Response of Desulfovibrio vulgaris to Alkaline Stress

Department of Civil and Environmental Engineering, University of Washington, Seattle, WA; Physical Bioscience Division, Lawrence Berkeley National Laboratory, CA; Department of Bioengineering, University of California, Berkeley, CA; Oak Ridge National Laboratory, TN; Department of Biochemistry, University of Missouri-Columbia, Columbia, MO; Department of Civil and Environmental Engineering, Temple University, PA; Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA; Institute for Environmental Genomics, Department of Botany and Microbiology University of Oklahoma, Norman, OK; Earth Science Division, Lawrence Berkeley National Laboratory, CA; Virtual Institute of Microbial Stress and Survival

^* To whom correspondence should be addressed. Email: sstolyar{at}washington.edu.

	Abstract

The response of exponentially growing Desulfovibrio vulgaris Hildenborough (DvH) to pH 10 stress was studied using oligonucleotide microarrays and a study set of mutants deleted in genes suggested by microarray data to be involved in alkaline stress response. These data showed that the response of D. vulgaris to increased pH is generally similar to E. coli, but apparently controlled by unique regulatory circuits since the alternative sigma factors (sigma S and E) contributing to this stress response in E. coli appear to be absent in D. vulgaris. Genes previously reported to be up-regulated in E. coli were up-regulated in D. vulgaris, including three ATPase genes and a tryptophan synthase gene. Transcription of chaperone and protease genes (ATP-dependent Clp and La proteases, and DnaK) were also elevated in D. vulgaris. As in E. coli, genes involved in flagella synthesis were down-regulated. The transcriptional data also identified regulators, distinct from sigma S and E, that are likely likely part of a DvH-specific stress response system. Characterization of a study set of mutants deleted in genes implicated in alkaline stress response confirmed a protective involvement of the sodium/proton antiporter NhaC-2, tryptophanase A, and two putative regulators/histidine kinases DVU0331 and DVU2580.