*30. A plant breeder wants to isolate mutants in tomatoes that are defective in DNA repair. However, this breeder does not have the expertise or equipment to study enzymes in DNA repair systems. How could the breeder identify tomato plants that are deficient in DNA repair? What are the traits to look for?

31. A genetics instructor designs a laboratory experiment to study the effects of UV radiation on mutation in bacteria. In the experiment, the students expose bacteria plated on petri plates to UV light for different lengths of time, place the plates in an incubator for 48 hours, and then count the number of colonies that appear on each plate. The plates that have received more UV radiation should have more pyrimidine dimers, which block replication; thus, fewer colonies should appear on the plates exposed to UV light for longer periods of time. Before the students carry out the experiment, the instructor warns them that, while the bacteria are in the incubator, the students must not open the incubator door unless the room is darkened. Why should the bacteria not be exposed to light?


32. Ochre and amber are two types of nonsense mutations. Before the genetic code was worked out, Sydney Brenner, Anthony O. Stretton, and Samuel Kaplan applied different types of mutagens to bacteriophages in an attempt to determine the bases present in the codons responsible for amber and ochre mutations. They knew that ochre and amber mutants were suppressed by different types of mutations, demonstrating that each was a different termination codon. They obtained the following results.

(1) A single-base substitution could convert an ochre mutation into an amber mutation.

(2) Hydroxylamine induced both ochre and amber mutations in wild-type phages.

(3) 2-Aminopurine caused ochre to mutate to amber.

(4) Hydroxylamine did not cause ochre to mutate to amber. These data do not allow the complete nucleotide sequence of the amber and ochre codons to be worked out, but they do provide some information about the bases found in the nonsense mutations.

(a) What conclusions about the bases found in the codons of amber and ochre mutations can be made from these observations?

(b) Of the three nonsense codons (UAA, UAG, UGA), which represents the ochre mutation.

33. To determine whether radiation associated with the atomic bombings of Hiroshima and Nagasaki produced recessive germ-line mutations, scientists examined the sex ratio of the children of the survivors of the blasts. Can you explain why an increase in germ-line mutations might be expected to alter the sex ratio?

34. The results of several studies provide evidence that DNA repair is rapid in genes that are undergoing transcription and that some proteins that play a role in transcription also participate in DNA repair. How are transcription and DNA repair related? Why might a gene that is being transcribed be repaired faster than a gene that is not being transcribed?


Balter, M. 1995. Filtering a river of cancer data. Science 267:1084-1086.

Article describing the nuclear disaster on the Techa river in Russia.

Beale, G. 1993. The discovery of mustard gas mutagenesis by Auerbach and Robson in 1941. Genetics 134:393-399. An informative and personal account of Auerbachs life and research.

Dovoret, R. 1979. Bacterial tests for potential carcinogens. Scientific American 241(2):40-49.

A discussion of the Ames tests and more recent tests of mutagenesis in bacteria. Drake, J.W., and R.H. Baltz. 1976. The biochemistry of mutagenesis. Annual Review of Biochemistry 45:11-37. A discussion of how mutations are produced by mutagenic agents.

Dubrova, Y.E., V.N. Nesterov, N.G. Krouchinsky, V.A. Ostapenko, R. Neumann, D.L. Neil, and A.J. Jeffreys. 1996. Human minisatellite mutation rate after the Chernobyl accident. Nature 380:683-686.

A report of increased germ-line mutation rate in people exposed to radiation in the Chernobyl accident.

Goodman, M.F. 1995. DNA models: mutations caught in the act. Nature 378:237-238.

A review of the role of tautomerization in replication errors. Hoeijmakers, J.H., and D. Bootsma. 1994. Incisions for excision. Nature 371:654-655.

Commentary on the proteins in eukaryotic nucleotide-excision repair.

Martin, J.B. 1993. Molecular genetics of neurological diseases. Science 262:674-676.

A discussion of expanding trinucleotide repeats as cause of neurological diseases.

Modrich, P. 1991. Mechanisms and biological effects of mismatch repair. Annual Review ofGenetics 25:229-253. A comprehensive review of mismatch repair. Neel, J.V., C. Satoh, H.B. Hamilton, M. Otake, K. Goriki, T. Kageoka, M. Fujita, S. Neriishi, and J. Asakawa. 1980. Search for mutations affecting protein structure in children of atomic bomb survivors: preliminary report. Proceedings of the National Academy of Sciences of the United States ofAmerica. 77:4221-4225.

A report of the gene mutations in the children of survivors of the atomic bombings in Japan.

Sancar, A. 1994. Mechanisms of DNA excision repair. Science 266:1954-1956.

An excellent review of research on excision repair. This issue of Science was about the "molecule of the year" for 1994, which was DNA repair (actually not a molecule). Schull, W.J., M. Otake, and J.V. Neel. 1981. Genetic effects of the atomic bombs: a reappraisal. Science 213:1220-1227. Research findings concerning the genetic effects of radiation exposure in survivors of the atomic bombings in Japan.

Shcherbak, Y.M. 1996. Ten years of the Chernobyl era. Scientific American 274(4):44-49.

Considers the long-term effects of the Chernobyl accident.

Sinden, R.R. 1999. Biological implications of DNA structures associated with disease-causing triplet repeats. American Journal of Human Genetics 64:346-353.

A good summary of disease-causing trinucleotide repeats and some models for how they might arise. Tanaka, K., and R.D. Wood. 1994. Xeroderma pigmentosum and nucleotide excision repair. Trends in Biochemical Sciences 19:84-86.

A review of the molecular basis of xeroderma pigmentosum.

Yu, S., J. Mulley, D. Loesch, G. Turner, A. Donnelly, A. Gedeon, D. Hillen, E. Kremer, M. Lynch, M. Pritchard, G.R. Sunderland, and R.I. Richards. 1992. Fragile-X syndrome: unique genetics of the heritable unstable element. American Journal of Human Genetics 50:968-980.

A research report describing the expanding trinucleotide repeat that causes fragile-X syndrome.

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