ArticleMicrobiologyOpen2014
σ(N) -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 σ(S) antagonist FliZ.
Article in MicrobiologyOpen, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- A Role for the RNA Polymerase Gene Specificity Factor σJournal of bacteriology · 2022Article
- Prediction and Inferred Evolution of Acid Tolerance Genes in the Biotechnologically ImportantFrontiers in microbiology · 2022Article
- Regulation ofEcoSal Plus · 2017Review
- Staphylococcus aureus SufT: an essential iron-sulphur cluster assembly factor in cells experiencing a high-demand for lipoic acid.Molecular microbiology · 2016Article
- Global Regulator of Virulence A (GrvA) Coordinates Expression of Discrete Pathogenic Mechanisms in Enterohemorrhagic Escherichia coli through Interactions with GadW-GadE.Journal of bacteriology · 2016Article
- Glycolysis for Microbiome Generation.Microbiology spectrum · 2015Article
- Investigating the genetic regulation of the ECF sigma factor σS in Staphylococcus aureus.BMC microbiology · 2014Article
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Authors and funding
7 authors.
Funding
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Abstract
In enterohemorrhagic Escherichia coli (EHEC), sigma factor N (σ(N)) regulates glutamate-dependent acid resistance (GDAR) and the locus of enterocyte effacement (LEE); discrete genetic systems that are required for transmission and virulence of this intestinal pathogen. Regulation of these systems requires nitrogen regulatory protein C, NtrC, and is a consequence of NtrC-σ(N) -dependent reduction in the activity of sigma factor S (σ(S)). This study elucidates pathway components and stimuli for σ(N)-directed regulation of GDAR and the LEE in EHEC. Deletion of fliZ, the product of which reduces σ(S) activity, phenocopied rpoN (σ(N)) and ntrC null strains for GDAR and LEE control, acid resistance, and adherence. Upregulation of fliZ by NtrC-σ(N) was shown to be indirect and required an intact flagellar regulator flhDC. Activation of flhDC by NtrC-σ(N) and FlhDC-dependent regulation of GDAR and the LEE was dependent on σ(N)-promoter flhDP 2 , and a newly described NtrC upstream activator sequence. Addition of ammonium chloride significantly altered expression of GDAR and LEE, acid resistance, and adherence, independently of rpoN, ntrC, and the NtrC sensor kinase, ntrB. Altering the availability of NtrC phosphodonor acetyl phosphate by growth without glucose, with acetate addition, or by deletion of acetate kinase ackA, abrogated NtrC-σ(N)-dependent control of flhDC, fliZ, GDAR, and the LEE.
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