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Feeding, fecundity and lifespan in female Drosophila melanogaster.

Barnes AI, Wigby S, Boone JM, Partridge L, Chapman T - Proc. Biol. Sci. (2008)

Bottom Line: 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.This conclusion was also supported by the increase in feeding of virgin females whose egg production was experimentally elevated.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.

View Article: PubMed Central - PubMed

Affiliation: Research Department of Genetics, Evolution and Environment, University College London, Darwin Building, Gower Street, London WC1E 6BT, UK.

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.

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Related in: MedlinePlus

Feeding rates in virgin females with silenced fru neurons. Feeding rates (mean per vial per observation±s.e.) for experimental (UAS-shits/+; fruGAL4/+) and control (UAS-shits/+ or fruGAL4/+) virgin females at (a) restrictive (29°C) and (b) permissive (18°C) temperatures.
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fig2: Feeding rates in virgin females with silenced fru neurons. Feeding rates (mean per vial per observation±s.e.) for experimental (UAS-shits/+; fruGAL4/+) and control (UAS-shits/+ or fruGAL4/+) virgin females at (a) restrictive (29°C) and (b) permissive (18°C) temperatures.

Mentions: 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’ (i.e. fru silenced versus control flies) and ‘genotype’ nested within experimental treatment as factors. The data were analysed separately for 18 and 29°C, as it was not possible to conduct simultaneous behavioural observations at both temperatures. The data from the 18°C experiment were Box–Cox transformed to improve normality. Feeding rates were much higher at 29°C than at 18°C (figure 2). At the restrictive temperature (29°C), the females with silenced fru neurons fed at a significantly higher frequency than controls (F1,45=5.78, p=0.02; figure 2a) and there was no significant effect of control genotype on feeding rate (F1,45=0.28, p=0.59). These results were consistent with the finding that other SP-like oviposition and receptivity PMRs are also activated in females in which fru neurons are silenced (Kvitsiani & Dickson 2006). At the permissive temperature there was no difference between the experimental and control females in feeding rate (F1,45=0.00, p=0.99; figure 2b) but there were differences between genotypes (F1,45=10.42, p=0.002). Although there was a significant difference in feeding rate between the two control female treatments (fruGAL4/+ control females fed significantly more than UAS-shits/+ control females; q45,3=4.56, p=0.007), there were no significant differences between the experimental (UAS-shits/+; fruGAL4/+) versus either of the control groups of females (q45,3<0.283, p>0.25 for both comparisons). It is unclear why the two control genotypes differed from one another in feeding rate at the permissive temperature; however, the 18°C results show that the increase in feeding rate of the fru silenced females seen at the restrictive temperature is not due to an effect of genetic background or position effects of transgenes used. Our results demonstrate that the experimental elevation of egg laying in virgin females by the silencing of fru neurons is associated with elevated feeding. This supports the finding from the first experiment that egg production is necessary for increased feeding following mating.


Feeding, fecundity and lifespan in female Drosophila melanogaster.

Barnes AI, Wigby S, Boone JM, Partridge L, Chapman T - Proc. Biol. Sci. (2008)

Feeding rates in virgin females with silenced fru neurons. Feeding rates (mean per vial per observation±s.e.) for experimental (UAS-shits/+; fruGAL4/+) and control (UAS-shits/+ or fruGAL4/+) virgin females at (a) restrictive (29°C) and (b) permissive (18°C) temperatures.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2452982&req=5

fig2: Feeding rates in virgin females with silenced fru neurons. Feeding rates (mean per vial per observation±s.e.) for experimental (UAS-shits/+; fruGAL4/+) and control (UAS-shits/+ or fruGAL4/+) virgin females at (a) restrictive (29°C) and (b) permissive (18°C) temperatures.
Mentions: 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’ (i.e. fru silenced versus control flies) and ‘genotype’ nested within experimental treatment as factors. The data were analysed separately for 18 and 29°C, as it was not possible to conduct simultaneous behavioural observations at both temperatures. The data from the 18°C experiment were Box–Cox transformed to improve normality. Feeding rates were much higher at 29°C than at 18°C (figure 2). At the restrictive temperature (29°C), the females with silenced fru neurons fed at a significantly higher frequency than controls (F1,45=5.78, p=0.02; figure 2a) and there was no significant effect of control genotype on feeding rate (F1,45=0.28, p=0.59). These results were consistent with the finding that other SP-like oviposition and receptivity PMRs are also activated in females in which fru neurons are silenced (Kvitsiani & Dickson 2006). At the permissive temperature there was no difference between the experimental and control females in feeding rate (F1,45=0.00, p=0.99; figure 2b) but there were differences between genotypes (F1,45=10.42, p=0.002). Although there was a significant difference in feeding rate between the two control female treatments (fruGAL4/+ control females fed significantly more than UAS-shits/+ control females; q45,3=4.56, p=0.007), there were no significant differences between the experimental (UAS-shits/+; fruGAL4/+) versus either of the control groups of females (q45,3<0.283, p>0.25 for both comparisons). It is unclear why the two control genotypes differed from one another in feeding rate at the permissive temperature; however, the 18°C results show that the increase in feeding rate of the fru silenced females seen at the restrictive temperature is not due to an effect of genetic background or position effects of transgenes used. Our results demonstrate that the experimental elevation of egg laying in virgin females by the silencing of fru neurons is associated with elevated feeding. This supports the finding from the first experiment that egg production is necessary for increased feeding following mating.

Bottom Line: 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.This conclusion was also supported by the increase in feeding of virgin females whose egg production was experimentally elevated.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.

View Article: PubMed Central - PubMed

Affiliation: Research Department of Genetics, Evolution and Environment, University College London, Darwin Building, Gower Street, London WC1E 6BT, UK.

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.

Show MeSH
Related in: MedlinePlus