REGULATORY CIRCUITRY CONTROLLING LUMINESCENCE AUTOINDUCTION IN VIBRIO-FISCHERI

Luminescence in the marine symbiotic bacterium Vibrio fischeri is subject to control by autoinduction, a regulatory mechanism that activates light production at high population density and suppresses light production at low population density. Several genetic, physiological and environmental factors contribute to autoinduction. Primary among these are a self-produced, membrane-permeable compound, N-3-oxohexanoyl-L-homoserine lactone, called autoinducer, which accumulates in a population density-dependent manner during growth of V. fischeri, and a transcriptional activator protein, LuxR, which with autoinducer activates transcription of the luminescence (lux) genes (luxICDABEG; encoding proteins for autoinducer synthesis and light production). Additional genetically defined regulatory elements involved in autoinduction include 3':5'-cyclic AMP (cAMP), which via cAMP receptor protein activates transcription of luxR, and the GroESL proteins, which stabilize LuxR in its active form. Evidence exists also for the involvement of LexA protein, for a second autoinducer, N-octanoyl-L-homoserine lactone, and under anaerobic conditions for Fnr protein. Besides these regulatory elements, nutrient limitation, presence of glucose, availability of iron and oxygen, temperature, salts and an autoinducer-LuxR protein-independent modulation also contribute to the autoinduction phenomenon. The multiplicity of genetic, physiological and environmental factors indicates that luminescence autoinduction is mediated by a complex regulatory circuitry, one that is highly integrated with and responsive to the physiological and ecological status of the cells. Long thought to be unique to V. fischeri and certain closely related marine luminous bacteria, luminescence autoinduction is now viewed as a model for understanding population density-responsive control of gene expression in a wide variety of terrestrial and marine bacteria in which N-acyl-L-homoserine lactones and homologs of LuxI and LuxR recently have been found.