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Journal of Bacteriology, September 2004, p. 6150-6158, Vol. 186, No. 18
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.18.6150-6158.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

RsbV-Independent Induction of the SigB-Dependent General Stress Regulon of Bacillus subtilis during Growth at High Temperature

Gudrun Holtmann,1,{dagger} Matthias Brigulla,1,2,3 Leif Steil,1,2,3 Alexandra Schütz,1,2 Karsta Barnekow,3 Uwe Völker,1,2,3 and Erhard Bremer1*

Laboratory for Microbiology, Department of Biology, Philipps-University Marburg,1 Max-Planck-Institute for Terrestrial Microbiology, Marburg,2 Laboratory for Functional Genomics, Medical Faculty, Ernst-Moritz-Arndt-University, Greifswald, Germany3

Received 17 March 2004/ Accepted 23 June 2004

General stress proteins protect Bacillus subtilis cells against a variety of environmental insults. This adaptive response is particularly important for nongrowing cells, to which it confers a multiple, nonspecific, and preemptive stress resistance. Induction of the general stress response relies on the alternative transcription factor, SigB, whose activity is controlled by a partner switching mechanism that also involves the anti-sigma factor, RsbW, and the antagonist protein, RsbV. Recently, the SigB regulon has been shown to be continuously induced and functionally important in cells actively growing at low temperature. With the exception of this chill induction, all SigB-activating stimuli identified so far trigger a transient expression of the SigB regulon that depends on RsbV. Through a proteome analysis and Northern blot and gene fusion experiments, we now show that the SigB regulon is continuously induced in cells growing actively at 51°C, close to the upper growth limit of B. subtilis. This heat induction of SigB-dependent genes requires the environmental stress-responsive phosphatase RsbU, but not the metabolic stress-responsive phosphatase RsbP. RsbU dependence of SigB activation by heat is overcome in mutants that lack RsbV. In addition, loss of RsbV alone or in combination with RsbU triggers a hyperactivation of the general stress regulon exclusively at high temperatures detrimental for cell growth. These new facets of heat induction of the SigB regulon indicate that the current view of the complex genetic and biochemical regulation of SigB activity is still incomplete and that SigB perceives signals independent of the RsbV-mediated signal transduction pathways under heat stress conditions.

* Corresponding author. Mailing address: Laboratory for Microbiology, Department of Biology, Philipps-University Marburg, Karl-von-Frisch-Str., D-35032 Marburg, Federal Republic of Germany. Phone: 49-6421-2821529. Fax: 49-6421-2828979. E-mail: bremer{at}staff.uni-marburg.de.

{dagger} Present address: 3M Deutschland GmbH, 41453 Neuss, Germany.

Journal of Bacteriology, September 2004, p. 6150-6158, Vol. 186, No. 18
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.18.6150-6158.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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