PqsE Functions Independently of PqsR-PseudomonasQuinolone Signal and Enhances therhlQuorum-Sensing System

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Abstract
Pseudomonas aeruginosais 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 threeP. aeruginosacell-to-cell signaling systems. The focus of this study, the quinolone signaling system, functions through thePseudomonasquinolone 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 thepqsABCDEoperon. The first four genes of this operon are required for PQS synthesis, but the fifth gene,pqsE, is not. The function of thepqsEgene 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 apqsEmutant can be complemented for pyocyanin production by a large excess of exogenousN-butyryl homoserine lactone (C4-HSL). Finally, we show that PqsE enhances the ability ofEscherichia coliexpressing 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 therhlquorum-sensing system.

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