This Article Full Text Full Text (PDF) Other Versions of this Article: JB.01161-06v1 189/4/1451    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Senadheera, M. D. Articles by Cvitkovitch, D. G. Search for Related Content PubMed PubMed Citation Articles by Senadheera, M. D. Articles by Cvitkovitch, D. G.

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,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.

Published ahead of print on 17 November 2006.

This article has been cited by other articles:

• Winkler, M. E., Hoch, J. A. (2008). Essentiality, Bypass, and Targeting of the YycFG (VicRK) Two-Component Regulatory System in Gram-Positive Bacteria. J. Bacteriol. 190: 2645-2648 [Full Text]  
• Sztajer, H., Lemme, A., Vilchez, R., Schulz, S., Geffers, R., Yip, C. Y. Y., Levesque, C. M., Cvitkovitch, D. G., Wagner-Dobler, I. (2008). Autoinducer-2-Regulated Genes in Streptococcus mutans UA159 and Global Metabolic Effect of the luxS Mutation. J. Bacteriol. 190: 401-415 [Abstract] [Full Text]  
• Merritt, J., Zheng, L., Shi, W., Qi, F. (2007). Genetic characterization of the hdrRM operon: a novel high-cell-density-responsive regulator in Streptococcus mutans. Microbiology 153: 2765-2773 [Abstract] [Full Text]  
• Deng, D.M., Liu, M.J., ten Cate, J.M., Crielaard, W. (2007). The VicRK System of Streptococcus mutans Responds to Oxidative Stress. J. Dent. Res. 86: 606-610 [Abstract] [Full Text]