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J. Bacteriol. doi:10.1128/JB.01354-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Nitric Oxide in Chemostat-Cultured Escherichia coli is Sensed by Fnr and Other Global Regulators; Unaltered Methionine Biosynthesis Indicates Lack of S-Nitrosation

Steven T. Pullan, Mark A. Gidley, Richard A. Jones, Jason Barrett, Tania M. Stevanin, Robert C. Read, Jeffrey Green, and Robert K. Poole*

Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield, S10 2TN, and Division of Immunity and Infectious Diseases, University of Sheffield Medical School, Royal Hallamshire Hospital, Sheffield, S10 2RX, UK

* To whom correspondence should be addressed. Email: r.poole{at}sheffield.ac.uk.


  Abstract

We previously elucidated the global transcriptional responses of Escherichia coli to the nitrosating agent S-nitrosoglutathione (GSNO) in both aerobic and anaerobic chemostats and demonstrated expression of NO-protective mechanisms and evidence of critical thiol nitrosation. The present study is the first to examine the transcriptome of NO-exposed E. coli in a chemostat. We have compared, under identical conditions, the GSNO stimulon with that of nitric oxide (NO) released from two NOC compounds simultaneously and demonstrate marked differences in the transcriptional responses to these distinct nitrosative stresses. Exposure to NO did not induce met genes, suggesting that, unlike GSNO, NO does not elicit homocysteine S-nitrosation and compensatory increases in methionine biosynthesis. Exogenous methionine, on entry into cells, afforded protection from GSNO- but not NO-mediated killing. Anaerobic exposure to NO led to up-regulation of multiple Fnr-repressed genes and down-regulation of Fnr-activated genes, including nrfA that encodes cytochrome c nitrite reductase, providing strong evidence for NO inactivation of Fnr. Other global regulators apparently affected by NO were IscR, Fur, SoxR, NsrR and NorR. Components of the NorR regulon were sought by microarray comparison of NO-exposed wild-type and norR mutant strains: only norVW, encoding the NO-detoxifying flavorubredoxin and its cognate reductase, were unambiguously identified. Mutation of norV or norR was without effect on E. coli survival in mouse macrophages. Thus, GSNO (a nitrosating agent) and NO exhibit distinct cellular effects: NO more effectively interacts with global regulators that mediate adaptive responses to nitrosative stress, but does not affect methionine requirements arising from homocysteine nitrosation.


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