LuxR-type quorum sensing receptors (LuxR-type QS receptors)

LuxR-type quorum sensing (QS) receptors in Pseudomonas aeruginosa, primarily LasR, RhlR, and QscR, are cytoplasmic transcription factors that regulate approximately 10% of the bacterial genome in response to population density [1.1.1, 1.2.2]. These receptors function by binding specific N-acyl-homoserine lactone (AHL) signaling molecules, such as N-(3-oxododecanoyl)-L-homoserine lactone (3-oxo-C12-HSL) and N-butyryl-L-homoserine lactone (C4-HSL), which stabilize the proteins and promote dimerization and DNA binding [1.1.2, 1.4.3, 1.5.1]. This regulatory network coordinates the expression of critical virulence factors, including pyocyanin, elastase, and rhamnolipids, and is essential for the formation and maturation of biofilms [1.3.1, 1.5.3]. Because these receptors are central to the pathogen's ability to establish chronic infections, particularly in cystic fibrosis and burn wounds, they are significant therapeutic targets for anti-virulence drugs [1.3.3, 1.4.1]. Experimental inhibitors like V-06-018, meta-bromo-thiolactone (mBTL), and norlobaridone aim to disrupt these pathways by competing for the ligand-binding site or destabilizing the receptor's quaternary structure [1.2.2, 1.4.3, 1.4.5]. Unlike traditional antibiotics, these quorum sensing inhibitors (QSIs) seek to attenuate pathogenicity without exerting strong selective pressure for survival, potentially reducing the emergence of resistance [1.4.2, 1.4.3].

Other names

LasRRhlRQscRLuxR homologsQuorum sensing transcription factorsAcyl-homoserine lactone receptors

Inhibition of signal binding, prevention of receptor dimerization, promotion of receptor degradation, and inhibition of DNA binding to attenuate virulence gene expression.