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Investigating the mechanism underlying the cost of mating in Drosophila: the contribution of the sex peptide juvenile hormone and immunity
Reference
BB/C516452/1
Principal Investigator / Supervisor
Professor Linda Partridge
Co-Investigators /
Co-Supervisors
Dr Stuart Wigby
Institution
University College London
Department
Genetics Evolution and Environment
Funding type
Research
Value (£)
194,856
Status
Completed
Type
Research Grant
Start date
24/03/2005
End date
23/06/2008
Duration
39 months
Abstract
An ideal organism would have the life history of a Darwinian Demon and reproduce at its maximum rate throughout its entire, long lifespan. Many potential constraints that prevent organisms from achieving this ideal life history have been identified, but in no case has the genetic basis of the constraints yet been identified. One of the most important determinants of female life history is the cost of reproduction. The finding within and across many taxa is that organisms that reproduce at an elevated rate tend to live less long. Our previous work has shown that the cost of mating is the major constituent of reproductive costs in female D. melanogaster fruit flies. This cost of mating is caused by the receipt of seminal fluid molecules from males, and we have recently identified the specific agent responsible: the male ejaculate sex peptide. This discovery allows us, for the first time, to probe the exact mechanisms underlying the reproductive costs that determine life history trade-offs. The mechanisms underlying the way in which the sex peptide harms females are also of interest in the study of sexual conflicts, as the SP is the first substance identified to simultaneously benefit males (by increasing paternity through increasing the interval between matings) whilst harming females (by causing mating costs). It is unclear exactly how mating is costly. The answer may lie in resource allocation: ie. each organism has a fixed amount of resources that can be allocated to eg. egg production or longevity, but not both. Alternatively, reproductive and lifespan-promoting processes might communicate adaptively with each other via hormones. The sex peptides could directly harm females. Alternatively, it could be that the higher level of circulating JH produced in response to the sex peptides leads to decreased lifespan in mated females, an association which has been noted in other insects. Another possibility is that elevated levels of JH are associated with decreased performance of other traits, such as the immune system. JH is reported to suppress the immune response in other insects. The immune system of mated male fruitflies is also less effective than in male virgins, and genes that encode insect antimicrobials show significant changes in expression after mating. Our hypotheses are that the harmful effects of the make sex peptide on females result from the consequences of elevated JH and or because the immune system is suppressed. We will investigate which of these possibilities are correct in the research we propose here. We will manipulate the levels of SP transferred to females by using males that lack SP or that transfer higher than normal levels of it (by RNAi and over-expression). We will alter JH levels by increasing or decreasing the level of Juvenile Hormone Esterase (JHE), the major enzyme responsible for catabolising circulating JH (again using RNAi and over-expression). This will allow us to test the immune response of females with reduced or elevated levels of JH that receive reduced or elevated levels of SP their mates. Immune responses will be measured by recording bacterial clearance rates following experimental injections of known numbers of bacteria. These tests will allow us to determine whether the female immune system is reduced after mating, and if it is, whether the reduction in immune function is related to the level of JH or to the level of SP received from males, or both. We will then test whether JH, vitellogenesis or immunity can, in the absence of SP, cause mating costs in females. The tests we propose are important: they will reveal exactly how females are harmed following mating. This will reveal the nature of reproductive constraints, which should have a profound effect on the way the wider community thinks about life histories. For example, our results should reveal whether it is correct to think of reproductive costs in terms of resource allocation or molecular signalling. If it is the latter, it would make many traditional models of life history evolution redundant. The results will also shed light on how it is that the SP, can benefit males whilst simultaneously harming females.
Summary
unavailable
Committee
Closed Committee - Animal Sciences (AS)
Research Topics
Immunology
Research Priority
X – Research Priority information not available
Research Initiative
X - not in an Initiative
Funding Scheme
X – not Funded via a specific Funding Scheme
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