PMID:2887548

Citation	Reitzer, LJ, Bueno, R, Cheng, WD, Abrams, SA, Rothstein, DM, Hunt, TP, Tyler, B and Magasanik, B (1987) Mutations that create new promoters suppress the sigma 54 dependence of glnA transcription in Escherichia coli. J. Bacteriol. 169:4279-84
Abstract	Escherichia coli rpoN mutants lack sigma 54 and are therefore unable to initiate the transcription of glnA at glnAp2, which is required for the production of a high intracellular concentration of glutamine synthetase. We have found that the dependence on sigma 54 can be overcome by mutations that have apparently created a new sigma 70-dependent promoter. The position -35 RNA polymerase contact site of this new promoter overlaps glnAp2. The initiation of transcription at the new promoter is inhibited by sigma 54-RNA polymerase even in the absence of nitrogen regulator I-phosphate, the activator required for the initiation of transcription at glnAp2. The results suggest that in cells growing with an excess of nitrogen and therefore lacking nitrogen regulator I-phosphate, sigma 54-RNA polymerase is bound at glnAp2.
Links	PubMed PMC213741
Keywords	Base Sequence; Culture Media; DNA, Bacterial/analysis; Escherichia coli/enzymology; Escherichia coli/genetics; Genes, Bacterial; Glutamate-Ammonia Ligase/analysis; Glutamate-Ammonia Ligase/genetics; Mutation; Promoter Regions, Genetic; Sigma Factor/genetics; Suppression, Genetic; Transcription Factors/genetics; Transcription, Genetic
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