It has long been appreciated that certain groups of bacteria exhibit cooperative behavioral patterns. For example, feeding and sporulation of both myxobacteria and actinomycetes seem optimized for large populations of cells behaving almost as a single multicellular organism. The swarming motility of microorganisms such as Vibrio parahaemolyticus and Proteus mirabilis provides another excellent example of multicellular behavior among bacteria (2). Intercellular communication likewise has been appreciated for several years in Vibrio fischeri, Myxococcus xanthus, Bacillus subtilis, Streptomyces spp., the eukaryotic slime mold Dictyostelium discoideum, and other species (44). Here we first review how the marine luminescent bacterium V. fischeri uses the LuxR and LuxI proteins for intercellular communication and then describe a newly discovered family of LuxR and LuxI homologs in diverse bacterial species. AUTOINDUCTION OF BACTERIAL LUMINESCENCEAutoinduction of luminescence in the marine bacteria V. fischeri and Vibrio harveyi was described in the early 1970s (26,57). When these bacteria are cultured in broth, they exhibit a lag in luminescence gene (lux) expression during early and mid-exponential growth, followed by a rapid increase in expression during the late exponential and early stationary growth phases. Luminescence in early-log-phase cultures is induced by the addition of cell-free fluid extracts from stationary-phase cultures. Furthermore, the extracts show strain specificity, in that the addition of a V harveyi extract to an early-log-phase culture of V fischeri (or vice versa) does not induce luminescence (26,55,57).Autoinduction should not be confused with autoregulation or autorepression, two similar terms that describe entirely different phenomena (for a review of autoregulation, see reference 49). Autoinduction defines an environmental sensing system that allows bacteria to monitor their own population density. The bacteria produce a diffusible compound termed autoinducer which accumulates in the surrounding environment during growth. At low cell densities this substance is in low concentration, while at high cell densities this substance accumulates to the critical concentration required for activation of luminescence genes (26,55 The V. fischeri autoinducer (VAI) is 3-oxo-N-(tetrahydro-2-oxo-3-furanyl)hexanamide (27), which is commonly referred to as N-3-(oxohexanoyl)homoserine lactone (Fig. 1). The cell membrane is permeable to VAI, and thus, it accumulates in the growth medium (45). At low cell densities, VAI passively diffuses out of cells down a concentration gradient, while at high cell densities, VAI accumulates (at an intracellular concentration equivalent to the extracellular concentration). A concentration on the order of 10 nM is sufficient to activate transcription of the luminescence genes (45). V. fischeri is the specific symbiont in the light organs of certain marine fishes and squids (for recent reviews, see references 24, 51, and 68) and also occurs free-living in sea water. In light...
Different species of bacteria were tested for production of extracellular autoinducer-like activities that could stimulate the expression of the luminescence genes in Vibrio harveyi. Several species of bacteria, including the pathogens Vibrio cholerae and Vibrio parahaemolyticus, were found to produce such activities. Possible physiological roles for the two V. harveyi detection-response systems and their joint regulation are discussed.At least two species of marine bacteria, Vibrio fischeri and Vibrio harveyi, express bioluminescence in response to cell density. These two vibrios are found in different environments in the ocean. V. harveyi is found free-living in the sea as well as in the gut tracts of marine animals, where it exists at high population densities in association with other species of bacteria. V. fischeri is found in these habitats and also lives in pure culture as a light organ symbiont of various fish and squid (8). V. fischeri and V. harveyi accomplish density-dependent lux regulation by the synthesis, excretion, and detection of small signal molecules called autoinducers, which accumulate in the environment (9). The autoinducer that controls light production in V. fischeri is N-(3-oxohexanoyl)-L-homoserine lactone. Two autoinducers control density-dependent lux expression in V. harveyi. One of the V. harveyi autoinducers is N-(3-hydroxybutanoyl)-L-homoserine lactone (AI-1), and the second autoinducer (AI-2) remains to be identified. Recently, a number of other bacteria have been shown to control cell density-dependent functions through the excretion of and response to acyl-homoserine lactone autoinducers. Cell density-dependent regulation of lux expression is an example of a phenomenon called quorum sensing (5).Genetic analysis of the density-sensing apparatus of V. harveyi has shown that two independent density-sensing systems exist, and each is composed of a sensor-autoinducer pair; system 1 is composed of sensor 1 and AI-1, and system 2 is composed of sensor 2 and AI-2 (1, 2). The two density-sensing systems are redundant, because a null mutation in either system alone results in Lux ϩ strains, whereas null mutations in both systems render the cells dark and incapable of density sensing. In 1979 Greenberg et al. (6) reported that V. harveyi was stimulated to produce light following the addition of cellfree culture fluid from several species of nonluminous bacteria. At the time of that study it was not known that two autoinducer-detection systems existed in V. harveyi. Because V. harveyi mutants capable of responding to only AI-1 or AI-2 now exist, it is possible to determine through which pathway(s) the signals from these other organisms flow. Now that we also appreciate that many bacteria communicate intercellularly and control gene expression through the use of autoinducers, it is of interest to understand how they might accomplish crossspecies communication and use it for survival in various niches. In this study we have used V. harveyi sensor mutants as reporters for specific autoinduc...
The Vibrio fischeri luminescence genes are activated by the transcription factor LuxR in combination with a diffusible signal compound, N-(3-oxohexanoyl) homoserine lactone, termed the autoinducer. We have synthesized a set of autoinducer analogs. Many analogs with alterations in the acyl side chain showed evidence of binding to LuxR. Some appeared to bind with an affinity similar to that of the autoinducer, but none showed a higher affinity, and many did not bind as tightly as the autoinducer. For the most part, compounds with substitutions in the homoserine lactone ring did not show evidence of binding to LuxR. The exceptions were compounds with a homocysteine thiolactone ring in place of the homoserine lactone ring. Many but not all of the analogs showing evidence of LuxR binding had some ability to activate the luminescence genes. None were as active as the autoinducer. While most showed little ability to induce luminescence, a few analogs with rather conservative substitutions had appreciable activity. Under the conditions we employed, some of the analogs showing little or no ability to induce luminescence were inhibitors of the autoinducer.Quorum sensing is used by a number of gram-negative bacterial genera to regulate expression of specific sets of genes in a cell density-dependent fashion (10,20,21). Certain pathogenic bacteria use quorum sensing in the regulation of genes encoding extracellular virulence factors (17,19). The cell density control of luminescence in the symbiotic marine bacterium Vibrio fischeri is the best-studied quorum sensing system, and although each of the known systems has unique features, the V. fischeri luminescence system is considered the model (10, 20, 21). There are two regulatory genes involved in quorum sensing, the I and R genes. The I gene directs the synthesis of an N-acyl homoserine lactone (HSL) signal molecule termed the autoinducer. The R gene codes for a transcription factor that is responsive to the N-acyl HSL signal. In V. fischeri, the luxI gene directs the synthesis of 3-oxohexanoyl HSL, the autoinducer signal required for luminescence gene activation (6,8,9). Cells are permeable to this signal, and thus high cell densities are required to achieve a critical concentration of the autoinducer required to bind the luxR product, which in turn activates transcription of the luminescence genes (1,8,13,15).Little is known about the interaction of the V. fischeri autoinducer, 3-oxohexanoyl HSL, and the LuxR protein. The LuxR polypeptide consists of two domains. The available evidence indicates that 3-oxohexanoyl HSL binds to the N-terminal domain and that this binding allows a productive interaction of the LuxR C-terminal domain with the transcription-initiation complex of the luminescence genes (4, 13). There is one previous study of the influence of autoinducer analogs on induction of luminescence in V. fischeri (7). The analogs showed a spectrum of activities: some were capable of inducing luminescence, some inhibited activation by 3-oxohexanoyl HSL, and others showe...
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The enzymes for luminescence in Vibrio fischeri are induced by the accumulation of a species-specific metabolite (autoinducer) in the culture medium. Tritium-labeled auteinducer was used to study the mechanism of autoinduction. When 3H-autoinducer was added to suspensions of V. fischeri or Escherichwa coli, cellular concentrations equaled external concentrations. For V. fischeri, equilibration of 3H-autoinducer was rapid (within 20 s), and >90% of the cellular tritium remained in unmodified autoinducer. When V. fischeri or E. coli cells containing 3H-autoinducer were transferred to autoinducer-free buffer, 85 to 99.5% of the radiotracer escaped from the cells, depending on the strain. Concentrations of autoinducer as low as 10 nM, which is equivalent to 1 or 2 molecules per cell, were sufficient for induction, and the maximal response to autoinducer occurred at about 200 nM. If external autoinducer concentrations were decreased to below 10 nM after induction had commenced, the induction response did not continue. Based on this study, a model for autoinduction is described wherein autoinducer association with cells is by simple diffusion and binding of autoinducer to its active site is reversible.
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