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Excision deficiency in the mutagen-sensitive mus (2) 201/sup D1/ mutant of Drosophila

Journal Article · · Genetics; (United States)
OSTI ID:5261933
Selection for mutants that are sensitive to chemical mutagens was conducted with the aid of stocks bearing translocations between the two major autosomes of Drosophila melanogaster. A mutant linked to the second chromosome has been designated mus (2) 201 /sup D1/. Larvae homozygous for this mutation are hypersensitive to methyl methanesulfonate, nitrogen mustard and 2-acetylaminofluorene. Analyses of DNA repair in primary cell cultures derived from homozygous mus (2) 201/sup D1/ embryos have revealed a strong deficiency for the excision of pyrimidine dimers. This defect has been detected by monitoring the resynthesis step of excision repair with unscheduled DNA synthesis. Complete retention of pyrimidine dimers in the DNA of irradiated mutant cells has also been demonstrated during post-irradiation incubation. During this same period cells from control stocks remove about 60% of the induced lesions from their DNA. Pyrimidine dimers were detected in this assay as sites sensitive to a uv-specific endonuclease preparation. Alkaline elution analysis has detected the induction of incision-related DNA breaks in control cells but not in mus (2) 201/sup D1/ cells following uv irradiation. In wild type cells the frequency of uv-induced breaks is elevated by inhibitors of DNA synthesis. This accumulation of breaks is not observed in mus (2) 201/sup D1/ cells. We, therefore, conclude that this mutant is deficient in the initial incision step of excision repair. DNA synthesis, postreplication repair and the repair of single strand breaks induced by x-rays are normal in this mutant.
Research Organization:
Univ. of California, Davis
DOE Contract Number:
AT(04-3)-34
OSTI ID:
5261933
Journal Information:
Genetics; (United States), Journal Name: Genetics; (United States) Vol. 91:4; ISSN GENTA
Country of Publication:
United States
Language:
English

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