Female sexual receptivity is defective in juvenile hormone-deficient mutants of the apterous gene of Drosophila melanogaster.
During reproductive maturation of female insects, the acquisition of sexual receptivity is coordinated with ovarian development. Juvenile hormone regulates vitellogenesis in the ovaries, but the action of this hormone in the development of sexual behavior is less well-understood. A strain of Drosophila melanogaster carrying a mutation in the apterous gene ( ap4) was known to exhibit arrested vitellogenesis (rescuable by applying exogenous juvenile hormone), sterility of both sexes, and a deficiency of juvenile hormone. In this study, we examined the effects of mutations of ap on female receptivity and its relationship to juvenile hormone. We observed abnormally low female receptivity in homozygous ap strains, and heteroallelic combinations of ap mutations exhibited low receptivity. For female receptivity, ap showed no dominance (i.e., ap/ ap+ was intermediate between ap/ ap and ap+/ap+). Low receptivity mapped genetically to the ap locus. The reduction in female receptivity in these mutants is positively correlated with levels of juvenile hormone synthesized by their corpora allata.[1]References
- Female sexual receptivity is defective in juvenile hormone-deficient mutants of the apterous gene of Drosophila melanogaster. Ringo, J., Werczberger, R., Altaratz, M., Segal, D. Behav. Genet. (1991) [Pubmed]
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