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Response of Desulfovibrio vulgaris to Alkaline Stress
Author(s) -
Sergey Stolyar,
Qiang He,
Marcin P. Joachimiak,
Zhili He,
Zamin K. Yang,
Sharon Borglin,
Dominique C. Joyner,
Katherine Huang,
Eric J. Alm,
Terry C. Hazen,
Jizhong Zhou,
Judy D. Wall,
Adam P. Arkin,
David A. Stahl
Publication year - 2007
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.00284-07
Subject(s) - biology , desulfovibrio vulgaris , sigma factor , mutant , gene , antiporter , response regulator , escherichia coli , microbiology and biotechnology , biochemistry , genetics , rna polymerase , bacteria , membrane
The response of exponentially growing Desulfovibrio vulgaris Hildenborough to pH 10 stress was studied using oligonucleotide microarrays and a study set of mutants with genes suggested by microarray data to be involved in the alkaline stress response deleted. The data showed that the response of D. vulgaris to increased pH is generally similar to that of Escherichia coli but is apparently controlled by unique regulatory circuits since the alternative sigma factors (sigma S and sigma 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; these genes included three ATPase genes and a tryptophan synthase gene. Transcription of chaperone and protease genes (encoding ATP-dependent Clp and La proteases and DnaK) was also elevated in D. vulgaris. As in E. coli, genes involved in flagellum synthesis were down-regulated. The transcriptional data also identified regulators, distinct from sigma S and sigma E, that are likely part of a D. vulgaris Hildenborough-specific stress response system. Characterization of a study set of mutants with genes implicated in alkaline stress response deleted confirmed that there was protective involvement of the sodium/proton antiporter NhaC-2, tryptophanase A, and two putative regulators/histidine kinases (DVU0331 and DVU2580).

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