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Journal of Bacteriology, August 2006, p. 5896-5903, Vol. 188, No. 16
0021-9193/06/$08.00+0     doi:10.1128/JB.01960-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Salicylic Acid Activates Sigma Factor B by rsbU-Dependent and -Independent Mechanisms

Marco Palma,^1, Arnold Bayer,^2,3* Leon I. Kupferwasser,^2, Tammy Joska,¹ Michael R. Yeaman,^2,3 and Ambrose Cheung¹

Department of Microbiology, Dartmouth Medical School, Hanover, New Hampshire 03755,¹ Division of Infectious Diseases, LA Biomedical Research Institute at Harbor-UCLA, Torrance, California 90502,² and Geffen School of Medicine at UCLA, Los Angeles, California 90024³

Received 21 December 2005/ Accepted 22 May 2006

Salicylic acid (SAL) may impact Staphylococcus aureus virulence by activating the sigB operon (rsbU-V-W-sigB), thus leading to reductions in alpha-toxin production and decreased fibronectin binding (L. I. Kupferwasser et al., J. Clin. Investig. 112:222-233, 2003). As these prior studies were performed in strain RN6390 (an rsbU mutant) and its rsbU-repaired variant, SH1000, the current investigation was designed to determine if the SAL effect occurs via rsbU- and/or rsbV-dependent pathways in an rsbU-intact S. aureus strain (FDA486). We thus quantified the transcription from two sigB-dependent promoters (asp23 and sarA P3) in FDA486 in response to SAL exposure in vitro, using isogenic single-knockout constructs of rsbU, rsbV, or rsbW and a green fluorescent protein reporter system. SAL induced sarA P3 and asp23 promoter activities in a dose-dependent manner in the parental strain. In contrast, sigB activation by SAL was progressively more mitigated in the rsbU and rsbV mutants. As predicted, SAL caused significant reductions in both alpha-toxin production and fibrinogen and fibronectin binding in the parental strain. The extent of these reductions, compared with the parent, was reduced in the rsb mutants (rsbV > rsbU), especially at low SAL concentrations. Since generation of the free SigB protein usually requires a sequential rsbU-V-W-sigB activation cascade, the present phenotypic and genotypic data suggest key roles for both rsbU and rsbV in SAL-mediated activation of sigB in strains with a fully intact sigB operon.

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* Corresponding author. Mailing address: LA Biomedical Research Institute at Harbor-UCLA, 1124 W. Carson Street, Bldg RB2, Room 225, Torrance, CA 90502. Phone: (310) 222-6422. Fax: (310) 782-2016. E-mail: Bayer{at}humc.edu.

Present address: Departments of Microbiology and Immunology, Medical College of Cornell University, New York, NY 10021.

Present address: Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048.

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Journal of Bacteriology, August 2006, p. 5896-5903, Vol. 188, No. 16
0021-9193/06/$08.00+0     doi:10.1128/JB.01960-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

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