Grant: Travel Awards - Institute Community Support

Streptococcus mutans is a major causative agent of dental caries. The ability of S. mutans to produce and tolerate acid and form biofilm are key attributes to its cariogenicity. K+ has been reported to play a vital role in glycolysis, cell shape, and recently, we identified the importance of K+ transport in biofilm formation and stress tolerance in S. mutans. In present study, four specific K+ transport systems were identified, two transporters similar to Trk transporters that are energy dependent moderate affinity high specificity transporters, one K+ channel like protein ((KcsA) and one Glutamate/ K+ co-transporter (GlnQHMP). These systems maintain K+ homeostasis of S. mutans and may modulate virulence attributes of S. mutans. We constructed knockout mutants for four K+ transport systems namely: Trk1, Trk2, KcsA and GlnQHMP and these strains were used to measure the intracellular concentration of K+, growth curves analysis under various stressors like paraquat and ability to form biofilms in K+ limiting condition. Interestingly, biofilm formation is impaired if medium is devoid of K+. Also, impaired biofilm formation was observed for knockout mutant strains of Trk2 and double knockout mutant strain of Trk1/Trk2 systems at concentration <25mM of K+. Through the growth curve analysis we observed the sensitivity towards paraquat, which lead us to identify a potential transcriptional regulator VicKR (TCSTS). VicK is a histidine kinase sensor that has intracellular PAS like sensing domain. Quantitative gene expression analysis in VicK knockout mutants substantiated the regulatory role of VicK on expression of kcsA as kcsA was upregulated 2 folds in stationary phase in VicK knockout mutants. Our future experiments aim to elucidate and characterize the role of each K+ transport system individually and also identify the putative regulators for these systems.