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Journal of Bacteriology, November 2006, p. 7823-7829, Vol. 188, No. 22
0021-9193/06/$08.00+0     doi:10.1128/JB.00525-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

plcR papR-Independent Expression of Anthrolysin O by Bacillus anthracis{triangledown}

Caná L. Ross and Theresa M. Koehler*

Department of Microbiology and Molecular Genetics, The University of Texas-Houston Health Science Center Medical School, Houston, Texas 77030

Received 12 April 2006/ Accepted 29 August 2006

Cholesterol-dependent cytolysins (CDCs) are secreted, pore-forming toxins that are associated with pathogenesis in a variety of gram-positive bacteria. Bacillus anthracis produces anthrolysin O (ALO), a CDC that is largely responsible for the hemolytic activity of culture supernates when the bacterium is cultured in appropriate conditions. B. cereus and B. thuringiensis, species closely related to B. anthracis, produce CDCs with significant amino acid sequence homology to ALO. Transcription of the B. cereus and B. thuringiensis CDC genes is controlled by PlcR, a transcription regulator that requires a pentapeptide derived from the papR gene product for binding to a consensus sequence (PlcR box) and transcriptional activation of downstream genes. A PlcR box precedes the B. anthracis alo gene, and the B. anthracis genome contains three plcR-like genes, one of which harbors a nonsense mutation that is predicted to result in a truncated, nonfunctional protein. We detected mRNA of alo, papR, and the three plcR-like genes in spleens of B. anthracis-infected mice, indicating gene expression in vivo. Analysis of alo transcription in batch culture revealed a potential transcription start located between the PlcR box and the translational start. Nevertheless, steady-state levels of alo transcripts and ALO protein were unaffected by deletion of papR or disruption of the PlcR box. Our data indicate that despite the presence of the transcriptionally active plcR and papR genes in B. anthracis and a PlcR box in the promoter region of the alo gene, alo expression is independent of this control system.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Genetics, University of Texas—Houston Medical School, 6431 Fannin St., JFB 1.765, Houston, TX 77030. Phone: (713) 500-5450. Fax: (713) 500-5499. E-mail: Theresa.M.Koehler{at}uth.tmc.edu.

{triangledown} Published ahead of print on 15 September 2006.

Journal of Bacteriology, November 2006, p. 7823-7829, Vol. 188, No. 22
0021-9193/06/$08.00+0     doi:10.1128/JB.00525-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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