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PhoR autokinase activity is controlled by an intermediate in wall teichoic acid metabolism that is sensed by the intracellular PAS domain during the PhoPR-mediated phosphate limitation response of Bacillus subtilis.

Authors :
Botella E
Devine SK
Hubner S
Salzberg LI
Gale RT
Brown ED
Link H
Sauer U
Codée JD
Noone D
Devine KM
Source :
Molecular microbiology [Mol Microbiol] 2014 Dec; Vol. 94 (6), pp. 1242-59. Date of Electronic Publication: 2014 Nov 11.
Publication Year :
2014

Abstract

The PhoPR two-component signal transduction system controls one of the major responses to phosphate limitation in Bacillus subtilis. When activated it directs expression of phosphate scavenging enzymes, lowers synthesis of the phosphate-rich wall teichoic acid (WTA) and initiates synthesis of teichuronic acid, a non-phosphate containing replacement anionic polymer. Despite extensive knowledge of this response, the signal to which PhoR responds has not been identified. Here we report that one of the main functions of the PhoPR two-component system in B. subtilis is to monitor WTA metabolism. PhoR autokinase activity is controlled by the level of an intermediate in WTA synthesis that is sensed through the intracellular PAS domain. The pool of this intermediate generated by WTA synthesis in cells growing under phosphate-replete conditions is sufficient to inhibit PhoR autokinase activity. However WTA synthesis is lowered upon phosphate limitation by the combined effects of PhoP ∼ P-mediated activation of tuaA-H transcription and repression of tagAB. These transcriptional changes combine to lower the level of the inhibitory WTA metabolite thereby increasing PhoR autokinase activity. This amplifies the PHO response with full induction being achieved ∼ 90 min after the onset of phosphate limitation.<br /> (© 2014 John Wiley & Sons Ltd.)

Details

Language :
English
ISSN :
1365-2958
Volume :
94
Issue :
6
Database :
MEDLINE
Journal :
Molecular microbiology
Publication Type :
Academic Journal
Accession number :
25315493
Full Text :
https://doi.org/10.1111/mmi.12833