Previous Article | Next Article ![]()
Journal of Bacteriology, November 2008, p. 7268-7274, Vol. 190, No. 21
0021-9193/08/$08.00+0 doi:10.1128/JB.00967-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Department of Oral Biology, College of Dentistry, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104,1 UCLA School of Dentistry, Department of Oral Biology, Los Angeles, California 90025,2 University of Iowa School of Dentistry, Department of Pediatric Dentistry, Iowa City, Iowa 522423
Received 14 July 2008/ Accepted 22 August 2008
Previous studies identified irvA as a normally repressed but highly inducible transcription regulator capable of repressing mutacin I gene expression in Streptococcus mutans. In this study, we aimed to identify and characterize the regulator(s) responsible for repressing the expression of irvA. An uncharacterized open reading frame (SMU.1398) located immediately adjacent to irvA and annotated as a putative transcription repressor was identified as a likely candidate. The results of mutation studies confirmed that the expression of irvA was greatly increased in the SMU.1398 background. Mutation of SMU.1398 ("irvR") abolished genetic competence and reduced the expression of the late competence genes/operons comEA, comY, and dprA without affecting the expression of the known competence regulators comC, comED, or comX. In addition, irvR was found to be a potent negative regulator of dextran-dependent aggregation (DDAG) and gbpC expression. Each of these irvR mutant phenotypes could be rescued with a double mutation of irvA or complemented by introducing a wild-type copy of irvR on a shuttle vector. These data indicate that the repression of irvA is critically dependent upon irvR and that irvA repression is essential for the development of genetic competence and the proper control of DDAG in S. mutans.
Published ahead of print on 29 August 2008.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»