LuxR controls the expression of Vibrio fischeri luxCDABE clone in Escherichia coli in the absence of luxI gene.

Abstract

We have recently suggested that the expression of V. fischeri right lux operon is initiated from two sites, the first located upstream of the luxI gene, while the second seems to be located upstream of the luxC gene. The transcription from both sites is negatively controlled by H-NS protein. E. coli MC4100 rpoS hns mutant harbouring the V. fischeri luxCDABE genes showed constitutive mode and 70,000-fold higher luminescence than the wild-type cells. The present study shows that the expression of luxCDABE genes in E. coli MC4100 wild-type cells is also controlled by LuxR protein in the absence of the autoinducer. The co-presence of a ptac-controlled luxR gene in a trans position to a plasmid carrying the luxCDABE genes resulted in 100,000 times higher luminescence. In the absence of the autoinducer, the presence of the luxR gene under its own regulated control resulted in about 100-200-fold increase of luminescence from the luxC upstream site. Taken together, it seems that the LuxR protein initiates the formation of the V. fischeri lux system cloned in E. coli from two sites located upstream and downstream of the luxI gene. Only the activation of the first site requires the presence of the autoinducer, whereas the second site is fully activated by LuxR protein in the absence of the autoinducer.