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dc.contributor.authorVarahan, Sriram
dc.contributor.authorIyer, Vljayalakshmi S.
dc.contributor.authorMoore, William T.
dc.contributor.authorHancock, Lynn E.
dc.date.accessioned2014-07-02T20:27:06Z
dc.date.available2014-07-02T20:27:06Z
dc.date.issued2013-05-03
dc.identifier.citationSriram Varahan et al. (2013). Eep confers lysozyme resistance to enterococcus faecalis via the activation of the extracytoplasmic function sigma factor SigV. Journal of bacteriology 195(14):3125-34. http://www.dx.doi.org/10.1128/JB.00291-13
dc.identifier.urihttp://hdl.handle.net/1808/14460
dc.description.abstractEnterococcus faecalis is a commensal bacterium found in the gastrointestinal tract of most mammals, including humans, and is one of the leading causes of nosocomial infections. One of the hallmarks of E. faecalis pathogenesis is its unusual ability to tolerate high concentrations of lysozyme, which is an important innate immune component of the host. Previous studies have shown that the presence of lysozyme leads to the activation of SigV, an extracytoplasmic function (ECF) sigma factor in E. faecalis, and that the deletion of sigV increases the susceptibility of the bacterium toward lysozyme. Here, we describe the contribution of Eep, a membrane-bound zinc metalloprotease, to the activation of SigV under lysozyme stress by its effects on the stability of the anti-sigma factor RsiV. We demonstrate that the eep mutant phenocopies the sigV mutant in lysozyme, heat, ethanol, and acid stress susceptibility. We also show, using an immunoblot analysis, that in an eep deletion mutant, the anti-sigma factor RsiV is only partially degraded after lysozyme exposure, suggesting that RsiV is processed by unknown protease(s) prior to the action of Eep. An additional observation is that the deletion of rsiV, which results in constitutive SigV expression, leads to chaining of cells, suggesting that SigV might be involved in regulating cell wall-modifying enzymes important in cell wall turnover. We also demonstrate that, in the absence of eep or sigV, enterococci bind significantly more lysozyme, providing a plausible explanation for the increased sensitivity of these mutants toward lysozyme.
dc.description.sponsorshipThis work was supported by National Institutes of Health grant 1R01 AI 77782 (L.E.H.).
dc.publisherAmerican Society of Microbiology
dc.titleEep confers lysozyme resistance to enterococcus faecalis via the activation of the extracytoplasmic function sigma factor SigV
dc.typeArticle
kusw.kuauthorHancock, Lynn E.
kusw.kudepartmentDepartment of Molecular Biosciences
kusw.oastatusna
dc.identifier.doi10.1128/JB.00291-13
kusw.oaversionScholarly/refereed, publisher version
kusw.oapolicyThis item does not meet KU Open Access policy criteria.
dc.rights.accessrightsopenAccess


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