The oral pathogen Streptococcus mutans employs a variety of mechanisms to maintain a competitive advantage over many other oral bacteria which occupy the same ecological niche. Production of the bacteriocin, mutacin I, is one such mechanism. However, little is known about the regulatory mechanisms associated with mutacin I production. Previous work has demonstrated that the production of mutacin I greatly increased with cell density. In this study, we found that high cell density also triggered high level mutacin I gene transcription. However, this response was abolished upon deletion of luxS. Further analysis using real-time reverse transcription polymerase chain reaction (RT-PCR) demonstrated that in the luxS mutant transcription of both the mutacin I structural gene mutA and the mutacin I transcriptional activator mutR was impaired. Through microarray analysis, a putative transcription repressor annotated as Smu1274 in the Los Alamos National Laboratory Oral Pathogens Sequence Database was identified, which was strongly induced in the luxS mutant. Characterization of Smu1274, which we referred to as irvA, suggested that it may act as an inducible repressor to suppress mutacin I gene expression. A luxS and irvA double mutant regained the ability to produce mutacin I; whereas a constitutive irvA-producing strain was impaired in mutacin I production. These findings reveal a novel regulatory pathway for mutacin I gene expression, which may provide clues to the regulatory mechanisms of other cellular functions regulated by luxS in S. mutans.
ASJC Scopus subject areas
- Molecular Biology