1,721,051 research outputs found

    Is there local adaptation in Drosophila-parasitoid interactions?

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    Local adaptation has received little attention in host-parasitoid associations. Here we combine data on the outcome of parasitism in 20 sympatric populations of Drosophila melanogaster and its parasitoid Asobara tabida. We present data on resistance and virulence when each host is tested against a single allopatric strain of parasitoid, and when each parasitoid is tested against a single allopatric strain of host. We argue that the extent to which these allopatric interactions can be used to predict sympatric interactions sets an upper bound to the importance of local adaptation. In a statistical model, we found that 56% of the variance in the outcome of sympatric interactions could be explained by parasitoid virulence and host resistance measured using the allopatric reference strains, with the former being the much more important of the two. The geographical distance between the provenances of the sympatric and reference parasitoid (but not host) populationswas also statistically significant and increased the variance explained to69%; but against expectation, parasitoid success was negatively correlatedwith distance. We also explore the factors determining the frequency with which neither host nor parasitoid survive. We conclude that, although the critical tests have yet to be performed, the available evidence points towards local adaptation not being of major importance in this system

    Potential life history costs of parasitoid avoidance in Drosophila melanogaster

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    Pupal parasitoids are a common natural enemy of Drosophila. As Drosophila pupae do not have an immunological defence against pupal parasitoids, they have to avoid being attacked. As a first step to identifying the costs of avoidance of parasitism by pupal parasitoids, we explored three traits that potentially influence the probability of D. melanogaster pupae to survive attack by Pachycrepoideus vindemiae. We found that larvae pupating on the food source had a higher probability of avoiding parasitism, but that the distance that larvae pupate away from the food had no effect on survival probability when exposed to pupal parasitoids. We also found no indication that the thickness of the puparial wall influences risk of parasitism. Pupal size, however, was correlated with the probability of surviving parasitoid attack, with smaller pupae having a higher survival probability. If pupal size is indeed the key trait influencing risk of parasitism of D. melanogaster pupae by P. vindemiae, the potential life-history costs of parasitoid avoidance are smaller adult size, leading to lower general fitnes

    Selection for resistance to a fungal pathogen in Drosophila melanogaster

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    An artificial selection experiment designed to explore the evolution of resistance to a fungal pathogen, Beauveria bassiana, in Drosophila melanogaster is reported here. The experiment was designed to test whether there is sufficient additive genetic variation in this trait for increased resistance to evolve, and, if so, whether there are correlated responses that might represent a cost to defence. After 15 generations of selection, flies from selected lines did not have higher overall fitness after infection compared with control lines. The response to selection for resistance against this pathogen is thus much weaker than against other species, in particular, parasitoids. There was, however, evidence for increased late-life fecundity in selected lines, which may indicate evolved tolerance of fungal infection. This increase was accompanied by reduced early-life fitness, which may reflect the well-known trade-off between early and late reproduction. In the absence of fungal infection, selected flies had lower fitness than control flies, and the possibility that this is also a trade-off with increased tolerance is explored

    Evolutionary interactions between Drosophila melanogaster and its parasitoid Asobara tabida

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    Drosophila melanogaster is attacked by parasitoids that develop internally in the larva. They can defend themselves by a cellular immune response (host resistance), although this can be disabled by parasitoid countermeasures (parasitoid virulence). D. melanogaster and its parasitoids are an excellent system in which to study coevolution experimentally. We designed an experiment to compare changes in resistance and virulence in replicate populations of flies and parasitoids maintained together for approximately 10 fly (five parasitoid) generations. The experiment had three treatments each with three replicates: (A) no parasitoids (B) outbred parasitoids (C) partially inbred parasitoids. Host resistance increased in treatments B and C but there was no difference between these treatments. Parasitoid virulence appeared not to change during the experiment. Host larvae in treatments B and C fed at lower rates than those in A, evidence of a trade-off between resistance and larval competitive ability. We found no evidence for local adaptation, as hosts from the different replicates of treatment C performed no differently against parasitoids from the same and other replicates. Also, we found no evidence for the evolution of behavioural traits in the host that could lead to lower probabilities of being attacked. Comparing the evolution of host resistance in these seminatural settings with that in artificial selection experiments provides insight into how the conflicting selection pressures on host resistance interact

    Experimental evolution shows Drosophila melanogaster resistance to a microsporidian pathogen has fitness costs

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    Most organisms experience strong selection to develop mechanisms to resist or tolerate their pathogens or parasites. Limits to adaptation are set by correlated responses to selection, for example reduced abilities to detect other parasites or trade-offs with other fitness components. For a few model systems it is now becoming possible to compare the evolutionary response to a broad range of natural enemies. In Drosophila, the evolutionary responses to ectoparasitic mites, parasitoids, and fungal and bacterial pathogens have previously been studied. Here replicate lines of D. melanogaster were exposed to the microsporidian parasite Tubulinosema kingi over a period of 61 weeks, with overlapping generations. Compared to controls, exposed lines had higher early-life fecundity and increased longevity when infected suggesting successful selection for resistance or tolerance. In the absence of the pathogen, exposed lines had lower fecundity when reared under harsh environmental conditions, and were poorer larval competitors than controls. They also had relatively higher densities of haemocytes, a component of the cellular immune system. Defense against this pathogen resembles more that against macroparasites than microsparasites, and this is interpreted in the light of what is known about the mechanisms of resistance to microsporidians

    Basis of the trade off between parasitoid resistance and larval competitive ability in Drosophila melanogaster

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    Drosophila melanogaster can be artificially selected for increased resistance against parasitoid wasps that attack the larvae. Lines selected for greater resistance are poorer larval competitors under conditions of resource scarcity. Here we investigated the mechanistic basis of this apparent trade-off. We found that resistant lines have approximately twice the density of haemocytes (blood cells) than that of controls. Haemocytes are involved in encapsulation, the chief cellular immune defence against parasitoids. We have previously shown that resistant lines feed more slowly than controls and hypothesize that limiting resources are being switched from trophic to defensive functions

    Costs of resistance in insect-parasite and insect-parasitoid interactions

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    Most, if not all, organisms face attack by natural enemies and will be selected to evolve some form of defence. Resistance may have costs as well as its obvious benefits. These costs may be associated with actual defence or with the maintenance of the defensive machinery irrespective of whether a challenge occurs. In this paper, the evidence for costs of resistance in insect-parasite and insect-parasitoid systems is reviewed, with emphasis on two host-parasitoid systems, based on Drosophila melanogaster and pea aphids as hosts. Data from true insect-parasite systems mainly concern the costs of actual defence; evidence for the costs of standing defences is mostly circumstantial. In pea aphids, the costs of standing defences have so far proved elusive. Resistance amongst clones is not correlated with life-time fecundity, whether measured on good or poor quality plants. Successful defence by a D. melanogaster larva results in a reduction in adult size and fecundity and an increased susceptibility to pupal parasitoids. Costs of standing defences are a reduction in larval competitive ability though these costs only become important when food is limited. It is concluded that costs of resistance can play a pivotal role in the evolutionary and population dynamic interactions between hosts and their parasites

    Costs of counterdefenses to host resistance in a parasitoid of Drosophila

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    AbstractThe ability of a parasitoid to evolve enhanced counterdefenses against host resistance and its possible costs were studied in a Drosophila-parasitoid system. We reared Asobara tabida (Braconidae, Hymenoptera) exclusively on D. melanogaster to impose artificial selection for improved counterdefenses against cellular encapsulation, the main host defense against parasitism. Controls were reared on D. subobscura, the main host of the population of wasps from which the laboratory culture was derived and a species that never encapsulates parasitoids. We observed improved survival and avoidance of encapsulation in all five selection lines compared to their paired control lines, although there was unexpected variation among pairs. Improved survival was associated with parasitoid eggs becoming embedded in host tissue, where they were protected from circulating haemocytes. There were no differences among lines in average adult size, fat content, egg load, or performance on D. subobscura. However, the duration of the egg stage in selection lines was longer than that of control lines, probably because of reduced nutrient and/or oxygen supply when eggs are embedded in host tissue. We suggest that this delay in hatching reduces the probability of parasitoid survival if another parasitoid egg is laid in the same host (superparasitism or multiparasitism) and hence is a cost of enhanced counterdefenses against host resistance.<br/
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