The contribution of melanization to Drosophila survival changes with Enterococcus faecalis V583 genomic content

Abstract

Enterococcus faecalis is a human opportunist pathogen able to infect and kill Drosophila. Previous studies proved that E. faecalis carrying the Fsr quorum sensing system are extremely virulent. Fsr is the regulator of two important virulence factors, gelatinase and serine protease, which cause death of Drosophila adult flies by decreasing its tolerance to infection. The exact mechanism underlying the toxicity of these E. faecalis virulence factors is nevertheless not known, in particular the way they interfere with the host immune response. In the present study, we investigated the influence of Fsr-GelE-SprE bacterial factors on different immunity responses, namely antimicrobial peptide production, phagocytosis and melanization. Using E. faecalis V583 wild type and E. faecalis V583 {Delta}fsrB{Delta}gelE{Delta}sprE mutant we showed that both drosomycin production and phagocytosis were activated to similar levels by the two bacterial strains. However, fly pupae infected with the mutant strain showed less melanization and higher survival rates when compared to pupae infected with wild type bacteria. Using adult flies carrying the PPO1{Delta} PPO2{Delta} mutation, we found that absence of melanization had a different impact in survival of the flies when infected with the two E. faecalis strains. PPO1{Delta}, PPO2{Delta} mutant flies were more tolerant to E. faecalis deprived of its major virulence factors. By showing that the presence of the E. faecalis proteases completely alters the impact of melanization activation on Drosophila tolerance, this study provides new clues on the interactions between E. faecalis virulence factors and the fly{acute}s immune system. Future studies on Drosophila immunity should consider the pathogen genomic content.