Identification of a second locus in Drosophila melanogaster required for excision repair.

摘要: The mur(2)201 locus in Drosophila is defined by two mutant alleles that render homozygous larvae hypersensitive to mutagens. Both confer strong vivo somatic sensitivity treatment methyl methanesulfonate, nitrogen mustard and ultraviolet radiation but only weak hypersensitivity X-radiation. Unlike the excision-defective mei-9 mutants identified previous studies, mus(2)102 do not affect female fertility appear influence recombination proficiency or chromosome segregation meiocytes. Three independent biochemical assays reveal cell cultures derived from embryos for mus(2)/sup D//sup 1/ allele are devoid of detectable excision repair. 1. Such cells quantitatively retain pyrimidine dimers their DNA 24 hr following UV exposure. 2. No measurable unscheduled synthesis induced treatment. 3. Single-strand breaks, which associated with normal repair after either N-acetoxy-N-acetyl-2-aminofluorene, much reduced these cultures. Mutant possess a capacity postreplication single-strand breaks X-rays.