Control of bioluminescence in Vibrio fischeri by the LuxO signal response regulator.

Bioluminescence in the marine bacterium Vibrio fischeri is controlled by the excretion of a N-acyl homoserine lactone (HSL) autoinducer which interacts with a regulator, LuxR, and activates transcription of the lux operon at high-cell density. This system has become the prototype for quorum sensing in many bacteria. Although light emission in Vibrio harveyi is also regulated by a N-acyl-HSL inducer, in sharp contrast, a completely different and more complex system is involved in quorum sensing which is mediated via LuxO, the response regulator of a phosphorelay signal transduction system. In the present work, luxO and the overlapping luxU gene, also involved in the phosphorelay system in V. harveyi, have been discovered in V. fischeri. By gene replacement technology, a V. fischeri luxO- mutant was generated whose phenotype was similar to that of V. harveyi luxO- showing that LuxO is involved in control of luminescence in V. fischeri. This mutant could be complemented with luxO from either V. fischeri or V. harveyi resulting in the restoration of the dependence of luminescence intensity on cell density. In contrast to V. harveyi luxO-, light emission of V. fischeri luxO- was stimulated by the N-acyl-HSL autoinducer indicating that luxO is part of a second signal transduction system controlling luminescence in this species. The presence of a luxO-based phosphorelay regulatory system as well as the luxR-based system in V. fischeri suggests that the former system, originally discovered in V. harveyi, may be a general regulatory mechanism in luminescent bacteria.