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Journal of Bacteriology, November 2008, p. 7043-7051, Vol. 190, No. 21
0021-9193/08/$08.00+0     doi:10.1128/JB.00753-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

PqsE Functions Independently of PqsR-Pseudomonas Quinolone Signal and Enhances the rhl Quorum-Sensing System

John M. Farrow III, Zoe M. Sund, Matthew L. Ellison, Dana S. Wade, James P. Coleman, and Everett C. Pesci^*

Department of Microbiology and Immunology, The Brody School of Medicine at East Carolina University, 600 Moye Boulevard, Greenville, North Carolina 27834

Received 27 May 2008/ Accepted 25 August 2008

Pseudomonas aeruginosa is an opportunistic pathogen that causes both acute and chronic infections in immunocompromised individuals. This gram-negative bacterium produces a battery of virulence factors that allow it to infect and survive in many different hostile environments. The control of many of these virulence factors falls under the influence of one of three P. aeruginosa cell-to-cell signaling systems. The focus of this study, the quinolone signaling system, functions through the Pseudomonas quinolone signal (PQS), previously identified as 2-heptyl-3-hydroxy-4-quinolone. This signal binds to and activates the LysR-type transcriptional regulator PqsR (also known as MvfR), which in turn induces the expression of the pqsABCDE operon. The first four genes of this operon are required for PQS synthesis, but the fifth gene, pqsE, is not. The function of the pqsE gene is not known, but it is required for the production of multiple PQS-controlled virulence factors and for virulence in multiple models of infection. In this report, we show that PqsE can activate PQS-controlled genes in the absence of PqsR and PQS. Our data also suggest that the regulatory activity of PqsE requires RhlR and indicate that a pqsE mutant can be complemented for pyocyanin production by a large excess of exogenous N-butyryl homoserine lactone (C₄-HSL). Finally, we show that PqsE enhances the ability of Escherichia coli expressing RhlR to respond to C₄-HSL. Overall, our data lead us to conclude that PqsE functions as a regulator that is independent of PqsR and PQS but dependent on the rhl quorum-sensing system.

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* Corresponding author. Mailing address: Department of Microbiology and Immunology, East Carolina University School of Medicine, BT 132, 600 Moye Blvd., Greenville, NC 27834. Phone: (252) 744-2351. Fax: (252) 744-3535. E-mail: pescie{at}ecu.edu

Published ahead of print on 5 September 2008.

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Journal of Bacteriology, November 2008, p. 7043-7051, Vol. 190, No. 21
0021-9193/08/$08.00+0     doi:10.1128/JB.00753-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

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