Journal of Bacteriology, August 1998, p. 4243-4251, Vol. 180, No. 16
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
D-Dependent Gene Expression in Bacillus
subtilis
Department of Biochemistry and Molecular Biology, Louisiana State University Medical Center, Shreveport, Louisiana
Received 23 February 1998/Accepted 28 May 1998
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
D-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
D levels are
observed in mecA mutants grown in competence medium, but no
change in
D 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
D-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
D activity. There likely exists another
comK-independent mechanism of hag transcription
that requires mecA and possibly affects the
D concentration in cells undergoing competence
development.
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