In vitro experimental study uncovers CiaH-mediated upregulation of lipoprotein OpcC in Streptococcus mutans, indicating a molecular pathway for bacterial acid tolerance.
Streptococcus mutans uses two-component signal transduction systems (TCSs) to monitor and respond to the fluctuating pH levels to survive the human oral cavity. The TCSs modulate the expression of genes encoding products crucial to cell survival. CiaRH is one of TCSs that is thought to be responsible for the acid tolerance of this pathogen; however, the target molecules modulated by the CiaRH have been still unclear. In this study, we identified that a lipoprotein OpcC contributes to the acid tolerance of S. mutans. The opcC-deficient mutant showed higher acid sensitivity than the wild-type 109c. In addition, deletion of the gene encoding prolipoprotein diacylglyceryl transferase (Lgt) eliminated OpcC on the cell surface of S. mutans. These results suggest that OpcC is an acid-tolerance related lipoprotein that is lipid anchored in the cell membrane by Lgt. Relationship between opcC and CiaRH was assessed by transcriptional analysis of S. mutans in the acidic or neutral conditions. The opcC expression was increased in the wild type and ciaR mutant in the acidic environment. However, the opcC expression was not increased in the ciaH mutant by the acidic stress. These results suggest that acidic stress sensing by CiaH is essential for the increased expression of opcC. Collectively, S. mutans OpcC is an acid tolerance-related lipoprotein whose gene-expression is enhanced via CiaH by sensing the acidic stress. In this study, we clarify the partial mechanism mediating S. mutans survival in acidic environments by showing the link between CiaRH and OpcC.
No takes yet. Share an insight, caveat, or question.
Taniguchi et al. (2013) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: