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. 1987 Sep;169(9):4279–4284. doi: 10.1128/jb.169.9.4279-4284.1987

Mutations that create new promoters suppress the sigma 54 dependence of glnA transcription in Escherichia coli.

L J Reitzer, R Bueno, W D Cheng, S A Abrams, D M Rothstein, T P Hunt, B Tyler, B Magasanik
PMCID: PMC213741  PMID: 2887548

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.

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Selected References

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