Genetic dissection of sexual orientation: behavioral, cellular, and molecular approaches in Drosophila melanogaster.

摘要: Insertional mutagenesis using P-element vectors yielded several independent mutations that cause male homosexuality in Drosophila melanogaster. Subsequent analyses revealed all of these insertions were located at the same chromosomal division, 91B, where one inversion breakpoints responsible for bisexual phenotype fruitless (fru) mutant has been mapped. In addition to altered sexual orientation, fru mutants displayed a range defects formation male-specific muscle, muscle Lawrence. Since this was dependent solely on sex innervating nerve and not itself, primary site action gene should be neural cells. satori, P-insertion alleles which we isolated, carried lacZ E. coli as reporter, beta-galactosidase expression found subset brain cells including those antennal lobe satori mutant. Targeted determination gene, transformer (tra), used produce chromosomally flies with certain feminized glomeruli lobe. Such sexually mosaic courted only females but also males when DM2, DA3 DA4 feminized, indicating substructures may involved orientation flies. Molecular cloning genomic complementary DNAs indicated transcription locus yields different transcripts, encodes putative regulator BTB domain two zinc finger motifs. 5' non-coding region, three Transformer binding sites identified. It appears plausible therefore is elements cascade controls fates neuronal Improper lead malformation muscle. Some implications results our study other organisms will discussed based research.