PROBLEMS

Question 35.1

1.  Mistakes were made. List some of the means by which mutations can be introduced into DNA.

Question 35.2

2.  Molecular insults. List the factors discussed in this chapter that can cause DNA damage.

Question 35.3

3.  As simple as 1,2,3. What are the steps required of all DNA-repair mechanisms? ✓ 5

Question 35.4

4.  DNA repair services. List the repair systems responsible for maintaining the integrity of DNA. ✓ 5

Question 35.5

5.  Sad, but true. Generations of children have been told by their mothers: “Get out of the house and play outside. Sunshine is good for you!” Why is that now sometimes considered questionable advice?

Question 35.6

6.  Flipped out. Describe the process of base-excision repair, which removes modified bases.

Question 35.7

7.  T time. Explain the benefit of using thymine in DNA instead of uracil. ✓ 5

Question 35.8

8.  A coincidence? I think not. Cytosine in eukaryotic DNA is frequently methylated in the 5 position as a means of transcription regulation. Eukaryotic cells also contain a specialized repair system that recognizes G–T mismatches and repairs them to G–C base pairs. Why is this repair system useful to the cell? ✓ 5

Question 35.9

9.  Corrections. Most of the time, the misincorporation of a nucleotide in the course of DNA synthesis in E. coli does not lead to mutated progeny. What is the mechanistic basis for this good fortune?

Question 35.10

10.  No wonder you’re so tired. The spontaneous cleavage of adenine or guanine from DNA, a process called spontaneous depurination, is a common form of DNA damage in mammalian cells. The rate of spontaneous depurination is estimated to be 3 × 10−9 per purine per minute. This damage must be repaired. A diploid human cell has 6 × 109 bp. How many spontaneous depurinations must be repaired per cell per day? ✓ 5

Question 35.11

11.  Induced spectrum. DNA photolyases convert the energy of light in the near-ultraviolet, or visible, region (300–500 nm) into chemical energy to break the cyclobutane ring of pyrimidine dimers. In the absence of substrate, these photoreactivating enzymes do not absorb light of wavelengths longer than 300 nm. Why is the substrate-induced absorption band advantageous? ✓ 5

Question 35.12

12.  Like Lewis and Clark. Match each term with its description.

Trinucleotide repeat
Mutagen
Mismatch repair
Direct repair
Base-excision repair
Nucleotide-excision repair
Tumor-suppressor gene
RAD51
Holliday junction
Recombination
Requires MutS, MutL, and MutH
DNA repair without the removal of any fragments of DNA
An ATPase that binds single-stranded DNA
Requires glycosylase activity
Recombination intermediate
Expansion of it causes Huntington disease
Repair mechanism encoded by the uvrABC gene in E. coli
Exchange of genetic information
Chemical agents that alter DNA
Often a gene for DNA repair

Data Interpretation and Challenge Problems

Question 35.13

13.  Ames test. The adjoining illustration shows four Petri plates used for the Ames test. A piece of filter paper (white circle in the center of each plate) was soaked in one of four preparations and then placed on a Petri plate.

The four preparations contained (A) purified water (control), (B) a known mutagen, (C) a chemical whose mutagenicity is under investigation, and (D) the same chemical after treatment with liver homogenate. The number of revertants, visible as colonies on the Petri plates, was determined in each case.

Unnumbered Figure

(a) What was the purpose of the control plate, which was exposed only to water?

(b) Why was it wise to use a known mutagen in the experimental system?

(c) How would you interpret the results obtained with the experimental compound?

(d) What liver components are likely responsible for the effects observed in preparation D?

Question 35.14

14.  Here comes the sun, and I say, it’s not alright. Skin cancer is the most common cancer in Caucasians, accounting for nearly half of all cancers in the United States per year. More than 2 million people are expected to develop nonmelanoma skin cancer this year in the United States. Fortunately, this skin cancer is readily treated. Sun exposure is the major environmental agent implicated in the induction of nonmelanoma skin cancer. The adjoining graph shows the cumulative percentage of patients with nonmelanoma skin cancer plotted against the age of onset of skin cancers in normal and xeroderma pigmentosum (XP) skin-cancer patients. ✓ 5

Unnumbered Figure

(a) Of the two groups of patients, which group is more susceptible to skin cancer?

(b) Explain your answer to part a.

(c) Hypothesize why it takes approximately six decades for skin cancer to develop in normal people.

Selected Readings for this chapter can be found online at www.whfreeman.com/tymoczko3e.

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