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Journal Article

Insulin signalling regulates remating in female Drosophila


Wigby,  S.
Max Planck Society;

Slack,  C.
Max Planck Society;

Grönke,  S.
Max Planck Society;

Martinez,  P.
Max Planck Society;

Calboli,  F. C.
Max Planck Society;

Chapman,  T.
Max Planck Society;

Partridge,  L.
Max Planck Society;

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Wigby, S., Slack, C., Grönke, S., Martinez, P., Calboli, F. C., Chapman, T., et al. (2011). Insulin signalling regulates remating in female Drosophila. Proc Biol Sci, 278(1704), 424-31. doi:rspb.2010.1390 [pii] 10.1098/rspb.2010.1390.

Cite as: http://hdl.handle.net/11858/00-001M-0000-0028-59F9-4
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.