Interconnection of competence, stress and CiaR regulons in Streptococcus pneumoniae: competence triggers stationary phase autolysis of ciaR mutant cells.
Of the 13 two-component signal transduction systems (TCS) identified in Streptococcus pneumoniae, two, ComDE and CiaRH, are known to affect competence for natural genetic transformation. ComD and ComE act together with the comC-encoded competence-stimulating peptide (CSP) and with ComAB, the CSP-dedicated exporter, to co-ordinate activation of genes required for differentiation to competence. Several lines of evidence suggest that the CiaRH TCS and competence regulation are interconnected, including the observation that inactivation of the CiaR response regulator derepresses competence. However, the nature of the interconnection remains poorly understood. Interpretation of previous transcriptome analyses of ciaR mutants was complicated by competence derepression in the mutants. To circumvent this problem, we have used microarray analysis to investigate the transition from non-competence to competence in a comC-null wild-type strain and its ciaR derivative after the addition of CSP. This study increased the number of known CSP-induced genes from approximately 47 to 105 and revealed approximately 42 genes with reduced expression in competent cells. Induction of the CiaR regulon, as well as the entire HrcA and part of the CtsR stress response regulons, was observed in wild-type competent cells. Enhanced induction of stress response genes was detected in ciaR competent cells. In line with these observations, CSP was demonstrated to trigger growth arrest and stationary phase autolysis in ciaR cells. Taken together, these data strongly suggest that differentiation to competence imposes a temporary stress on cells, and that the CiaRH TCS is required for the cells to exit normally from the competent state.
Dagkessamanskaia
Adilia
A
Laboratoire de Microbiologie et Génétique Moléculaires, UMR 5100 CNRS-Université Paul Sabatier, Toulouse Cedex, France.
Moscoso
Miriam
M
Hénard
Vincent
V
Guiral
Sébastien
S
Overweg
Karin
K
Reuter
Mark
M
Martin
Bernard
B
Wells
Jerry
J
Claverys
Jean-Pierre
JP
D001426:Bacterial Proteins / Q000235:genetics / Q000494:pharmacology / Q000502:physiology*; D001433:Bacteriolysis; D004268:DNA-Binding Proteins / Q000235:genetics / Q000494:pharmacology / Q000502:physiology; D017353:Gene Deletion; D020869:Gene Expression Profiling; D005798:Genes, Bacterial; D006360:Heat-Shock Proteins / Q000235:genetics / Q000502:physiology*; D000071677:Histidine Kinase; D007700:Kinetics; D009154:Mutation; D020411:Oligonucleotide Array Sequence Analysis; D010675:Pheromones / Q000235:genetics / Q000494:pharmacology / Q000502:physiology; D011494:Protein Kinases / Q000235:genetics / Q000502:physiology*; D018085:Regulon; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D013296:Streptococcus pneumoniae / Q000235:genetics / Q000254:growth & development / Q000502:physiology*; D014169:Transformation, Bacterial
D001426:Bacterial Proteins; C061262:ComA protein, Bacteria; C103179:ComE protein, Streptococcus pneumoniae; C118338:CtsR protein, bacteria; D004268:DNA-Binding Proteins; D006360:Heat-Shock Proteins; D010675:Pheromones; D012097:Repressor Proteins; D011494:Protein Kinases; D000071677:Histidine Kinase; C088910:CiaR protein, Streptococcus pneumoniae