Mutagenesis in spermatozoa of Drosophila melanogaster by cross-linking agents depends on the mus(1)101+ gene product in the oocyte.

ABSTRACT

In Drosophila melanogaster the sex-linked gene must(1)101+ is essential for mutagenesis induced by a cross-linking agent mature sperm mutagenized by nitrogen mustard (HN2) yield high frequencies of induced sex-linked recessive lethals if tested with wild-type oocytes but practically no recessive lethals if tested with homozygous mus(1)101D1 oocytes. In the absence of mus(1)101+ at least some cross-links act as lethal lesions, whereas in the presence of mus(1)101+ some act as premutational lesions. The lack of delayed mutations in mutant oocytes indicates that the lesions are efficiently eliminated and do not lead to mutagenesis in later post-fertilization nuclear divisions. The mutation mus(1)101D1 is not a null allele because, in tests with heterozygotes, it reduces mutagenesis to a lesser extent than a deletion including the mus(1)101 locus. It is a leaky allele with such a reduced activity that, in homozygous condition, mutagenesis is practically absent. In deletion heterozygotes the mus(1)101+ gene is not dosage-compensated.