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1 Laboratoire de Microbiologie de l'Environnement, EA 956 soutenue par l'INRA, IRBA, Université de Caen, 14032 Caen Cedex, France
2 Institute of Microbiology, Catholic University of Sacred Heart, L. go F. Vito 1, 00168, Rome, Italy
Correspondence
Jean-Christophe Giard
jean-christophe.giard{at}unicaen.fr
PerR is one of the most important transcriptional regulators involved in the oxidative-stress response in Bacillus subtilis. Here, the homologous gene in Enterococcus faecalis, ranked among the leading causes of nosocomial infection, was characterized and analysed. Phenotype analysis showed that the perR mutant was significantly more resistant to H2O2 challenge (P<0·05). Expression of eight genes with potential roles in the oxidative-stress response was determined in the wild-type and perR-mutant strains by real-time quantitative PCR. Surprisingly, low quantitative differences in the transcriptional activity of these genes in the mutant versus wild-type were observed. Likewise, this locus was not involved in survival within murine macrophages, but in the mouse peritonitis model, the perR mutant appeared less lethal than the JH2-2 wild-type strain. The combined results show that PerR affects E. faecalis virulence and that its implication in the transcriptional regulation in this bacterium deviates from the B. subtilis model.
The GenBank/EMBL/DDBJ accession number for the perR sequence of E. faecalis JH2-2 reported in this paper is DQ064645.
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