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Expression oface (a dhesin toc ollagen ofE nterococcus faecalis), encoding a virulence factor in endocarditis and urinary tract infection models, has been shown to increase under certain conditions, such as in the presence of serum, bile salts, urine, and collagen and at 46°C. However, the mechanism oface /Ace regulation under different conditions is still unknown. In this study, we identified a two-component regulatory system GrvRS as the main regulator oface expression under these stress conditions. Using Northern hybridization and β-galactosidase assays of anace promoter-lacZ fusion, we found transcription oface to be virtually absent in agrvR deletion mutant under the conditions that increaseace expression in wild-type OG1RF and in the complemented strain. Moreover, agrvR mutant revealed decreased collagen binding and biofilm formation as well as attenuation in a murine urinary tract infection model. Here we show that GrvR plays a major role in control oface expression andE. faecalis virulence.

The Two-Component System GrvRS (EtaRS) Regulates ace Expression in Enterococcus faecalis OG1RF