σN‐dependent control of acid resistance and the locus of enterocyte effacement in enterohemorrhagic Escherichia coli is activated by acetyl phosphate in a manner requiring flagellar regulator FlhDC and the σS antagonist FliZ

• DOI: 10.1002/mbo3.183
• Publication Date: 2014-06-16T22:41:05Z
• Authors: Avishek Mitra; Pamela A. Fay; Khoury W. Vendura; Zimrisha Alla; Ronan K. Carroll; Lindsey N. Shaw; James T. Riordan
• Keywords: rpoN; Sigma factor

Abstract In enterohemorrhagic Escherichia coli ( EHEC ), sigma factor N σ ) regulates glutamate‐dependent acid resistance GDAR and the locus of enterocyte effacement LEE ); discrete genetic systems that are required for transmission virulence this intestinal pathogen. Regulation these requires nitrogen regulatory protein C, NtrC, is a consequence NtrC‐ ‐dependent reduction in activity S ). This study elucidates pathway components stimuli ‐directed regulation . Deletion fliZ , product which reduces activity, phenocopied rpoN ntrC null strains control, resistance, adherence. Upregulation by was shown to be indirect an intact flagellar regulator flh DC Activation Flh dependent on ‐promoter D P 2 newly described NtrC upstream activator sequence. Addition ammonium chloride significantly altered expression adherence, independently sensor kinase, ntrB Altering availability phosphodonor acetyl phosphate growth without glucose, with acetate addition, or deletion kinase ackA abrogated control