LuxR-family quorum sensing receptor (LuxR)

LuxR-family quorum sensing receptors are bacterial transcription factors that play a central role in density-dependent gene regulation, primarily in Gram-negative bacteria (Papenfort & Bassler, 2016). These receptors function by binding small signaling molecules known as N-acyl homoserine lactones (AHLs) produced by the bacteria themselves (Churchill & Chen, 2011). Once the AHL concentration reaches a critical threshold, the LuxR-type protein undergoes a conformational change, often leading to dimerization and subsequent binding to specific DNA promoter regions called lux boxes (UniProt P12746). This process triggers the synchronized expression of genes responsible for virulence, biofilm development, and antibiotic resistance (Defoirdt, 2018). Because LuxR-family receptors control the pathogenic potential of bacteria like Pseudomonas aeruginosa and Burkholderia cepacia, they are highly attractive targets for anti-virulence drug development (Hentzer et al., 2003). Targeting these receptors aims to disarm the bacteria rather than killing them, which may exert less selective pressure for the development of resistance compared to traditional antibiotics (Galloway et al., 2011).

Other names

LuxR-type transcriptional regulatorLuxR homologAHL-responsive transcriptional regulatorQuorum-sensing transcriptional activatorLuxR-family protein

Antagonism of the N-acyl homoserine lactone (AHL) binding site, inhibition of receptor dimerization, or blocking of the C-terminal DNA-binding domain to prevent the transcriptional activation of virulence and biofilm-related genes (Defoirdt, 2018; Churchill & Chen, 2011).