HAL is a multi-disciplinary open access archive for the deposit and dissemination of scientific research documents, whether they are published or not. The documents may come from teaching and research institutions in France or abroad, or from public or private research centers. L'archive ouverte pluridisciplinaire HAL, est destinée au dépôt et à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.

When feeds on, some bacteria cross the intestinal barrier and eventually proliferate in the hemocoel. This process is limited by hemocytes through phagocytosis. requires the quorum-sensing regulator RhlR to elude the cellular immune response of the fly. RhlI synthesizes the autoinducer signal that activates RhlR. Here, we show that mutants are unexpectedly more virulent than mutants, both in fly and in nematode intestinal infection models, suggesting that RhlR has RhlI-independent functions. We also report that RhlR protects from opsonization mediated by the thioester-containing protein 4 (Tep4). mutant bacteria show higher levels of mediated opsonization, as compared to mutants, which prevents lethal bacteremia in the hemocoel. In contrast, in a septic model of infection, in which bacteria are introduced directly into the hemocoel, mutant flies are more resistant to wild-type but not to the mutant. Thus, depending on the infection route, the Tep4 opsonin can either be protective or detrimental to host defense.

No abstract

No abstract

We present the draft genome sequence of Tubulinosema ratisbonensis, a microsporidium species infecting Drosophila melanogaster. A total of 3,013 protein-encoding genes and an array of transposable elements were identified. This work represents a necessary step to develop a novel model of host-parasite relationships using the highly tractable genetic model D. melanogaster.

Microsporidia are obligate intracellular parasites able to infest specifically a large range of species, including insects. The knowledge about the biology of microsporidial infections remains confined to mostly descriptive studies, including molecular approaches such as transcriptomics or proteomics. Thus, functional data to understand insect host defenses are currently lacking. Here, we have undertaken a genetic analysis of known host defenses of the Drosophila melanogaster using an infection model whereby Tubulinosema ratisbonensis spores are directly injected in this insect. We find that phagocytosis does confer some protection in this infection model. In contrast, the systemic immune response, extracellular reactive oxygen species, thioester proteins, xenophagy, and intracellular antiviral response pathways do not appear to be involved in the resistance against this parasite. Unexpectedly, several genes such as PGRP-LE seem to promote this infection. The prophenol oxidases that mediate melanization have different functions; PPO1 presents a phenotype similar to that of PGRP-LE whereas that of PPO2 suggests a function in the resilience to infection. Similarly, eiger and Unpaired3, which encode two cytokines secreted by hemocytes display a resilience phenotype with a strong susceptibility to T. ratisbonensis.

No abstract

When Drosophila flies feed on Pseudomonas aeruginosa strain PA14, some bacteria cross the intestinal barrier and start proliferating inside the hemocoel. This process is limited by hemocytes through phagocytosis. We have previously shown that the PA14 quorum-sensing regulator RhlR is required for these bacteria to elude the cellular immune response. RhlI synthesizes the auto-inducer signal that activates RhlR. Here, we compare the null mutant phenotypes of rhlR and rhlI in a variety of infection assays in Drosophila and in the nematode Caenorhabditis elegans. Surprisingly, in Drosophila, unlike ΔrhlR mutants, ΔrhlI mutants are only modestly attenuated for virulence and are poorly phagocytosed and opsonized in a Thioester-containing Protein4-dependent manner. Likewise, ΔrhlI but not ΔrhlR mutants colonize the digestive tract of C. elegans and kill it as efficiently as wild-type PA14. Thus, RhlR has an RhlI-independent function in eluding detection or counter-acting the action of the immune system. In contrast to the intestinal infection model, Tep4 mutant flies are more resistant to PA14 in a septic injury model, which also depends on rhlR. Thus, the Tep4 putative opsonin can either be protective or detrimental to host defense depending on the infection route.