The following acknowledgments section should have been included. ACKNOWLEDGMENTS We thank Paula Fives-Taylor at the University of Vermont for providing the SloC antiserum. In addition, we thank Tim Hunter and coworkers at the Vermont Cancer Center DNA Analysis Facility for their assistance with the analysis of real-time qRT-PCR experiments, Joel Tilley at the University of Vermont for inductively coupled argon plasma analysis, Michele Von Turkovitch at the University of Vermont for preparing the scanning electron micrographs, Dilani Senadheera at the University of Toronto Faculty of Dentistry for assistance with growth curve determination, Gary Nelson for figure preparation, and Frank Spatafora for laboratory assistance.

Metal ion availability in the human oral cavity plays a putative role in Streptococcus mutans virulence gene expression and in appropriate formation of the plaque biofilm. In this report, we present evidence that supports such a role for the DtxR-like SloR metalloregulator (called Dlg in our previous publications) in this oral pathogen. Specifically, the results of gel mobility shift assays revealed the sloABC, sloR, comDE, ropA, sod, and spaP promoters as targets of SloR binding. We confirmed differential expression of these genes in a GMS584 SloR-deficient mutant versus the UA159 wild-type progenitor by real-time semiquantitative reverse transcriptase PCR experiments. The results of additional expression studies support a role for SloR in S. mutans control of glucosyltransferases, glucan binding proteins, and genes relevant to antibiotic resistance. Phenotypic analysis of GMS584 revealed that it forms aberrant biofilms on an abiotic surface, is compromised for genetic competence, and demonstrates heightened incorporation of iron and manganese as well as resistance to oxidative stress compared to the wild type. Taken together, these findings support a role for SloR in S. mutans adherence, biofilm formation, genetic competence, metal ion homeostasis, oxidative stress tolerance, and antibiotic gene regulation, all of which contribute to S. mutans-induced disease.