title: Mutations that create new promoters suppress the sigma 54 dependence of glnA transcription in Escherichia coli.
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.
mesh_terms: 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
chemical_list: D003470:Culture Media; D004269:DNA, Bacterial; D012808:Sigma Factor; D014157:Transcription Factors; D005974:Glutamate-Ammonia Ligase