RhlR

RhlR is a transcriptional regulator of the quorum-sensing system in the bacterium Pseudomonas aeruginosa. It belongs to the LuxR family of cytoplasmic transcription factors and acts as the receptor for the autoinducer N-butyryl-L-homoserine lactone (C4-HSL), produced by the synthase RhlI. Upon accumulation of C4-HSL, RhlR binds the ligand, dimerizes, and binds to promoter regions containing LuxR-type DNA binding motifs to regulate transcription.

The primary regulon of RhlR includes genes required for rhamnolipid biosynthesis, notably the rhlAB operon, and several other loci involved in biofilm maturation, swarming motility, and virulence factor production. The activity of RhlR is integrated with the Las quorum-sensing system (LasI/LasR) as LasR positively influences rhlI expression, linking the two networks, as well as with the Pseudomonas quinolone signal (PQS) system in a complex regulatory circuit. In some contexts, RhlR-dependent regulation can persist in otherwise LasR-defective strains, underscoring its potential role in virulence when Las signaling is compromised.

Structure-function: Like other LuxR-type regulators, RhlR has an N-terminal autoinducer binding domain and a C-terminal DNA-binding domain. Ligand binding promotes conformational change and dimerization, enabling binding to target promoters and transcriptional control.

Clinical and scientific significance: RhlR contributes to the production of rhamnolipids, biofilm architecture, motility, and virulence traits. Because it can drive pathogenic behavior in LasR-defective backgrounds, RhlR is of interest as a target for anti-virulence strategies aimed at disarming rather than killing P. aeruginosa.