Pseudomonas aeruginosa is an opportunistic bacterial pathogen. Many of its virulence genes are regulated by quorum sensing (QS), a form of cell-to-cell communication. P. aeruginosa QS consists of three interlinked circuits, LasI-R, Rhl-R, and Pseudomonas quinolone signal (PQS). Additionally, its QS system is interconnected with other regulatory networks, which help optimize gene expression under variable conditions. The numbers of genes regulated by QS differ substantially among P. aeruginosa strains. We show that a regulatory factor MexT, which is activated in response to certain antibiotics, downregulates the RhlI-R circuit and in turn measurably lowers virulence in a nematode worm infection model. Our findings help understand how existing and future therapeutic interventions for P. aeruginosa infections may impact this bacterium's gene regulation and physiology.
Keywords: acyl-homoserine lactone; bacterial communication; gene regulation.