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Journal of Bacteriology, November 2007, p. 7720-7732, Vol. 189, No. 21
0021-9193/07/$08.00+0     doi:10.1128/JB.01081-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Abh and AbrB Control of Bacillus subtilis Antimicrobial Gene Expression{triangledown}

Mark A. Strauch,1* Benjamin G. Bobay,2 John Cavanagh,2 Fude Yao,1,{dagger} Angelo Wilson,1 and Yoann Le Breton1

Department of Biomedical Sciences, Dental School, University of Maryland, Baltimore, 650 W. Baltimore Street, Baltimore, Maryland 21201,1 Department of Molecular and Structural Biochemistry, North Carolina State University, 128 Polk Hall, Raleigh, North Carolina 276952

Received 9 July 2007/ Accepted 10 August 2007

The Bacillus subtilis abh gene encodes a protein whose N-terminal domain has 74% identity to the DNA-binding domain of the global regulatory protein AbrB. Strains with a mutation in abh showed alterations in the production of antimicrobial compounds directed against some other Bacillus species and gram-positive microbes. Relative to its wild-type parental strain, the abh mutant was found deficient, enhanced, or unaffected for the production of antimicrobial activity. Using lacZ fusions, we examined the effects of abh upon the expression of 10 promoters known to be regulated by AbrB, including five that transcribe well-characterized antimicrobial functions (SdpC, SkfA, TasA, sublancin, and subtilosin). For an otherwise wild-type background, the results show that Abh plays a negative regulatory role in the expression of four of the promoters, a positive role for the expression of three, and no apparent regulatory role in the expression of the other three promoters. Binding of AbrB and Abh to the promoter regions was examined using DNase I footprinting, and the results revealed significant differences. The transcription of abh is not autoregulated, but it is subject to a degree of AbrB-afforded negative regulation. The results indicate that Abh is part of the complex interconnected regulatory system that controls gene expression during the transition from active growth to stationary phase.

* Corresponding author. Mailing address: Department of Biomedical Sciences, Dental School, University of Maryland, Baltimore, 650 W. Baltimore Street, Baltimore, MD 21201. Phone: (410) 706-1815. Fax: (410) 706-0865. E-mail: mstrauch{at}umaryland.edu

{triangledown} Published ahead of print on 24 August 2007.

{dagger} Present address: Biotechnology Research Institute, Guangxi Academy of Agricultural Sciences, 44 Daxue Rd. West, Nanning, Guangxi 530007, People's Republic of China.

Journal of Bacteriology, November 2007, p. 7720-7732, Vol. 189, No. 21
0021-9193/07/$08.00+0     doi:10.1128/JB.01081-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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