1,721,114 research outputs found

    Infection of Drosophila melanogaster by Tubulinosema kingi: stage-specific susceptibility and within-host proliferation

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    Despite its importance as a model organism very little is known about the interaction between Drosophila and its microsporidian pathogens. Here we report on the relative susceptibility of D. melanogaster life-history stages to infection by Tubulinosema kingi, and on patterns of pathogen proliferation. We find that only larvae can be infected, and that this susceptibility decreases with larval age. Following infection, the pathogen shows little subsequent proliferation in larvae, a limited amount in pupae while it replicates greatly in adults. We present evidence that the host launches a cellular immune response after infection with the pathogen, although its effectiveness remains to be demonstrated

    Evolution of host resistance and parasitoid counter-resistance

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    By their nature, parasitoids will exert a selection pressure on their hosts to evolve a mechanism through which to resist parasitoid attack. In turn, such a resistance mechanism will lead to parasitoids evolving counter-resistance. In this chapter, we present an overview of the research on the (co)evolutionary interaction between Drosophila and their parasitoids, with the main focus on the cellular immune response of D. melanogaster, and the counter-resistance mechanism of one of its main parasitoids, Asobara tabida. A key aspect of this interaction is the existence of genetic variation: in the field, host resistance and parasitoid counter-resistance vary, both between and within populations. Host resistance and parasitoid counter-resistance are costly, and both these costs turn out to be density dependent. These tradeoffs can explain the existence of genetic variation. We briefly touch upon behavioral aspects of the interaction and the parasites and pathogens that the parasitoids themselves suffer from. We end this chapter by considering the data coming from gene chip experiments: early indications suggest that the genes involved in the actual immune response against parasitoids are mostly different from the genes involved in the evolution of resistance. © 2009 Elsevier Ltd. All rights reserved

    Evolutionary change in parasitoid resistance under crowded conditions in Drosophila melanogaster

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    Patterns of investment of limiting resources in such processes as competing for food and defense against natural enemies are shaped by trade-offs and constraints. In Drosophila melanogaster artificial selection for increased resistance to parasitoids results in a correlated decrease in larval competitive ability. Here we ask whether selection for competitive ability leads to a correlated reduction in parasitoid resistance. Replicated lines of D. melanogaster were maintained under crowded or uncrowded conditions for eight generations. As expected, the crowded lines evolved higher competitive ability (when tested against a common strain of fly). But instead of parasitoid resistance decreasing, we found a significant increase, and that this was associated with elevated densities of haemocytes in second-instarlarvae. To understand these results we measured a variety of life-history traits in the two sets of lines. We find evidence that directly and indirectly selected changes in competitive ability are due to different mechanisms. We also ask why crowded conditions should select for increased resistance to parasitism, and conclude that it is unlikely to be due to correlated selection for resistance to other natural enemies, but might be due to correlated selection for better wound responses

    Requirements for Driving Antipathogen Effector Genes into Populations of Disease Vectors by Homing

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    There is a need for new interventions against the on-going burden of vector-borne diseases such as malaria and dengue. One suggestion has been to develop genes encoding effector molecules that block parasite development within the vector, and then use the nuclease-based homing reaction as a form of gene drive to spread those genes through target populations. If the effector gene reduces the fitness of the mosquito and does not contribute to the drive, then loss-of-function mutations in the effector will eventually replace functional copies, but protection may nonetheless persist sufficiently long to provide a public health benefit. Here we present a quantitative model allowing one to predict the duration of protection as a function of the probabilities of different molecular processes during the homing reaction, various fitness effects, and the efficacy of the effector in blocking transmission. Factors that increase the duration of protection include reducing the frequency of pre-existing resistant alleles, the probability of non-recombinational DNA repair, the probability of homing-associated loss of the effector, the fitness costs of the nuclease and effector, and the completeness of parasite blocking. For target species that extend over an area much larger than the typical dispersal distance, the duration of protection is expected to be highest at the release site, and decrease away from there, eventually falling to zero, as effector-less drive constructs replace effector-containing ones. We also model an alternative strategy of using the nuclease to target an essential gene, and then linking the effector to a sequence that restores the essential function and is resistant to the nuclease. Depending upon parameter values, this approach can prolong the duration of protection. Our models highlight the key design criteria needed to achieve a desired level of public health benefit

    Parasitoids: Behavioral and Evolutionary Ecology/ H. Charles J. Godfray.

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    In English.Parasitoids lay their eggs on or in the bodies of other species of insect, and the parasitoid larvae develop by feeding on the host, causing its eventual death. Known for a long time to applied biologists for their importance in regulating the population densities of economic pests, parasitoids have recently proven to be valuable tools in testing many aspects of evolutionary theory. This book synthesizes the work of both schools of parasitoid biology and asks how a consideration of evolutionary biology can help us understand the behavior, ecology, and diversity of the approximately one to two million species of parasitoid found on earth. After a general introduction to parasitoid natural history and taxonomy, the first part of the book treats the different components of the reproductive strategy of parasitoids: searching for a host, host selection, clutch size, and the sex ratio. Subsequent chapters discuss pathogens and non-Mendelian genetic elements that affect sexual reproduction; evolutionary aspects of the physiological interactions between parasitoid and host; mating strategies; life history theory and community ecology. A special effort is made to discuss the theoretical background to the subject, but without the use of mathematics.Frontmatter -- Contents -- Acknowledgments -- 1.Introduction -- 2. Host Location -- 3. Oviposition Behavior -- 4. Sex Ratio -- 5. Selfish Genetic Elements -- 6. The Immature Parasitoid -- 7. The Adult Parasitoid -- 8. Life Histories and Community Patterns -- References -- Author Index -- Subject Index -- Taxonomic Index1 online resource

    Diversity and competitive interactions in experimentally evolved bacterial populations

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    Laboratory bacterial populations provide ideal opportunities to experimentally test theories in ecology and evolutionary biology. I used a model laboratory microbial system, Pseudomonas fluorescens SBW25, to address an array of questions on the origin, maintenance, and functional role of biodiversity, and the evolution of biotic interactions. My thesis reports experiments with the following conclusions. (1) The extent of diversification in P. fluorescens populations is not affected by the presence of an interspecific competitor P. putida, although the early stage of the diversification in one environment (spatially homogeneous environment) could be speeded up by the competitor. (2) Niche and neutral mechanisms simultaneously contribute to the maintenance of phenotypic diversity in P. fluorescens populations; but the operation of niche processes does not lead to a positive effect of biodiversity on ecosystem functioning. (3) The competitive interactions among bacterial phenotypes are generally transitive, and competitive hierarchies inferred from pair-wise competition are fairly consistent to those from multi-species competition. (4) The niche complementarity and selection effects evaluated by random assembly biodiversity experiments can be used to predict the functional consequences of particular non-random species extinction scenarios. (5) P. fluorescens does not show an evolutionary trade-off in using several carbon substrates (glucose, galactose and trehalose), and evolution in environments containing these resources results in imperfect generalists; migration among populations may speed up fitness evolution of some generalists. (6) Biofilm formation at the air-broth interface by wrinkly spreader phenotypes in P. fluorescens is a cooperative behaviour which is costly to individuals but benefits the group; this behaviour could be exploited by smooth morph phenotypes. The cooperators and cheats in this system show reciprocal antagonistic coevolution in resistance and cheating performance
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