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Journal of Bacteriology, April 2009, p. 2285-2295, Vol. 191, No. 7
0021-9193/09/$08.00+0     doi:10.1128/JB.01490-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Pseudomonas aeruginosa Sensor Kinase KinB Negatively Controls Alginate Production through AlgW-Dependent MucA Proteolysis{triangledown}

F. Heath Damron,1 Dongru Qiu,1 and Hongwei D. Yu1,2,3*

Departments of Biochemistry and Microbiology,1 Pediatrics, Joan C. Edwards School of Medicine at Marshall University, Huntington, West Virginia 25755-9320,2 Progenesis Technologies, LLC, Bldg. 740, Rm. 4136, Dow Technology Park, 3200 Kanawha Turnpike, South Charleston, West Virginia 253033

Received 22 October 2008/ Accepted 4 January 2009

Mucoidy, or overproduction of the exopolysaccharide known as alginate, in Pseudomonas aeruginosa is a poor prognosticator for lung infections in cystic fibrosis. Mutation of the anti-{sigma} factor MucA is a well-accepted mechanism for mucoid conversion. However, certain clinical mucoid strains of P. aeruginosa have a wild-type (wt) mucA. Here, we describe a loss-of-function mutation in kinB that causes overproduction of alginate in the wt mucA strain PAO1. KinB is the cognate histidine kinase for the transcriptional activator AlgB. Increased alginate production due to inactivation of kinB was correlated with high expression at the alginate-related promoters PalgU and PalgD. Deletion of alternative {sigma} factor RpoN ({sigma}54) or the response regulator AlgB in kinB mutants decreased alginate production to wt nonmucoid levels. Mucoidy was restored in the kinB algB double mutant by expression of wt AlgB or phosphorylation-defective AlgB.D59N, indicating that phosphorylation of AlgB was not required for alginate overproduction when kinB was inactivated. The inactivation of the DegS-like protease AlgW in the kinB mutant caused loss of alginate production and an accumulation of the hemagglutinin (HA)-tagged MucA. Furthermore, we observed that the kinB mutation increased the rate of HA-MucA degradation. Our results also indicate that AlgW-mediated MucA degradation required algB and rpoN in the kinB mutant. Collectively, these studies indicate that KinB is a negative regulator of alginate production in wt mucA strain PAO1.

* Corresponding author. Mailing address: Robert C. Byrd Biotechnology Science Center, 1 John Marshall Drive, Huntington, WV 25755-9320. Phone: (304) 696-7356. Fax: (304) 696-7207. E-mail: yuh{at}marshall.edu

{triangledown} Published ahead of print on 23 January 2009.

Journal of Bacteriology, April 2009, p. 2285-2295, Vol. 191, No. 7
0021-9193/09/$08.00+0     doi:10.1128/JB.01490-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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