Quorum sensing and its potential application to vibriosis

Abstract

Quorum sensing is a gene regulatory mechanism by which certain pathogenic and symbiotic bacteria respond to population density and host association. By mediating the ability of bacteria such as Vibrio harveyi to infect larval shrimp, quorum sensing could have application to the problem of vibriosis in shrimp mariculture. Knowledge of quorum sensing developed from studies of luminescence in the marine bacteria Vibrio fischeri and V. harveyi. In both species, luminescence is controlled by a quorum-sensing mechanism involving two signal molecules and several genetically defined and physiological factors. In V. fischeri, luminescence is regulated by LuxR protein and the Luxl-dependent 3-oxo-hexanoyl-homoserine lactone (3- oxo-C6-HSL), which together activate transcription of luxICDABEG (the lux operon, genes for LuxI and the luminescence enzymes). A second acyl-HSL, octanoyl-HSL, product of AinS, blocks premature lux operon induction by interfering with 3-oxo-C6-HSL binding to LuxR. In V. harveyi, quorumsensing control of luminescence involves the luxLM-dependent 3-hydroxy- butyryl-HSL and an unidentified luxS-dependent signal molecule. These signals, through independent branches of a phosphorylation cascade, control the phosphorylation state of LuxO. In the absence of the signals, LuxO, in phosphorylated form, represses lux operon (luxCDABEGH) expression. The presence of the signals operates to dephosphorylate LuxO, relieving the repression. A LuxR protein then activates lux operon transcription. Targets for blocking the quorum-sensing mechanism in these bacteria and potentially blocking vibriosis include the activity, production and persistence of the signals, the production and activity of the response proteins, and the activity of specific downstream quorum-sensing controlled proteins involved in host infection.