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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 .

Phagocytosis Is the Sole Arm of Drosophila melanogaster Known Host Defenses That Provides Some Protection Against Microsporidia Infection