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B

Department of Food Science and Technology, University of California, Davis, CA 95616, USA
ABSTRACT
The general stress response of Bacillus subtilis is triggered by a variety of environmental and metabolic stresses which activate the
B transcription factor. Among the more than 100 genes controlled by
B (the csb genes), the functions identified thus far include resistance to oxidative stress, resistance to protein denaturation and resistance to osmotic stress. To understand the breadth of functions in which csb genes participate, the transcriptional organization and predicted products of two such genes previously identified in a screen for
B-dependent lacZ fusions were analysed. The csb-22::Tn917lacZ and csb-34::Tn917lacZ fusions are unusual among csb genes in that their expression appears to be completely dependent upon
B. By plasmid-integration experiments, fusion analyses and site-directed mutagenesis, stress-inducible,
B-dependent promoters for both these fusions were identified. The csb-34 fusion marked an ORF (yxcC or csbC) which by sequence analysis lay in a monocistronic transcriptional unit. This ORF encoded a predicted 461-residue product which had high identity with Class I sugar transporters of the major facilitator superfamily. It was speculated that the csbC product could serve either a nutritional or an osmotic protection function. In contrast, the csb-22 fusion identified an ORF (ywmG or csbD) which appeared to be the second gene of a two-gene operon. This ORF encoded a predicted 62-residue product which resembled a small Escherichia coli protein of unknown function. The
B-dependent promoter lay immediately upstream from csbD and appeared to be an internal promoter for the operon.
Author for correspondence: Chester W. Price. Tel: + 1 530 752 1596. Fax: + 1 530 752 4759. e-mail: cwprice@ucdavis.edu
Present address: Department of Biological Chemistry, School of Medicine, University of California, Davis, CA 95616, USA.
Present address: College of Pharmacy, Seoul National University, Seoul, South Korea.
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