The regulatory control of the bacterial luminescence system--a new view.

We have recently shown that the transcription of the PR lux operon for Vibrio fischeri luminescence is positively controlled by the htpR (sigma 32) protein. It was suggested that the LexA protein might negatively control the lux genes. This paper extends these findings. It was found that Escherichia coli cells that contain the entire lux operon (pChv1) in RecA or LexA mutants which are unable to remove the LexA protein are considerably dimmer than the wild-type strain. Mutants that do not make LexA or form a weakly bound LexA are very bright. The role of sigma 32 protein was studied on luxR-luxI genes that are fused to beta-galactosidase. The addition of V. fischeri inducer brings about the formation of beta-galactosidase activity in htpR+ but not in htpR- strains of E. coli/pMJ3. Similar to the effect of starvation on the induction of luminescence in marine bacteria and in E. coli/pChv1 cells, beta-galactosidase activity in such constructs is preferentially induced by low nutrient concentrations. A new model for the regulatory control of the V. fischeri luminescence system is discussed.