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Enterohemorrhagic  Escherichia coli  (EHEC) is dependent on acid resistance for gastric passage and low oral infectious dose, and the locus of enterocyte effacement (LEE) for intestinal colonization. Mutation of  rpoN , encoding sigma factor N (σ N ), dramatically alters the growth-phase dependent regulation of both acid resistance and the LEE. This study reports on the determinants of σ N -directed acid resistance and LEE expression, and the underlying mechanism attributable to this phenotype. Glutamate-dependent acid resistance (GDAR) in TW14359Δ rpoN  correlated with increased expression of the  gadX - gadW  regulatory circuit during exponential growth, whereas upregulation of arginine-dependent acid resistance (ADAR) genes  adiA  and  adiC  in TW14359Δ rpoN  did not confer acid resistance by the ADAR mechanism. LEE regulatory ( ler ), structural ( espA  and  cesT ) and effector ( tir ) genes were downregulated in TW14359Δ rpoN , and mutation of  rpoS  encoding sigma factor 38 (σ S ) in TW14359Δ rpoN  restored acid resistance and LEE genes to WT levels. Stability, but not the absolute level, of σ S  was increased in TW14359Δ rpoN ; however, increased stability was not solely attributable to the GDAR and LEE expression phenotype. Complementation of TW14359Δ rpoN  with a σ N  allele that binds RNA polymerase (RNAP) but not DNA, did not restore WT levels of σ S  stability,  gadE ,  ler  or GDAR, indicating a dependence on transcription from a σ N  promoter(s) and not RNAP competition for the phenotype. Among a library of σ N  enhancer binding protein mutants, only TW14359Δ ntrC , inactivated for nitrogen regulatory protein NtrC, phenocopied TW14359Δ rpoN  for σ S  stability, GDAR and  ler  expression. The results of this study suggest that during exponential growth, NtrC-σ N  regulate GDAR and LEE expression through downregulation of σ S  at the post-translational level; likely by altering σ S  stability or activity. The regulatory interplay between NtrC, other EBPs, and σ N –σ S , represents a mechanism by which EHEC can coordinate GDAR, LEE expression and other cellular functions, with nitrogen availability and physiologic stimuli.

Sigma Factor N, Liaison to an ntrC and rpoS Dependent Regulatory Pathway Controlling Acid Resistance and the LEE in Enterohemorrhagic Escherichia coli