The transcription of bacterial luminescence is regulated by sigma 32

Publisher Website
Google Scholar
Abstract
Luminescence in the marine bacterium, Vibrio fischeri, is regulated by a small molecule, the autoinducer. The transcription of the V. fischeri lux genes also requires a regulatory protein, (luxR), cAMP and CRP. We show that, apart from these components, the transcription of the PR lux operon is also controlled by the activity of σ32 (htpR protein). In luminescent Escherichia coli (E. coli/pChv1), as well as in different marine luminous bacteria and their naturally occurring dark (K) variants, the luminescence system can be induced by starvation under microaerophilic conditions. Heat shock also induces luminescence in htpR+ but not in htpR− strains of E. coli/pChv1.An htpR− mutant of E. coli containing pChv1 is very dim and its luminescence is not induced by starvation or heat shock. The addition of a plasmid bearing the gene for htpR+ into such cells restores their response to starvation and heat shock. Cells of wild type E. coli/pChv1 that have been starved or heat shocked respond to lower concentrations of V. fischeri inducer than untreated cells. These cultures also produce more extracellular inducer than untreated cells. Starvation, heat shock and the presence of σ32 do not induce luminescence in luxl deleted E. coli/pChv1 cells.SOS‐inducing agents advance the onset of luminescence in both htpR+ and htpR− strains but not in luxl deleted E. coli/pChvi cells.DNA sequencing of the luxR‐luxl region reveals the presence of a promoter region of the kind typical for σ32 at the beginning of the luxl gene. In addition we find a LexA protein‐DNA binding site in the non‐consensus sequence for the −35 region of the PR operon. It is proposed that the regulatory protein‐inducer complex displaces the LexA protein and allows the transcription of the right operon. SOS‐inducing agents result in proteolysis of LexA protein and advance the onset of luminescence. σ32 enhances the transcription from the PR operon and thus initiates a positive control circuit. It seems that σ32 is the major controlling element in determining the onset of luminescence both in vivo and in vitro.