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. 1986 Mar;112(3):505–522. doi: 10.1093/genetics/112.3.505

DNA Repair Dependence of Somatic Mutagenesis of Transposon-Caused WHITE Alleles in DROSOPHILA MELANOGASTER after Treatment with Alkylating Agents

Kazuo Fujikawa 1,2, Sohei Kondo 1,2
PMCID: PMC1202761  PMID: 3007278

Abstract

DNA repair-defective alleles of the mei-9, mei-41, mus-104 and mus-101 loci of Drosophila melanogaster were introduced into stocks bearing the UZ and SZ marker sets. Males with the UZ marker set, z1 (zeste allele) and w+(TE) (genetically unstable white allele presumably caused by a transposable element), or the SZ marker set, z1 and w+R (semistable white allele caused by partial duplication of the w+ locus plus transposon insert), were exposed to EMS at the first instar. After emergence, adult males bearing red spots on lemon-yellow eyes were scored as flies with somatic reversions of w+(TE) or w +R. The relative mutabilities (relative values of reversion frequency at an equal EMS dose) of either w+(TE) or w+R in a repair-proficient strain and in mei-9, mei-41, mus-104 and mus-101 strains were 1:∼1.2:0.3:0.3:0.7, despite the fact that w+(TE) reverted two to three times as frequently as w+R under both the repair-proficient and repair-deficient genetic conditions. Similarly, after treatment with MMS, MNNG and ENNG, w+(TE) was somatically more mutable in the mei-9 strain and less mutable in the mei-41 and mus-104 strains than in the repair-proficient strain. From these results, we propose that mutagenic lesions produced in DNA by treatment with these chemicals are converted to mutant DNA sequences via the error-prone repair mechanisms dependent on the products of the genes mei-41+ (mei-41 and mus-104 being alleles of the same locus) and mus-101+, whereas they are eliminated by mei-9+-dependent excision repair. In contrast to the approximately linear responses of induced reversions of w+( TE) with ENNG in the repair-proficient, mei-9, and mei-41 strains, seemingly there were dosage insensitive ranges for induced reversion with MNNG in the repair-proficient and mei-41 strains, but not for reversion in the mei-9 strain; w+( TE) in the mus-104 strain was virtually nonmutable with MNNG and ENNG. These results suggest that O6-methylguanine (O6MeG) produced in DNA with MNNG, but not O 6-ethylguanine produced with ENNG, is almost completely repaired in a low dose range by constitutive activity of DNA O6MeG transmethylase. From the distribution of clone sizes of spontaneous revertant spots and other data, we propose that both w+(TE) and w+R have a similar tendency to spontaneously revert more frequently at early rather than at late developmental stages, probably reflecting a common property of their inserted transposons.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Baker B. S., Smith D. A. The effects of mutagen-sensitive mutants of Drosophila melanogaster in nonmutagenized cells. Genetics. 1979 Jul;92(3):833–847. doi: 10.1093/genetics/92.3.833. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Bowman J. T., Jr Spontaneous reversion of the white-ivory mutant of Drosophila melanogaster. Genetics. 1965 Nov;52(5):1069–1079. doi: 10.1093/genetics/52.5.1069. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Boyd J. B., Golino M. D., Setlow R. B. The mei-9 alpha mutant of Drosophila melanogaster increases mutagen sensitivity and decreases excision repair. Genetics. 1976 Nov;84(3):527–544. doi: 10.1093/genetics/84.3.527. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Boyd J. B., Shaw K. E. Postreplication repair defects in mutants of Drosophila melanogaster. Mol Gen Genet. 1982;186(2):289–294. doi: 10.1007/BF00331864. [DOI] [PubMed] [Google Scholar]
  5. Brown T. C., Boyd J. B. Postreplication repair-defective mutants of Drosophila melanogaster fall into two classes. Mol Gen Genet. 1981;183(2):356–362. doi: 10.1007/BF00270640. [DOI] [PubMed] [Google Scholar]
  6. Gatti M., Pimpinelli S., Baker B. S. Relationships among chromatid interchanges, sister chromatid exchanges, and meiotic recombination in Drosophila melanogaster. Proc Natl Acad Sci U S A. 1980 Mar;77(3):1575–1579. doi: 10.1073/pnas.77.3.1575. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Goldberg M. L., Sheen J. Y., Gehring W. J., Green M. M. Unequal crossing-over associated with asymmetrical synapsis between nomadic elements in the Drosophila melanogaster genome. Proc Natl Acad Sci U S A. 1983 Aug;80(16):5017–5021. doi: 10.1073/pnas.80.16.5017. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Harris P. V., Boyd J. B. Excision repair in Drosophila. Analysis of strand breaks appearing in DNA of mei-9 mutants following mutagen treatment. Biochim Biophys Acta. 1980 Nov 14;610(1):116–129. doi: 10.1016/0005-2787(80)90061-1. [DOI] [PubMed] [Google Scholar]
  9. Ishii Y., Kondo S. Comparative analysis of deletion and base-change mutabilities of Escherichia coli B strains differing in DNA repair capacity (wild-type, uvrA-, polA-, recA-) by various mutagens. Mutat Res. 1975 Jan;27(1):27–44. doi: 10.1016/0027-5107(75)90271-7. [DOI] [PubMed] [Google Scholar]
  10. Kondo S., Ichikawa H., Iwo K., Kato T. Base-change mutagenesis and prophage induction in strains of Escherichia coli with different DNA repair capacities. Genetics. 1970 Oct;66(2):187–217. doi: 10.1093/genetics/66.2.187. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Prakash L., Higgins D. Role of DNA repair in ethyl methanesulfonate-induced mutagenesis in Saccharomyces cerevisiae. Carcinogenesis. 1982;3(4):439–444. doi: 10.1093/carcin/3.4.439. [DOI] [PubMed] [Google Scholar]
  12. Prakash L. Lack of chemically induced mutation in repair-deficient mutants of yeast. Genetics. 1974 Dec;78(4):1101–1118. doi: 10.1093/genetics/78.4.1101. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Rasmuson B., Svahlin H., Rasmuson A., Montell I., Olofsson H. The use of a mutationally unstable X-chromosome in Drosophila melanogaster for mutagenicity testing. Mutat Res. 1978 Aug;54(1):33–38. doi: 10.1016/0165-1161(78)90132-2. [DOI] [PubMed] [Google Scholar]
  14. Shukla P. T., Auerbach C. Genetical tests for the frequency of small deletions among ems-induced point mutations in Drosophila. Mutat Res. 1981 Aug;83(1):81–89. doi: 10.1016/0027-5107(81)90073-7. [DOI] [PubMed] [Google Scholar]
  15. Singer B., Kuśmierek J. T. Chemical mutagenesis. Annu Rev Biochem. 1982;51:655–693. doi: 10.1146/annurev.bi.51.070182.003255. [DOI] [PubMed] [Google Scholar]
  16. Smith P. D., Baumen C. F., Dusenbery R. L. Mutagen sensitivity of Drosophila melanogaster. VI. Evidence from the excision-defective mei-9AT1 mutant for the timing of DNA-repair activity during spermatogenesis. Mutat Res. 1983 Mar;108(1-3):175–184. doi: 10.1016/0027-5107(83)90119-7. [DOI] [PubMed] [Google Scholar]

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