RpiRc is a pleiotropic effector of virulence determinant synthesis and attenuates pathogenicity in Staphylococcus aureus

Rosmarie Gaupp, Jessica Wirf, B. Wonnenberg, Tanja Biegel, J. Eisenbeis, J. Graham, M. Herrmann, C. Y. Lee, C. Beisswenger, C. Wolz, T. Tschernig, M. Bischoff, G. A. Somerville

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

In Staphylococcus aureus, metabolism is intimately linked with virulence determinant biosynthesis, and several metabolite-responsive regulators have been reported to mediate this linkage. S. aureus possesses at least three members of the RpiR family of transcriptional regulators. Of the three RpiR homologs, RpiRc is a potential regulator of the pentose phosphate pathway, which also regulates RNAIII levels. RNAIII is the regulatory RNA of the agr quorum-sensing system that controls virulence determinant synthesis. The effect of RpiRc on RNAIII likely involves other regulators, as the regulators that bind the RNAIII promoter have been intensely studied. To determine which regulators might bridge the gap between RpiRc and RNAIII, sarA, sigB, mgrA, and acnA mutations were introduced into an rpiRc mutant background, and the effects on RNAIII were determined. Additionally, phenotypic and genotypic differences were examined in the single and double mutant strains, and the virulence of select strains was examined using two different murine infection models. The data suggest that RpiRc affects RNAIII transcription and the synthesis of virulence determinants in concert with σB, SarA, and the bacterial metabolic status to negatively affect virulence.

Original languageEnglish (US)
Pages (from-to)2031-2041
Number of pages11
JournalInfection and immunity
Volume84
Issue number7
DOIs
StatePublished - 2016

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

Fingerprint

Dive into the research topics of 'RpiRc is a pleiotropic effector of virulence determinant synthesis and attenuates pathogenicity in Staphylococcus aureus'. Together they form a unique fingerprint.

Cite this