@article{mbs:/content/journal/micro/10.1099/00221287-148-4-1119, author = "Manefield, Michael and Rasmussen, Thomas Bovbjerg and Henzter, Morten and Andersen, Jens Bo and Steinberg, Peter and Kjelleberg, Staffan and Givskov, Michael", title = "Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover", journal= "Microbiology", year = "2002", volume = "148", number = "4", pages = "1119-1127", doi = "https://doi.org/10.1099/00221287-148-4-1119", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/00221287-148-4-1119", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", keywords = "3-oxo-C6-HSL, N-3-oxo-hexanoyl-homoserine lactone", keywords = "intercellular signal", keywords = "AHL, N-acyl-L-homoserine lactone", keywords = "homoserine lactone", keywords = "RFU, relative fluorescence unit", keywords = "Delisea pulchra", abstract = " 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.", }