title: Insulin signalling regulates remating in female Drosophila.
abstract: Mating rate is a major determinant of female lifespan and fitness, and is predicted to optimize at an intermediate level, beyond which superfluous matings are costly. In female Drosophila melanogaster, nutrition is a key regulator of mating rate but the underlying mechanism is unknown. The evolutionarily conserved insulin/insulin-like growth factor-like signalling (IIS) pathway is responsive to nutrition, and regulates development, metabolism, stress resistance, fecundity and lifespan. Here we show that inhibition of IIS, by ablation of Drosophila insulin-like peptide (DILP)-producing median neurosecretory cells, knockout of dilp2, dilp3 or dilp5 genes, expression of a dominant-negative DILP-receptor (InR) transgene or knockout of Lnk, results in reduced female remating rates. IIS-mediated regulation of female remating can occur independent of virgin receptivity, developmental defects, reduced body size or fecundity, and the receipt of the female receptivity-inhibiting male sex peptide. Our results provide a likely mechanism by which females match remating rates to the perceived nutritional environment. The findings suggest that longevity-mediating genes could often have pleiotropic effects on remating rate. However, overexpression of the IIS-regulated transcription factor dFOXO in the fat body-which extends lifespan-does not affect remating rate. Thus, long life and reduced remating are not obligatorily coupled.
authors.affiliation: Institute of Healthy Ageing and , Department of Genetics, Evolution and Environment, University College London, UK. stuart.wigby@zoo.ox.ac.uk
authors.forename: Stuart
authors.initials: S
authors.lastname: Wigby
authors.forename: Cathy
authors.initials: C
authors.lastname: Slack
authors.forename: Sebastian
authors.initials: S
authors.lastname: Grönke
authors.forename: Pedro
authors.initials: P
authors.lastname: Martinez
authors.forename: Federico C F
authors.initials: FC
authors.lastname: Calboli
authors.forename: Tracey
authors.initials: T
authors.lastname: Chapman
authors.forename: Linda
authors.initials: L
authors.lastname: Partridge
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D029721:Drosophila Proteins / Q000502:physiology*; D004331:Drosophila melanogaster / Q000502:physiology*; D005260:Female; D005298:Fertility / Q000502:physiology*; D007328:Insulin / Q000502:physiology*; D016014:Linear Models; D008297:Male; D015735:Mifepristone / Q000494:pharmacology; D009752:Nutritional Status / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D014161:Transduction, Genetic
chemical_list: D029721:Drosophila Proteins; D007328:Insulin; D015735:Mifepristone