Drosophila Host Model Reveals New Enterococcus faecalis Quorum-Sensing Associated Virulence Factors
Gorman, Matthew J.
Palmer, Kelli L.
Hancock, Lynn E.
de Fátima Silva Lopes, MariaNote: Order does not necessarily reflect citation order of authors.
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CitationTeixeira, N., S. Varahan, M. J. Gorman, K. L. Palmer, A. Zaidman-Remy, R. Yokohata, J. Nakayama, et al. 2013. “Drosophila Host Model Reveals New Enterococcus faecalis Quorum-Sensing Associated Virulence Factors.” PLoS ONE 8 (5): e64740. doi:10.1371/journal.pone.0064740. http://dx.doi.org/10.1371/journal.pone.0064740.
AbstractEnterococcus faecalis V583 is a vancomycin-resistant clinical isolate which belongs to the hospital-adapted clade, CC2. This strain harbours several factors that have been associated with virulence, including the fsr quorum-sensing regulatory system that is known to control the expression of GelE and SprE proteases. To discriminate between genes directly regulated by Fsr, and those indirectly regulated as the result of protease expression or activity, we compared gene expression in isogenic mutants of V583 variously defective in either Fsr quorum sensing or protease expression. Quorum sensing was artificially induced by addition of the quorum signal, GBAP, exogenously in a controlled manner. The Fsr regulon was found to be restricted to five genes, gelE, sprE, ef1097, ef1351 and ef1352. Twelve additional genes were found to be dependent on the presence of GBAP-induced proteases. Induction of GelE and SprE by GBAP via Fsr resulted in accumulation of mRNA encoding lrgAB, and this induction was found to be lytRS dependent. Drosophila infection was used to discern varying levels of toxicity stemming from mutations in the fsr quorum regulatory system and the genes that it regulates, highlighting the contribution of LrgAB and bacteriocin EF1097 to infection toxicity. A contribution of SprE to infection toxicity was also detected. This work brought to light new players in E. faecalis success as a pathogen and paves the way for future studies on host tolerance mechanisms to infections caused by this important nosocomial pathogen.
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