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M is induced by phosphate depletion in Bacillus subtilis W23

Département de Microbiologie Fondamentale, Bâtiment de Biologie, Université de Lausanne, CH-1015 Lausanne, Switzerland
Correspondence
Kathrin Minnig
kathrin.minnig{at}hispeed.ch
The expression of the Bacillus subtilis W23 tar genes specifying the biosynthesis of the major wall teichoic acid, the poly(ribitol phosphate), was studied under phosphate limitation using lacZ reporter fusions. Three different regulation patterns can be deduced from these
-galactosidase activity data: (i) tarD and tarL gene expression is downregulated under phosphate starvation; (ii) tarA and, to a minor extent, tarB expression after an initial decrease unexpectedly increases; and (iii) tarO is not influenced by phosphate concentration. To dissect the tarA regulatory pattern, its two promoters were analysed under phosphate limitation: The PtarA-ext promoter is repressed under phosphate starvation by the PhoPR two-component system, whereas, under the same conditions, the PtarA-int promoter is upregulated by the action of an extracytoplasmic function (ECF)
factor,
M. In contrast to strain 168,
M is activated in strain W23 in phosphate-depleted conditions, a phenomenon indirectly dependent on PhoPR, the two-component regulatory system responsible for the adaptation to phosphate starvation. These results provide further evidence for the role of
M in cell-wall stress response, and suggest that impairment of cell-wall structure is the signal activating this ECF
factor.
The GenBank/EMBL/DDBJ accession number for the sequence reported in this paper is AJ889011
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