title: Knockout mutations of insulin-like peptide genes enhance sexual receptivity in Drosophila virgin females.
abstract: In the fruitfly Drosophila melanogaster, females take the initiative to mate successfully because they decide whether to mate or not. However, little is known about the molecular and neuronal mechanisms regulating sexual receptivity in virgin females. Genetic tools available in Drosophila are useful for identifying molecules and neural circuits involved in the regulation of sexual receptivity. We previously demonstrated that insulin-producing cells (IPCs) in the female brain are critical to the regulation of female sexual receptivity. Ablation and inactivation of IPCs enhance female sexual receptivity, suggesting that neurosecretion from IPCs inhibits female sexual receptivity. IPCs produce and release insulin-like peptides (Ilps) that modulate various biological processes such as metabolism, growth, lifespan and behaviors. Here, we report a novel role of the Ilps in sexual behavior in Drosophila virgin females. Compared with wild-type females, females with knockout mutations of Ilps showed a high mating success rate toward wild-type males, whereas wild-type males courted wild-type and Ilp-knockout females to the same extent. Wild-type receptive females retard their movement during male courtship and this reduced female mobility allows males to copulate. Thus, it was anticipated that knockout mutations of Ilps would reduce general locomotion. However, the locomotor activity in Ilp-knockout females was significantly higher than that in wild-type females. Thus, our findings indicate that the high mating success rate in Ilp-knockout females is caused by their enhanced sexual receptivity, but not by improvement of their sex appeal or by general sluggishness.
authors.affiliation: Department of Biological Sciences, Tokyo Metropolitan University.
authors.forename: Kazuki
authors.initials: K
authors.lastname: Watanabe
authors.forename: Takaomi
authors.initials: T
authors.lastname: Sakai
mesh_terms: D000818:Animals; D004330:Drosophila / Q000235:genetics / Q000502:physiology*; D029721:Drosophila Proteins / Q000235:genetics*; D005260:Female; D055786:Gene Knockout Techniques; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D061385:Insulins / Q000235:genetics*; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics*; D008297:Male; D009043:Motor Activity; D009154:Mutation; D009479:Neuropeptides; D012726:Sexual Behavior, Animal / Q000502:physiology*
chemical_list: D029721:Drosophila Proteins; C544178:ILP2 protein, Drosophila; C542424:ILP3 protein, Drosophila; C570846:Ilp5 protein, Drosophila; D007328:Insulin; D061385:Insulins; D036341:Intercellular Signaling Peptides and Proteins; D009479:Neuropeptides