A developmental analysis of behavioural mutations in Drosophila Melanogaster

Two types of sex-linked recessive mutations in Drosophila melanogaster have been investigated in the present study. The first type includes 5 different mutations which exhibit a stress-sensitive (ses) phenotype. Flies of all five mutant stocks become paralyzed when their containers are lightly tapped; wild type flies are unaffected by the same treatment. The five mutations form three complementation groups (cistrons). Flies mosaic for mutant and non-mutant tissue were studied to determine the foci of their action in embryos by fate mapping. These studies suggest that the mutation ses D² has 6 foci in the presumptive nervous system of the blastoderm. Each focus corresponds to a site in the thoracic ganglion which controls the movement of one leg. The focus for ses E¹ mutation is rather diffuse and occupies a larger area in the thoracic nervous system of the blastoderm fate map. Focus mapping studies with the ses B¹ mutation were inconclusive because of the highly variable expressions of the adult behavioural phenotype in mosaic individuals. Developmental studies, involving temperature shifts from 22°C to 29°C (permissive to restrictive temperatures) revealed that the ses E¹ mutation has 2 temperature-sensitive periods (TSPs) for lethality during its development, one in the late 2nd larval instar stage and the other in the late pupal stage. In addition to developmental TSPs of ses B² at the embryonic, 1st larval instar and pre-pupal stage, temperature-shift studies also revealed a ts maternal- effect lethal for ses B². The second type of mutation studied has a temperature-sensitive (ts) phenotype of adult death induced by shifting up to the restrictive temperature. The add Atsl flies have normal behaviour and longevity at 22°C but die within 24 hours after shift-up to 29°C. In contrast, the ses E¹ flies are less active and require 168 hours at 29°C to induce death. Both mutations studied have a 3rd larval instar-pupal TSP with add Atsl and ses E¹ also having an additional TSP at the embryonic and 1st larval instar-2nd larval instar stage respectively. Fate mapping studies suggest that the adult lethal phenotype of add Atsl is caused by a lesoon in tissues derived from the mesodermal cells of the blastoderm, and for ses E¹ the lesion is in the neural cells.Science, Faculty ofZoology, Department ofGraduat