RT Journal Article SR Electronic(1) A1 Manefield, Michael A1 Rasmussen, Thomas Bovbjerg A1 Henzter, Morten A1 Andersen, Jens Bo A1 Steinberg, Peter A1 Kjelleberg, Staffan A1 Givskov, MichaelYR 2002 T1 Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover JF Microbiology, VO 148 IS 4 SP 1119 OP 1127 DO https://doi.org/10.1099/00221287-148-4-1119 PB Microbiology Society, SN 1465-2080, AB N-acyl-L-homoserine lactones (AHLs) are co-regulatory ligands required for control of the expression of genes encoding virulence traits in many Gram-negative bacterial species. Recent studies have indicated that AHLs modulate the cellular concentrations of LuxR-type regulatory proteins by binding and fortifying these proteins against proteolytic degradation (Zhu & Winans, 2001 R43 ). Halogenated furanones produced by the macroalga Delisea pulchra inhibit AHL-dependent gene expression. This study assayed for an in vivo interaction between a tritiated halogenated furanone and the LuxR protein of Vibrio fischeri overproduced in Escherichia coli. Whilst a stable interaction between the algal metabolite and the bacterial protein was not found, it was noted by Western analysis that the half-life of the protein is reduced up to 100-fold in the presence of halogenated furanones. This suggests that halogenated furanones modulate LuxR activity but act to destabilize, rather than protect, the AHL-dependent transcriptional activator. The furanone-dependent reduction in the cellular concentration of the LuxR protein was associated with a reduction in expression of a plasmid encoded P luxI –gfp(ASV) fusion suggesting that the reduction in LuxR concentration is the mechanism by which furanones control expression of AHL-dependent phenotypes. The mode of action by which halogenated furanones reduce cellular concentrations of the LuxR protein remains to be characterized., UL https://www.microbiologyresearch.org/content/journal/micro/10.1099/00221287-148-4-1119