Mapping candidate genes for <i>Drosophila melanogaster</i> resistance to the parasitoid wasp <i>Leptopilina boulardi</i>

Hita, M.; Espagne, Eric; Lemeunier, Françoise; Pascual, Luis Alberto Malvárez; Carton, Y.; Périquet, Georges; Poirié, Marylène

doi:10.1017/s001667230600841x

Cited by 21 publications

(20 citation statements)

References 31 publications

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“…Likewise, the gene edl , which was previously implicated in the immune response against L. boulardi [56], plays a regulatory role in and is itself regulated by the Ras pathway signaling [57], and was more than 2-fold up-regulated after Lb17 attack but not Lh14 attack. In the 35B-E region, the Toll/JAK/STAT-regulated complement-like protein TepI [52] is greater than 10-fold up-regulated after Lb17 attack, but is not differentially regulated after Lh14 attack.…”

Section: Resultsmentioning

confidence: 99%

Contrasting Infection Strategies in Generalist and Specialist Wasp Parasitoids of Drosophila melanogaster

et al. 2007

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Although host–parasitoid interactions are becoming well characterized at the organismal and cellular levels, much remains to be understood of the molecular bases for the host immune response and the parasitoids' ability to defeat this immune response. Leptopilina boulardi and L. heterotoma, two closely related, highly infectious natural parasitoids of Drosophila melanogaster, appear to use very different infection strategies at the cellular level. Here, we further characterize cellular level differences in the infection characteristics of these two wasp species using newly derived, virulent inbred strains, and then use whole genome microarrays to compare the transcriptional response of Drosophila to each. While flies attacked by the melanogaster group specialist L. boulardi (strain Lb17) up-regulate numerous genes encoding proteolytic enzymes, components of the Toll and JAK/STAT pathways, and the melanization cascade as part of a combined cellular and humoral innate immune response, flies attacked by the generalist L. heterotoma (strain Lh14) do not appear to initiate an immune transcriptional response at the time points post-infection we assayed, perhaps due to the rapid venom-mediated lysis of host hemocytes (blood cells). Thus, the specialist parasitoid appears to invoke a full-blown immune response in the host, but suppresses and/or evades downstream components of this response. Given that activation of the host immune response likely depletes the energetic resources of the host, the specialist's infection strategy seems relatively disadvantageous. However, we uncover the mechanism for one potentially important fitness tradeoff of the generalist's highly immune suppressive infection strategy.

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Section: Resultsmentioning

confidence: 99%

Contrasting Infection Strategies in Generalist and Specialist Wasp Parasitoids of Drosophila melanogaster

et al. 2007

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“…In Drosophila , parasitoid wasps are one of the main causes of mortality in natural populations [46], and both linkage mapping and artificial selection experiments suggest that resistance against these parasites is controlled by a few major-effect loci [18], [47], [48]. There is also extensive variation in bacterial resistance, and polymorphisms in immune system genes explain a substantial proportion of this variation [49], [50].…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Association Studies Reveal a Simple Genetic Basis of Resistance to Naturally Coevolving Viruses in Drosophila melanogaster

Magwire¹,

Fabian²,

Schweyen³

et al. 2012

PLoS Genet

159

237

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Variation in susceptibility to infectious disease often has a substantial genetic component in animal and plant populations. We have used genome-wide association studies (GWAS) in Drosophila melanogaster to identify the genetic basis of variation in susceptibility to viral infection. We found that there is substantially more genetic variation in susceptibility to two viruses that naturally infect D. melanogaster (DCV and DMelSV) than to two viruses isolated from other insects (FHV and DAffSV). Furthermore, this increased variation is caused by a small number of common polymorphisms that have a major effect on resistance and can individually explain up to 47% of the heritability in disease susceptibility. For two of these polymorphisms, it has previously been shown that they have been driven to a high frequency by natural selection. An advantage of GWAS in Drosophila is that the results can be confirmed experimentally. We verified that a gene called pastrel—which was previously not known to have an antiviral function—is associated with DCV-resistance by knocking down its expression by RNAi. Our data suggest that selection for resistance to infectious disease can increase genetic variation by increasing the frequency of major-effect alleles, and this has resulted in a simple genetic basis to variation in virus resistance.

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“…Variation in both Drosophila resistance and parasitoid virulence is observed in the field [12]–[14], and some major genes involved in these traits have been characterized [15]–[18]. Based on these data, we address here the question of the origin of intraspecific variation of virulence of Drosophila parasitoids.…”

Section: Introductionmentioning

confidence: 95%

The Origin of Intraspecific Variation of Virulence in an Eukaryotic Immune Suppressive Parasite

et al. 2010

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Occurrence of intraspecific variation in parasite virulence, a prerequisite for coevolution of hosts and parasites, has largely been reported. However, surprisingly little is known of the molecular bases of this variation in eukaryotic parasites, with the exception of the antigenic variation used by immune-evading parasites of mammals. The present work aims to address this question in immune suppressive eukaryotic parasites. In Leptopilina boulardi, a parasitic wasp of Drosophila melanogaster, well-defined virulent and avirulent strains have been characterized. The success of virulent females is due to a major immune suppressive factor, LbGAP, a RacGAP protein present in the venom and injected into the host at oviposition. Here, we show that an homologous protein, named LbGAPy, is present in the venom of the avirulent strain. We then question whether the difference in virulence between strains originates from qualitative or quantitative differences in LbGAP and LbGAPy proteins. Results show that the recombinant LbGAPy protein has an in vitro GAP activity equivalent to that of recombinant LbGAP and similarly targets Drosophila Rac1 and Rac2 GTPases. In contrast, a much higher level of both mRNA and protein is found in venom-producing tissues of virulent parasitoids. The F1 offspring between virulent and avirulent strains show an intermediate level of LbGAP in their venom but a full success of parasitism. Interestingly, they express almost exclusively the virulent LbGAP allele in venom-producing tissues. Altogether, our results demonstrate that the major virulence factor in the wasp L. boulardi differs only quantitatively between virulent and avirulent strains, and suggest the existence of a threshold effect of this molecule on parasitoid virulence. We propose that regulation of gene expression might be a major mechanism at the origin of intraspecific variation of virulence in immune suppressive eukaryotic parasites. Understanding this variation would improve our knowledge of the mechanisms of transcriptional evolution currently under active investigation.

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Mapping candidate genes for Drosophila melanogaster resistance to the parasitoid wasp Leptopilina boulardi

Cited by 21 publications

References 31 publications

Contrasting Infection Strategies in Generalist and Specialist Wasp Parasitoids of Drosophila melanogaster

Contrasting Infection Strategies in Generalist and Specialist Wasp Parasitoids of Drosophila melanogaster

Genome-Wide Association Studies Reveal a Simple Genetic Basis of Resistance to Naturally Coevolving Viruses in Drosophila melanogaster

The Origin of Intraspecific Variation of Virulence in an Eukaryotic Immune Suppressive Parasite

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