Streptococcus mutans is a primary pathogen associated with dental caries. Its bacteriocin (mutacin) production ability is thought to play an important role in maintaining competitiveness in the multispecies oral biofilm. Previous studies have demonstrated that the production of the lantibiotic, mutacin I, is responsive to multiple input signals and that a putative inducible repressor, irvA, seems to be involved in the luxS-mediated mutacin I gene regulation pathway. In this study, we demonstrate that these multiple inputs can be divided into two pathways: irvA-dependent and irvA-independent. Similar to luxS, signals mediated through vicK, pttB and hk03 exert their effect possibly through modulating irvA transcription, whereas signals mediated through ciaH, hrcA, adhE, and Smu1281 exert their effect through an unknown mechanism independent of irvA.