Regulation of bacteriocin production and cell death by the VicRK signaling system in Streptococcus mutans.

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Regulation of bacteriocin production and cell death by the VicRK signaling system in Streptococcus mutans.

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dc.contributor.author Senadheera, Dilani B sv
dc.contributor.author Cordova, Martha sv
dc.contributor.author Ayala, Eduardo A sv
dc.contributor.author Chávez de Paz, Luis Eduardo sv
dc.contributor.author Singh, Kalpana sv
dc.contributor.author Downey, Jennifer S sv
dc.contributor.author Goodman, Steven D sv
dc.contributor.author Cvitcovitch, Dennis sv
dc.contributor.author Svensäter, Gunnel en_US
dc.date.accessioned 2013-01-15T10:55:38Z
dc.date.available 2013-01-15T10:55:38Z
dc.date.issued 2012 en_US
dc.identifier.issn 0021-9193
dc.identifier.uri http://hdl.handle.net/2043/14936
dc.description.abstract The VicRK two-component signaling system modulates biofilm formation, genetic competence, and stress tolerance in Streptococcus mutans. We show here that the VicRK modulates bacteriocin production and cell viability, in part by direct modulation of competence-stimulating peptide (CSP) production in S. mutans. Global transcriptome and real-time transcriptional analysis of the VicK-deficient mutant (SmuvicK) revealed significant modulation of several bacteriocin-related loci, including nlmAB, nlmC, and nlmD (P < 0.001), suggesting a role for the VicRK in producing mutacins IV, V, and VI. Bacteriocin overlay assays revealed an altered ability of the vic mutants to kill related species. Since a well-conserved VicR binding site (TGTWAH-N(5)-TGTWAH) was identified within the comC coding region, we confirmed VicR binding to this sequence using DNA footprinting. Overexpression of the vic operon caused growth-phase-dependent repression of comC, comDE, and comX. In the vic mutants, transcription of nlmC/cipB encoding mutacin V, previously linked to CSP-dependent cell lysis, as well as expression of its putative immunity factor encoded by immB, were significantly affected relative to the wild type (P < 0.05). In contrast to previous reports that proposed a hyper-resistant phenotype for the VicK mutant in cell viability, the release of extracellular genomic DNA was significantly enhanced in SmuvicK (P < 0.05), likely as a result of increased autolysis compared with the parent. The drastic influence of VicRK on cell viability was also demonstrated using vic mutant biofilms. Taken together, we have identified a novel regulatory link between the VicRK and ComDE systems to modulate bacteriocin production and cell viability of S. mutans. en_US
dc.format.extent 10
dc.language.iso eng en_US
dc.publisher American Society for Microbiology
dc.subject.classification Medicine en_US
dc.title Regulation of bacteriocin production and cell death by the VicRK signaling system in Streptococcus mutans. en_US
dc.type Article, peer reviewed scientific en_US
dc.contributor.department Malmö University. Faculty of Odontology
dc.identifier.doi 10.1128/JB.06071-11 en_US
dc.subject.srsc Research Subject Categories::MEDICINE en_US
dc.relation.ispartofpublication Journal of Bacteriology;6
dc.relation.ispartofpublicationvolume 194
dc.format.ePage 1316
dc.format.sPage 1307
mahlocal.rights.oaType bronze
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