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The LuxR protein is a transcriptional activator which, together with a diffusible small molecule termed the autoinducer [N-(3-oxohexanoyl)-L-homo-serine lactone], represents the primary level of regulation of the bioluminescence genes in Vibrio fischeri. LuxR, in the presence of autoinducer, activates transcription of the luxICDABEG gene cluster and both positively and negatively autoregulates transcription of the divergently oriented luxR gene, activating transcription at low levels of autoinducer, and repressing synthesis at high autoinducer concentration. Seven LuxR point mutants which activate V. fischeri lux transcription in the absence of autoinducer (LuxR*) have been characterized. The LuxR* proteins activated transcription of the bioluminescence genes to levels 1.5-40 times that achieved by wild-type LuxR without autoinducer. All of the LuxR* mutants retained responsiveness to autoinducer. However, in each case the degree of stimulation in response to autoinducer was lower than that observed for wild-type LuxR. The LuxR* proteins retained the requirement for autoinducer for autoregulation of the luxR gene. We propose that the LuxR protein exists in two conformations, an inactive form, and an active form which predominates in the presence of autoinducer. The LuxR* mutations appear to shift the equilibrium distribution of these two forms so as to increase the amount of the active form in the absence of autoinducer, while autoinducer can still convert inactive to active species. The differential effects of the LuxR* proteins at the two lux promoters suggest that LuxR stimulates PluxR transcription by a different mechanism to that used at the PluxI promoter, implying that binding of LuxR to its binding site, known to be necessary for transcriptional activation, may not be sufficient.

The conditioning of culture medium by the production of growth-regulatory substances is a well-established phenomenon with eukaryotic cells. It has recently been shown that many prokaryotes are also capable of modulating growth, and in some cases sensing cell density, by production of extracellular signaling molecules, thereby allowing single celled prokaryotes to function in some respects as multicellular organisms. As Escherichia coli shifts from exponential growth to stationary growth, many changes occur, including cell division leading to formation of short minicells and expression of numerous genes not expressed in exponential phase. An understanding of the coordination between the morphological changes associated with cell division and the physiological and metabolic changes is of fundamental importance to understanding regulation of the prokaryotic cell cycle. The ftsQA genes, which encode functions required for cell division in E. coli, are regulated by promoters P1 and P2, located upstream of the ftsQ gene. The P1 promoter is rpoS-stimulated and the second, P2, is regulated by a member of the LuxR subfamily of transcriptional activators, SdiA, exhibiting features characteristic of an autoinduction (quorum sensing) mechanism. The activity of SdiA is potentiated by N-acyl-homoserine lactones, which are the autoinducers of luciferase synthesis in luminous marine bacteria as well as of pathogenesis functions in several pathogenic bacteria. A compound(s) produced by E. coli itself during growth in Luria Broth stimulates transcription from P2 in an SdiA-dependent process. Another substance(s) enhances transcription of rpoS and (perhaps indirectly) of ftsQA via promoter P1. It appears that this bimodal control mechanism may comprise a fail-safe system, such that transcription of the ftsQA genes may be properly regulated under a variety of different environmental and physiological conditions.

The phenomenon of cell-density-dependent control of gene expression, called autoinduction, has long been a subject of interest and investigation in bioluminescent marine bacteria. It is now becoming clear that many other bacteria, including animal and plant pathogens, use an autoinduction mechanism to regulate a variety of functions. Cell-density-dependent gene expression provides an excellent example of multicellular behaviour in the prokaryotic kingdom where a single cell is able to communicate and sense when a minimal population unit, a 'quorum' of bacteria, is achieved in order for certain behaviour of the population to be performed efficiently. Regulation of bacterial bioluminescence has been studied for many years and represents the best model system for understanding the mechanism of cell-density-dependent gene expression. This review will focus on transcriptional regulation of the Vibrio fischeri luminescence genes emphasizing the role of the transcriptional activator LuxR and possible autoinduction mechanisms that occur in E. coli. Alternative views and opinions regarding the molecular details of the autoinduction mechanism will be discussed.