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Department of Oral Biology, College of Dentistry, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104; UCLA School of Dentistry, Department of Oral Biology, Los Angeles, CA 90025; University of Iowa School of Dentistry, Department of Pediatric Dentistry, Iowa City, IA 52242
* To whom correspondence should be addressed. Email:
justin-merritt{at}ouhsc.edu.
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 ORF (SMU.1398) located immediately adjacent to irvA and annotated as a putative transcription repressor was identified as a likely candidate. 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, comE/D, or comX. In addition, irvR was also 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 dextran-dependent aggregation in S. mutans.
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Characterization of irvR, a novel regulator of the irvA-dependent pathway required for genetic competence and dextran-dependent aggregation in Streptococcus mutans
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