ABSTRACT
Juvenile hormone (JH) is a major regulator of insect development and reproduction and its titer is determined largely by central nervous system regulation of JH synthesis by the corpora allata. To establish the basis for a molecular genetic dissection of the neuroendocrine system responsible for modulating JH titer, a radiochemical assay was utilized to examine JH synthesis in vitro by the isolated corpus allatum as well as the regulation of this synthesis by brain extracts of wild-type and apterous mutant Drosophila melanogaster females during reproductive maturation. JH production by glands of wild-type females increases in parallel with the progress of ovarian maturation, the major product of the adult corpus allatum being juvenile hormone 3 bis-epoxide (JHB3). Gland activity appears to be regulated by both the availability of JH precursors and the level of terminal oxidase(s) in the JH biosynthetic pathway. The brain contains an allatostatic factor, that is transmitted to the glands via nervous connections. Allatostatin production in the brain appears to be positively regulated by JHB3. Adult corpora allata from the mutants ap4 and ap56f synthesize very low levels of JH; additionally, brains of ap56f homozygotes lack allatostatic activity.
Subject(s)
Corpora Allata/metabolism , Drosophila melanogaster/metabolism , Gene Expression Regulation , Juvenile Hormones/genetics , Neurosecretory Systems/metabolism , Animals , Biological Assay , Brain/metabolism , Drosophila melanogaster/genetics , Fatty Acids, Monounsaturated/metabolism , Fatty Acids, Unsaturated/pharmacology , Female , Infertility, Female/genetics , Mutation , Vitellogenesis/physiologyABSTRACT
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.
