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Peptide alarmone signalling triggers an auto‐active bacteriocin necessary for genetic competence
Author(s) -
Perry Julie A.,
Jones Marcus B.,
Peterson Scott N.,
Cvitkovitch Dennis G.,
Lévesque Céline M.
Publication year - 2009
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2009.06693.x
Subject(s) - biology , bacteriocin , lytic cycle , streptococcus mutans , regulon , effector , microbiology and biotechnology , population , prophage , genetics , lysogenic cycle , gene , gene expression , bacteria , bacteriophage , virus , demography , escherichia coli , sociology
Summary The induction of genetic competence is a strategy used by bacteria to increase their genetic repertoire under stressful environmental conditions. Recently, Streptococcus pneumoniae has been shown to co‐ordinate the uptake of transforming DNA with fratricide via increased expression of the peptide pheromone responsible for competence induction. Here, we document that environmental stress‐induced expression of the peptide pheromone competence‐stimulating peptide (CSP) in the oral pathogen Streptococcus mutans . We showed that CSP is involved in the stress response and determined the CSP‐induced regulon in S. mutans by microarray analysis. Contrary to pneumococcus, S. mutans responds to increased concentrations of CSP by cell lysis in only a fraction of the population. We have focused on the mechanism of cell lysis and have identified a novel bacteriocin as the ‘death effector’. Most importantly, we showed that this bacteriocin causes cell death via a novel mechanism of action: intracellular action against self. We have also identified the cognate bacteriocin immunity protein, which resides in a separate unlinked genetic locus to allow its differential regulation. The role of the lytic response in S. mutans competence is also discussed. Together, these findings reveal a novel autolytic pathway in S. mutans which may be involved in the dissemination of fitness‐enhancing genes in the oral biofilm.