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J. Bacteriol. doi:10.1128/JB.01161-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The Streptococcus mutans vicX gene product modulates gtfB/C Expression, Biofilm Formation, Genetic Competence and Oxidative Stress Tolerance

Dental Research Institute, University of Toronto, 124 Edward Street, Toronto, ON M51G6, Canada; Department of Biology, Middlebury College, 276 Bicentennial Way, BIH354, Middlebury, VT 05753; Division of Diagnostic Science, Norris School of Dentistry, University of Southern California, 925 West 34^th, Los Angeles, California 90089

^* To whom correspondence should be addressed. Email: dennis.cvitkovitch{at}utoronto.ca.

	Abstract

Streptococcus mutans is considered one of the primary etiologic agents of dental caries. Previously, we characterized the VicRK two-component signal transduction system, which regulates multiple virulence factors of S. mutans. This study is focused on the vicX of the vicRKX tricistronic operon. To characterize vicX, we constructed a non-polar deletion mutation in the vicX coding region in S. mutans UA159. Growth kinetics of the mutant (designated SmuvicX) demonstrated a longer doubling time and considerable sensitivity to paraquat-induced oxidative stress. Supplementing the wild-type UA159 strain with paraquat significantly increased the expression of vicX (p<0.05; ANOVA) thus confirming its role in oxidative stress tolerance in S. mutans. Examination of mutant biofilms revealed architecturally altered cell clusters that were seemingly denser relative to the wild type. Interestingly, vicX-deficient cells grown in a glucose-supplemented medium showed significantly increased glucosyltransferase B/C (gtfB/C) expression relative to wild-type (p<0.05; ANOVA). Moreover, a sucrose-dependent adhesion assay performed using an S. mutans GS5-derived vicX-null mutant demonstrated enhanced adhesiveness compared with the parent strain, and its isogenic mutants lacking gtfB and/or gtfC. Also, disruption of vicX significantly reduced the genetic transformability of the mutant by approximately 10-fold compared with its parent strain (p<0.05; ANOVA). Taken collectively, these findings provide insight into important phenotypes controlled by the vicX gene product that can impact S. mutans pathogenicity.

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