Feeding, fecundity and lifespan in female Drosophila melanogaster

Andrew I Barnes,James M Boone,Stuart Wigby,Linda Partridge,Tracey Chapman

doi:10.1098/rspb.2008.0139

Andrew I Barnes, James M Boone + Show 3 more

Open Access

https://doi.org/10.1098/rspb.2008.0139

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Abstract

Male seminal fluid proteins induce a profound remodelling of behavioural, physiological and gene signalling pathways in females of many taxa, and typically cause elevated egg production and decreased sexual receptivity. In Drosophila melanogaster, these effects can be mediated by an ejaculate ‘sex peptide’ (SP), which, in addition, contributes significantly to the cost of mating in females. Recent research has revealed that SP can stimulate female post-copulatory feeding, raising the possibility that the widespread female cost of mating could be due to over-feeding. In this study, we used D. melanogaster as a model to test this hypothesis. We first show that elevated post-mating feeding is dependent upon egg production and does not occur in sterile ovoD1 mutant females. This conclusion was also supported by the increase in feeding of virgin females whose egg production was experimentally elevated. We then demonstrated that sterile ovoD1 and fertile females experienced identical survival costs of mating, related to their frequency of mating and not to female feeding rate or to egg production. We conclude that female mating costs are not the result of over-feeding, but may be due to other, potentially more direct, effects of ejaculate molecules.

Highlights

We examined the feeding rates of virgin females whose sex peptide’ (SP)-like egg production and receptivity post-mating responses (PMRs) were activated by silencing fruitless neurons (Kvitsiani & Dickson 2006; Yapici et al 2008)
Our results show that egg production is required for the effect of SP on female feeding to be observed. (b) Effect of silencing fru neurons on female feeding rate To test whether the silencing of fru neurons, which activates SP-like receptivity and egg-laying PMRs (Kvitsiani & Dickson 2006), is sufficient to increase feeding rate, we analysed the number of feeds per vial in a nested ANOVA with ‘experimental treatment’ and ‘genotype’ nested within experimental treatment as factors
The lack of association between egg production and survival costs of mating is consistent with previous studies (Chapman et al 1995; Chapman & Partridge 1996) and that lifespan and fecundity do not show an obligate trade-off (e.g. Hwangbo et al 2004; Mair et al 2004; Barnes et al 2006)

Summary

Introduction

The male seminal fluid proteins of invertebrates can profoundly remodel female behaviour, physiology and gene expression, and females of a wide range of taxa typically show increased egg production and decreased sexual receptivity following mating (e.g. Wolfner 1997, 2002; Chapman et al 1998; Chapman 2001; Gillot 2003; Kubli 2003; Lawniczak & Begun 2004; McGraw et al 2004). We tested the hypothesis that the magnitude of female mating costs in fertile and sterile ovoD1 females is associated with female feeding rate and/or egg production.

Results

Conclusion