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Journal of Bacteriology, October 2003, p. 5714-5721, Vol. 185, No. 19
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.19.5714-5721.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

RelA Is a Component of the Nutritional Stress Activation Pathway of the Bacillus subtilis Transcription Factor {sigma}B

Shuyu Zhang and W. G. Haldenwang*

Department of Microbiology and Immunology, University of Texas Health Science Center, San Antonio, Texas 78229-3900

Received 6 March 2003/ Accepted 3 July 2003

The general stress regulon of Bacillus subtilis is induced by the activation of the {sigma}B transcription factor. Activation of {sigma}B occurs when one of two phosphatases (RsbU and RsbP), each responding to a unique type of stress, actuates a positive regulator of {sigma}B by dephosphorylation. Nutritional stress triggers the RsbP phosphatase. The mechanism by which RsbP becomes active is unknown; however, its activation coincides with culture conditions that are likely to reduce the cell's levels of high-energy nucleotides. We now present evidence that RelA, a (p)ppGpp synthetase and the key enzyme of the stringent response, plays a role in nutritional stress activation of {sigma}B. An insertion mutation that disrupts relA blocks the activation of {sigma}B in response to PO4 or glucose limitation and inhibits the drop in ATP/GTP levels that normally accompanies {sigma}B induction under these conditions. In contrast, the activation of {sigma}B by physical stress (e.g., ethanol treatment) is not affected by the loss of RelA. RelA's role in {sigma}B activation appears to be distinct from its participation in the stringent response. Amino acid analogs which induce the stringent response and RelA-dependent (p)ppGpp synthesis do not trigger {sigma}B activity. In addition, neither a missense mutation in relA (relA240GE) nor a null mutation in rplK (rplK54), either of which is sufficient to inhibit the stringent response and RelA-dependent (p)ppGpp synthesis, fails to block {sigma}B activation by PO4 or glucose limitation.

* Corresponding author. Mailing address: Department of Microbiology & Immunology, MSC 7758, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900. Phone: (210) 567-3957. Fax: (210) 567-6612. E-mail: haldenwang{at}uthscsa.edu.

Journal of Bacteriology, October 2003, p. 5714-5721, Vol. 185, No. 19
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.19.5714-5721.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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