A molecular switch controlling competence and motility: competence regulatory factors ComS, MecA, and ComK control sigmaD-dependent gene expression in Bacillus subtilis.

Bacillus subtilis, like many bacteria, will choose among several response pathways when encountering a stressful environment. Among the processes activated under growth-restricting conditions are sporulation, establishment of motility, and competence development. Recent reports implicate ComK and MecA-ClpC as part of a system that regulates both motility and competence development. MecA, while negatively controlling competence by inhibiting ComK, stimulates sigmaD-dependent transcription of genes that function in motility and autolysin production. Both ComK-dependent and -independent pathways have been proposed for MecA's role in the regulation of motility. Mutations in mecA reduce the transcription of hag. encoding flagellin, and are partially suppressed by comK in both medium promoting motility and medium promoting competence. Reduced sigmaD levels are observed in mecA mutants grown in competence medium, but no change in sigmaD concentration is detected in a comK mutant. The comF operon, transcription of which requires ComK, is located immediately upstream of the operon that contains the flgM gene, encoding the sigmaD-specific antisigma factor. An insertion mutation that disrupts the putative comF-flgM transcription unit confers a phenotype identical to that of the comK mutant with respect to hag-lacZ expression. Expression of a flgM-lacZ operon fusion is reduced in both sigD and comK mutant cells but is abolished in the sigD comK double mutant. Reverse transcription-PCR examination of the comF-flgM transcript indicates that readthrough from comF into the flgM operon is dependent on ComK. ComK negatively controls the transcription of hag by stimulating the transcription of comF-flgM, thereby increasing the production of the FlgM antisigma factor that inhibits sigmaD activity. There likely exists another comK-independent mechanism of hag transcription that requires mecA and possibly affects the sigmaD concentration in cells undergoing competence development.