The Relationship ofpqsGene Expression to Acylhomoserine Lactone Signaling inPseudomonas aeruginosa

Abstract

ABSTRACTThe opportunistic pathogenPseudomonas aeruginosahas complex quorum sensing (QS) circuitry, which involves two acylhomoserine lactone (AHL) systems, the LasI AHL synthase and LasR AHL-dependent transcriptional activator system and the RhlI AHL synthase-RhlR AHL-responsive transcriptional activator. There is also a quinoline signaling system (thePseudomonasquinolone signal, PQS, system). Although there is a core set of genes regulated by the AHL circuits, there is substantial strain-to-strain variation in the non-core QS regulated genes. Reductive evolution of the QS regulon, and variation in specific genes activated by QS, occurs in laboratory evolution experiments with the model strain PAO1. We used a transcriptomics approach to test the hypothesis that reductive evolution in the PAO1 QS regulon can in large part be explained by a simple null mutation inpqsR, the gene encoding the transcriptional activator of thepqsoperon. We found that PqsR had very little influence on the AHL QS regulon. This was a surprising finding because the last gene in the PqsR-dependentpqsoperon,pqsE, codes for a protein, which physically interacts with RhlR and this interaction is required for RhlR-dependent activation of some genes. We used comparative transcriptomics to examine the influence of apqsEmutation on the QS regulon and identified only three transcripts, which were strictly dependent on PqsE. By using reporter constructs we showed that the PqsE influence on other genes was dependent on experimental conditions and we have gained some insight about those conditions. This work adds to our understanding of the plasticity of theP. aeruginosaQS regulon and to the role PqsE plays in RhlR-dependent gene activation.