Activating virulence pathways in response to surface contact is an efficient strategy for the survival of Pseudomonas aeruginosa (PA) during its transition from planktonic to sessile growth, both in the environment and in human infections. We have previously shown that retraction of the type IV pilus (TFP) leads to activation of the Chp chemosensory system.  This in turn activates the membrane-bound adenylate cyclase CyaB, the primary source of cyclic AMP (cAMP) in PA. cAMP binds to the transcriptional activator Vfr to induce transcription of >200 genes, including virulence-associated secretion systems. We have employed multiple approaches to dissect this mechanochemical signaling (MCS) pathway. Our work suggests that the chemoreceptor PilJ functions as an unconventional receptor with multiple direct binding partners. PilJ couples mechanical input (depolymerized pilin monomer) to activation of a complex phosphorelay. In addition, PilJ binds directly to two additional outputs,  PilH and to CyaB, thus coupling phosphorelay to cAMP production and activation of virulence genes.