A)
Yes, especially in children, where vitamin D formation is critical of bone growth.
B)
Yes, the incidence of xeroderma pigmentosa is extremely rare and the mutation rate in
the affected genes is low.
C)
No, defects can arise through UV entering the eyes, which is not protected by sunscreen.
D)
No, defects in DNA-repair systems increase with multiple exposures to mutagens.
E)
No, the defective gene in xeroderma pigmentosa is highly susceptible to UV-mutation
and can be acquired later in life.
Ans: D Section: 35.3
35.
If you could look at individual strands of DNA and you saw a Holliday junction, what would
that tell you?
A)
A region of DNA that contains a thymidine dimer is undergoing repair.
B)
DNA repair of a double stranded break is occurring via a recombination mechanism.
C)
DNA with a point mutation is undergoing base-excision repair.
D)
DNA with a point mutation is undergoing nucleotide-excision repair.
E)
Mutagenic reversal is occurring, as seen in the Ames Test.
Ans: B Section: 35.3
Short-Answer Questions
36.
Describe the difficulties in dealing with halts in DNA replication.
Ans:
Replication pauses occur with error-prone but faster polymerases. This often causes
errors but these polymerases are able to read across the lesions due to the pauses.
Section: 35.1
Ans: E Section: 35.2
Chapter 35 DNA Repair and Recombination
6
37.
What is DNA adduct and how is it formed?
38.
How are breaks in DNA sealed that were formed during nucleotide-excision repair?
end of the original part of the DNA strand.
Section: 35.2
39.
Deamination of adenine causes what kind of mutations in DNA?
substitution of cytosine for thymidine in the complementary strand of DNA.
Section: 35.1
40.
What are the enzymes needed for base-excision repair?
phosphodiesterase, DNA polymerase, DNA ligase
Section: 35.2
41.
Tumor-suppressor genes have a dominant negative genetic trait. What does this mean?
mutated, tumors develop at an accelerated rate.
Section: 35.2
42.
Describe the Ames test.
acquire the ability to grow on histidine (−) plates.
Section: 35.2
43.
Describe the consequences of incorrect DNA replication or DNA damage.
generations.
Section: Introduction
44.
Name the types of DNA repair, categorized in groups.
Ans:
The types include direct repair, base-excision repair, and nucleotide-excision repair.
Section: 35.2
45.
Why is thymine used in DNA instead of uracil?
recognized as foreign and is repaired.
formed by alkylation reactions, such as occurs at guanine residues due to aflatoxin B1.
Section: 35.1
Chapter 35 DNA Repair and Recombination
7
46.
To what does the phrase “recombination of genetic material” refer?
47.
What role does the protein RAD51 play in recombination?
promotes strand invasion and leads to the formation of the displacement loop (the D-
loop).
Section: 35.3
48.
Give examples of types of damage to DNA that have led to the development of a variety of
DNA-repair systems.
More complex forms include chemical modification of bases, chemical crosslinks
between DNA strands, and blockage of the process of DNA replication.
Section: Introduction
49.
How do double-strand breaks occur during replication?
x-rays or gamma rays.
Section: 35.3
50.
How is recombination used as a biochemical tool?
Section: 35.3
Ans:
It refers to the situation in which two daughter molecules are formed by the exchange of
genetic material between two parent molecules.
Section: 35.3