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

MicrobiologyOpen

Avishek Mitra¹  Pamela A. Fay¹  Khoury W. Vendura¹  Zimrisha Alla¹  Ronan K. Carroll¹  Lindsey N. Shaw¹ 

[1] Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, Florida

关键词: acid resistance;    EHEC O157;    H7;    LEE;    NtrC;    rpoN;    sigma factor N;   

DOI  :  10.1002/mbo3.183

来源: Wiley

【 摘 要 】

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 flhD_P2, 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.

【 授权许可】

CC BY   
© 2014 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd.

Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.