This Article Full Text Full Text (PDF) Other Versions of this Article: JB.00756-07v1 189/17/6168    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Reeves, A. Articles by Haldenwang, W. G. Search for Related Content PubMed PubMed Citation Articles by Reeves, A. Articles by Haldenwang, W. G.

ClpP Modulates the Activity of the Bacillus subtilis Stress Response Transcription Factor, ^B

Department of Microbiology and Immunology, MC7758, University of Texas Health Science Center, San Antonio, Texas 78229-3900,¹ Institute for Microbiology,² Interfacultary Institute for Genetics and Functional Genomics, Ernst Moritz Arndt University Interfaculty, Greifswald, Germany³

Received 14 May 2007/ Accepted 18 June 2007

The general stress regulon of Bacillus subtilis is controlled by the activity state of ^B, a transcription factor that is switched on following exposure to either physical or nutritional stress. ClpP is the proteolytic component of an ATP-dependent protease that is essential for the proper regulation of multiple adaptive responses in B. subtilis. Among the proteins whose abundance increases in ClpP^– B. subtilis are several known to depend on ^B for their expression. In the current work we examine the relationship of ClpP to the activity of ^B. The data reveal that the loss of ClpP in otherwise wild-type B. subtilis results in a small increase in ^B activity during growth and a marked enhancement of ^B activity following its induction by either physical or nutritional stress. It appears to be the persistence of ^B's activity rather than its induction that is principally affected by the loss of ClpP. ^B-dependent reporter gene activity rose in parallel in ClpP⁺ and ClpP^– B. subtilis strains but failed to display its normal transience in the ClpP^– strain. The putative ClpP targets are likely to be stress generated and novel. Enhanced ^B activity in ClpP^– B. subtilis was triggered by physical stress but not by the induced synthesis of the physical stress pathway's positive regulator (RsbT). In addition, Western blot analyses failed to detect differences in the levels of the principal known ^B regulators in ClpP⁺ and ClpP^– B. subtilis strains. The data suggest a model in which ClpP facilitates the turnover of stress-generated factors, which persist in ClpP's absence to stimulate ongoing ^B activity.

Published ahead of print on 22 June 2007.