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Journal of Bacteriology, September 2007, p. 6266-6275, Vol. 189, No. 17
0021-9193/07/$08.00+0     doi:10.1128/JB.00629-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Expression of hurP, a Gene Encoding a Prospective Site 2 Protease, Is Essential for Heme-Dependent Induction of bhuR in Bordetella bronchiseptica{triangledown}

Natalie D. King-Lyons, Kelsy F. Smith, and Terry D. Connell*

The Witebsky Center for Microbial Pathogenesis and Immunology and The Department of Microbiology and Immunology, The School of Medicine and Biomedical Sciences, The University at Buffalo, The State University of New York, Buffalo, New York 14214

Received 23 April 2007/ Accepted 15 June 2007

Expression of the hurIR bhuRSTUV heme utilization locus in Bordetella bronchiseptica is coordinately controlled by the global iron-dependent regulator Fur and the extracytoplasmic function sigma factor HurI. Activation of HurI requires transduction of a heme-dependent signal via HurI, HurR, and BhuR, a three-component heme-dependent regulatory system. In silico searches of the B. bronchiseptica genome to identify other genes that encode additional participants in this heme-dependent regulatory cascade revealed hurP, an open reading frame encoding a polypeptide with homology to (i) RseP, a site 2 protease (S2P) of Escherichia coli required for modifying the cytoplasmic membrane protein RseA, and (ii) YaeL, an S2P of Vibrio cholerae required for modification of the cytoplasmic membrane protein TcpP. A mutant of B. bronchiseptica defective for hurP was incapable of regulating expression of BhuR in a heme-dependent manner. Furthermore, the hurP mutant was unable to utilize hemin as a sole source of nutrient Fe. These defects in hemin utilization and heme-dependent induction of BhuR were restored when recombinant hurP (or recombinant rseP) was introduced into the mutant. Introduction of hurP into a yaeL mutant of V. cholerae also complemented its S2P defect. These data provided strong evidence that protease activity and cleavage site recognition was conserved in HurP, RseP, and YaeL. The data are consistent with a model in which HurP functionally modifies HurR, a sigma factor regulator that is essential for heme-dependent induction of bhuR.

* Corresponding author. Mailing address: 138 Farber Hall, Department of Microbiology and Immunology, The University at Buffalo, 3435 Main St., Buffalo, NY 14221. Phone: (716) 829-3364. Fax: (716) 829-2158. E-mail: connell{at}acsu.buffalo.edu

{triangledown} Published ahead of print on 22 June 2007.

Journal of Bacteriology, September 2007, p. 6266-6275, Vol. 189, No. 17
0021-9193/07/$08.00+0     doi:10.1128/JB.00629-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





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