Mutations that create new promoters suppress the sigma 54 dependence of glnA transcription in Escherichia coli.
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.
D001483:Base Sequence; D003470:Culture Media; D004269:DNA, Bacterial / Q000032:analysis; D004926:Escherichia coli / Q000201:enzymology / Q000235:genetics*; D005798:Genes, Bacterial; D005974:Glutamate-Ammonia Ligase / Q000032:analysis / Q000235:genetics*; D009154:Mutation; D011401:Promoter Regions, Genetic; D012808:Sigma Factor / Q000235:genetics*; D013489:Suppression, Genetic; D014157:Transcription Factors / Q000235:genetics*; D014158:Transcription, Genetic
D003470:Culture Media; D004269:DNA, Bacterial; D012808:Sigma Factor; D014157:Transcription Factors; D005974:Glutamate-Ammonia Ligase