RhlRRhlI

RhlRRhlI refers to the quorum-sensing components RhlR and RhlI in Pseudomonas aeruginosa, collectively forming the RhlR–RhlI system. RhlI encodes an autoinducer synthase that produces N-butyryl-L-homoserine lactone (C4-HSL). RhlR encodes a LuxR-type transcription factor that binds C4-HSL; the RhlR–C4-HSL complex activates transcription of a regulon involved in virulence, surface behaviors, and metabolism, including genes for rhamnolipid biosynthesis (rhlA and rhlB) and other virulence factors such as pyocyanin and proteases. In the absence of C4-HSL, RhlR can act as a repressor for certain targets, while binding of the ligand generally converts it into a transcriptional activator.

The RhlI/RhlR system operates within a broader quorum-sensing network that is hierarchically organized with the Las system. LasI/LasR synthesize and respond to 3-oxo-C12-HSL, which promotes expression of rhlR and, indirectly, rhlI. The C4-HSL–RhlR complex then gates the expression of a subset of genes that coordinate virulence factor production, rhamnolipid synthesis, swarming motility, and biofilm architecture. This arrangement allows P. aeruginosa to tailor community behaviors to cell density and environmental cues.

Mutants lacking RhlI fail to produce C4-HSL and show reduced activation of RhlR-regulated genes; providing exogenous C4-HSL can restore some activities in certain contexts. Conversely, RhlR mutants cannot respond to C4-HSL, effectively blocking the RhlR regulon. Because the RhlR–RhlI module controls key pathogenic traits, it is a focus of research into antivirulence strategies and quorum-sensing inhibitors.