Abstract

Bacteria are considered “social” organisms able to communicate with one another using small hormone-like molecules (pheromones) in a process called quorum-sensing (QS). These signaling molecules increase in concentration as a function of bacterial cell density. For most human pathogens, QS is critical for virulence and biofilm formation, and the opportunity to interfere with bacterial QS could provide a sophisticated means for manipulating the composition of pathogenic biofilms, and possibly eradicating the infection. Streptococcus mutans is a well-characterized resident of the dental plaque biofilm, and is the major pathogen of dental caries (cavities). In S. mutans, its CSP QS signaling peptide does not act as a classical QS signal by accumulating passively in proportion to cell density. In fact, particular stresses such as those encountered in the oral cavity, induce the production of the CSP pheromone, suggesting that the pheromone most probably functions as a stress-inducible alarmone by triggering the signaling to the bacterial population to initiate an adaptive response that results in different phenotypic outcomes. This mini-review discusses two different CSP-induced phenotypes, bacterial “suicide” and dormancy, and the underlying mechanisms by which S. mutans utilizes the same QS signaling peptide to regulate two opposite phenotypes.

Highlights

  • Oral streptococci are pioneer colonizers of the oral cavity and are abundant in the dental plaque, a tooth-associated biofilm (Lazarevic et al, 2009)

  • It is quite obvious that S. mutans utilizes its CSP-ComDE QS system as a means to convey an adaptive stress response that yields phenotypic heterogeneity within a given clonal population

  • One of the cell subpopulations undergoes suicide as a potentially altruistic act to eliminate damaged individual cells upon the exposure to adverse environmental conditions, and possibly provide nutrients to benefit the bacterial population as a whole

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Summary

INTRODUCTION

Oral streptococci are pioneer colonizers of the oral cavity and are abundant in the dental plaque, a tooth-associated biofilm (Lazarevic et al, 2009). The fact that most bacteria do not live solitary lives but live in biofilms, suggest that bacterial biofilms most likely act as multicellular organisms Particular environmental stressors, such as those encountered in the oral cavity, induce the expression of the CSP-encoding gene (comC). CipB activates expression of SigX-dependent genes such as lytFSm involved in CSP-induced PCD, it is unclear how both quorum-sensing systems are linked in a peptide-rich medium. The permeabilization of the cell membrane would enable the import of XIP, which, in association with ComR regulator, would directly activate SigX responsible for the development of genetic competence, stress-induced persisters, and CSP-induced PCD. It was demonstrated that the viability of a ∆lytFSm mutant in a long-term survival assay was significantly lower than that observed for the parent strain, suggesting that surviving cells may benefit from the nutrients released through the action of the autolysin activated by the CSP-induced PCD pathway (Dufour and Lévesque, 2013)

SURVIVAL THROUGH DORMANCY
Findings
CONCLUDING REMARKS
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