𝔖 Bobbio Scriptorium
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The regulatory control of the bacterial luminescence system—A new view

✍ Scribed by Ulitzur, S.

Publisher
John Wiley and Sons
Year
1989
Weight
531 KB
Volume
4
Category
Article
ISSN
0884-3996

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✦ Synopsis

We have recently shown that the transcription of the PR lux operon for Vibrio fischeri luminescence is positively controlled by the htpR (d2) 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 (pChvl) i n RecA or LexA mutants which are unable t o 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 d2 protein was studied on IuxR-lux1 genes that are fused t o B-galactosidase. The addition of V. fischeri inducer brings about the formation of 0galactosidase activity in htpw but not in htpRstrams of E. coli/pMJ3. Similar to the effect of starvation on the induction of luminescence in marine bacteria and in E. co/i/pChvl cells, Pgalactosidase activity in such constructs is preferentially induced by l o w nutrient concentrations. A new model for the regulatory control of the W. fischeri luminescence system is discussed.

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