Toward a molecular genetic analysis of spermatogenesis in Drosophila melanogaster: characterization of male-sterile mutants generated by single P element mutagenesis.

TLDR

This collection of male‑sterile mutants provides the basis for a molecular genetic analysis of spermatogenesis. The authors used reversion analyses and complementation tests with chromosomal deficiencies, and examined mutant phenotypes by light microscopy. The study identified 83 recessive autosomal male‑sterile mutations, grouped into 63 complementation groups (58 essential for spermatogenesis), with 12 loci affecting germline proliferation, spermatocyte growth, or meiosis, and 46 loci disrupting spermatid differentiation and maturation, all mapped to specific polytene map subdivisions and confirmed to be caused by P‑element insertions.

Abstract

Abstract We describe 83 recessive autosomal male-sterile mutations, generated by single P element mutagenesis in Drosophila melanogaster. Each mutation has been localized to a lettered subdivision of the polytene map. Reversion analyses, as well as complementation tests using available chromosomal deficiencies, indicate that the insertions are responsible for the mutant phenotypes. These mutations represent 63 complementation groups, 58 of which are required for spermatogenesis. Phenotypes of the spermatogenesis mutants were analyzed by light microscopy. Mutations in 12 loci affect germline proliferation, spermatocyte growth, or meiosis. Mutations in 46 other loci disrupt differentiation and maturation of spermatids into motile sperm. This collection of male-sterile mutants provides the basis for a molecular genetic analysis of spermatogenesis.