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Journal of Bacteriology, February 2007, p. 1451-1458, Vol. 189, No. 4
0021-9193/07/$08.00+0     doi:10.1128/JB.01161-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The Streptococcus mutans vicX Gene Product Modulates gtfB/C Expression, Biofilm Formation, Genetic Competence, and Oxidative Stress Tolerance{triangledown}

M. Dilani Senadheera,1 Andrew W. C. Lee,1 David C. I. Hung,3 Grace A. Spatafora,2 Steven D. Goodman,3 and Dennis G. Cvitkovitch1*

Dental Research Institute, University of Toronto, 124 Edward Street, Toronto, ON M51G6, Canada,1 Department of Biology, Middlebury College, 276 Bicentennial Way, BIH354, Middlebury, Vermont 05753,2 Division of Diagnostic Science, Norris School of Dentistry, University of Southern California, 925 West 34th, Los Angeles, California 900893

Received 29 July 2006/ Accepted 9 November 2006

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. In this study, we focused on the vicX gene of the vicRKX tricistronic operon. To characterize vicX, we constructed a nonpolar deletion mutation in the vicX coding region in S. mutans UA159. The growth kinetics of the mutant (designated SmuvicX) showed that the doubling time was longer and that there was considerable sensitivity to paraquat-induced oxidative stress. Supplementing a culture of the wild-type UA159 strain with paraquat significantly increased the expression of vicX (P < 0.05, as determined by analysis of variance [ANOVA]), confirming the role of this gene in oxidative stress tolerance in S. mutans. Examination of mutant biofilms revealed architecturally altered cell clusters that were seemingly denser than the wild-type cell clusters. Interestingly, vicX-deficient cells grown in a glucose-supplemented medium exhibited significantly increased glucosyltransferase B/C (gtfB/C) expression compared with the expression in the wild type (P < 0.05, as determined by ANOVA). Moreover, a sucrose-dependent adhesion assay performed using an S. mutans GS5-derived vicX null mutant demonstrated that the adhesiveness of this mutant was enhanced compared with that of the parent strain and isogenic mutants of the parent strain lacking gtfB and/or gtfC. Also, disruption of vicX reduced the genetic transformability of the mutant approximately 10-fold compared with that of the parent strain (P < 0.05, as determined by ANOVA). Collectively, these findings provide insight into important phenotypes controlled by the vicX gene product that can impact S. mutans pathogenicity.

* Corresponding author. Mailing address: Rm. 449A, Dental Research Institute, 124 Edward Street, Toronto, ON M51G6, Canada. Phone: (416) 979-4917, ext. 4592. Fax: (416) 979-4936. E-mail: dennis.cvitkovitch{at}utoronto.ca.

{triangledown} Published ahead of print on 17 November 2006.

Journal of Bacteriology, February 2007, p. 1451-1458, Vol. 189, No. 4
0021-9193/07/$08.00+0     doi:10.1128/JB.01161-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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