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Journal of Bacteriology, November 2002, p. 6123-6129, Vol. 184, No. 22
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.22.6123-6129.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Regulation of the Bacillus subtilis bcrC Bacitracin Resistance Gene by Two Extracytoplasmic Function {sigma} Factors

Min Cao and John D. Helmann*

Department of Microbiology, Cornell University, Ithaca, New York 14853-8101

Received 17 June 2002/ Accepted 20 August 2002

Bacitracin resistance is normally conferred by either of two major mechanisms, the BcrABC transporter, which pumps out bacitracin, or BacA, an undecaprenol kinase that provides C55-isoprenyl phosphate by de novo synthesis. We demonstrate that the Bacillus subtilis bcrC (ywoA) gene, encoding a putative bacitracin transport permease, is an important bacitracin resistance determinant. A bcrC mutant strain had an eightfold-higher sensitivity to bacitracin. Expression of bcrC initiated from a single promoter site that could be recognized by either of two extracytoplasmic function (ECF) {sigma} factors, {sigma}X or {sigma}M. Bacitracin induced expression of bcrC, and this induction was dependent on {sigma}M but not on {sigma}X. Under inducing conditions, expression was primarily dependent on {sigma}M. As a consequence, a sigM mutant was fourfold more sensitive to bacitracin, while the sigX mutant was only slightly sensitive. A sigX sigM double mutant was similar to a bcrC mutant in sensitivity. These results support the suggestion that one function of B. subtilis ECF {sigma} factors is to coordinate antibiotic stress responses.

* Corresponding author. Mailing address: Department of Microbiology, Cornell University, Ithaca, NY 14853-8101. Phone: (607) 255-6570. Fax: (607) 255-3904. E-mail: jdh9{at}cornell.edu.

Journal of Bacteriology, November 2002, p. 6123-6129, Vol. 184, No. 22
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.22.6123-6129.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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