The Two-Component System GrvRS (EtaRS) RegulatesaceExpression in Enterococcus faecalis OG1RF release_yqlszg236ngddh3sz6rsrs5k3e

by Jung Hyeob Roh, Kavindra V. Singh, Sabina Leanti La Rosa, Ana Luisa V. Cohen, Barbara E. Murray


Expression of<jats:italic>ace</jats:italic>(<jats:underline>a</jats:underline>dhesin to<jats:underline>c</jats:underline>ollagen of<jats:named-content content-type="genus-species"><jats:underline>E</jats:underline>nterococcus faecalis</jats:named-content>), 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 of<jats:italic>ace</jats:italic>/Ace regulation under different conditions is still unknown. In this study, we identified a two-component regulatory system GrvRS as the main regulator of<jats:italic>ace</jats:italic>expression under these stress conditions. Using Northern hybridization and β-galactosidase assays of an<jats:italic>ace</jats:italic>promoter-<jats:italic>lacZ</jats:italic>fusion, we found transcription of<jats:italic>ace</jats:italic>to be virtually absent in a<jats:italic>grvR</jats:italic>deletion mutant under the conditions that increase<jats:italic>ace</jats:italic>expression in wild-type OG1RF and in the complemented strain. Moreover, a<jats:italic>grvR</jats:italic>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 of<jats:italic>ace</jats:italic>expression and<jats:named-content content-type="genus-species">E. faecalis</jats:named-content>virulence.
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Published in Infection and Immunity by American Society for Microbiology
ISSN-L 0019-9567
Volume 83
Page(s) 389-395
Release Date 2014-11-10
Publisher American Society for Microbiology
Primary Language en (lookup)

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Type  article-journal
Stage   published
Date   2014-11-10
DOI  10.1128/iai.02587-14
PubMed  25385790
PMC  PMC4288885
Wikidata  Q34889914
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ISSN-L:  0019-9567
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