Regulation of nrf operon expression in pathogenic enteric bacteria: sequence divergence reveals new regulatory complexity

Research output: Contribution to journalArticle

Authors

Colleges, School and Institutes

External organisations

  • School of Biosciences and Institute of Microbiology and Infection; University of Birmingham; Edgbaston Birmingham B15 2TT UK

Abstract

The Escherichia coli K-12 nrf operon encodes a periplasmic nitrite reductase, the expression of which is driven from a single promoter, pnrf. Expression from pnrf is activated by the FNR transcription factor in response to anaerobiosis and further increased in response to nitrite by the response regulator proteins, NarL and NarP. FNR-dependent transcription is suppressed by the binding of two nucleoid associated proteins, IHF and Fis. As Fis levels increase in cells grown in rich medium, the positioning of its binding site, overlapping the promoter -10 element, ensures that pnrf is sharply repressed. Here, we investigate the expression of the nrf operon promoter from various pathogenic enteric bacteria. We show that pnrf from enterohaemorrhagic E. coli is more active than its K-12 counterpart, exhibits substantial FNR-independent activity and is insensitive to nutrient quality, due to an improved -10 element. We also demonstrate that the Salmonella enterica serovar Typhimurium core promoter is more active than previously thought, due to differences around the transcription start site, and that its expression is repressed by downstream sequences. We identify the CsrA RNA binding protein as being responsible for this, and show that CsrA differentially regulates the E. coli K-12 and Salmonella nrf operons.

Details

Original languageEnglish
Pages (from-to)580–594
JournalMolecular Microbiology
Volume104
Issue number4
Early online date1 Mar 2017
Publication statusPublished - 11 May 2017

Keywords

  • Journal Article