The absence of somatic effects of P-M hybrid dysgenesis in Drosophila melanogaster.
The wings and abdomens of dysgenic and nondysgenic control flies were scored for the presence of clones of cells mutant for first and third chromosome markers. These exceptional clones can arise from mitotic recombination, de novo mutation or deletion, and P-M hybrid dysgenesis has been shown to increase the frequency of parallel processes occurring in germ-line cells. Particular attention was given to careful genetic and molecular characterization of all stocks and to providing adequate and appropriate controls so that even very small increases in somatic clone frequency due to P-M hybrid dysgenesis would be detected. No difference was found in the frequency, size distribution or anatomical distribution of mutant somatic clones correlated to hybrid dysgenesis, confirming previous indications. The potential adaptive significance of a germ-line restriction of P-M hybrid dysgenesis is discussed.
D000483:Alleles; D000818:Animals; D002874:Chromosome Mapping; D004331:Drosophila melanogaster / Q000235:genetics*; D005260:Female; D005838:Genotype; D006059:Gonadal Dysgenesis; D006824:Hybridization, Genetic; D008297:Male; D009154:Mutation; D010641:Phenotype; D011995:Recombination, Genetic; D014960:X Chromosome