Open AccessMutations that create new promoters suppress the sigma 54 dependence of glnA transcription in Escherichia coli
Author(s) -
Larry Reitzer,
R Bueno,
Wu Cheng,
S A Abrams,
David M. Rothstein,
T P Hunt,
Bonnie Tyler,
Boris Magasanik
Publication year - 1987
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.169.9.4279-4284.1987
Subject(s) - sigma factor , biology , rna polymerase , rpon , transcription (linguistics) , promoter , microbiology and biotechnology , mutant , glutamine synthetase , rna polymerase ii holoenzyme , general transcription factor , activator (genetics) , escherichia coli , genetics , gene , gene expression , glutamine , linguistics , philosophy , amino acid
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.