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J. Bacteriol. doi:10.1128/JB.01368-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Regulation of denitrification genes in Neisseria meningitidis by nitric oxide and the repressor NsrR

Department of Biology, University of York, Heslington, York, YO10 5YW, UK.; School of Medicine and Biomedical Science, University of Sheffield, Beech Hill Road, Sheffield, S10 2RX, UK

^* To whom correspondence should be addressed. Email: jm46{at}york.ac.uk.

	Abstract

The human pathogen Neisseria meningitidis is capable of growth using denitrification of nitrite to nitrous oxide under microaerobic conditions. This process is catalysed by two reductases: nitrite reductase (encoded by aniA) and nitric oxide reductase (encoded by norB). Here we show that in N. meningitidis MC58 norB is regulated by nitric oxide via the product of gene NMB0437 which encodes NsrR. NsrR is a repressor in the absence of NO, but norB expression is de-repressed by NO in an NsrR-dependent manner. nsrR deficient mutants grow by denitrification more rapidly than wild-type N. meningitidis, and this is coincident with both NO reductase and nitrite reductase being up-regulated even under aerobic conditions in the absence of nitrite or NO. The NsrR-dependent repression of aniA (unlike that of norB) is not lifted in the presence of NO. The role of NsrR in the control of expression of aniA is linked to the function of the anaerobic activator protein FNR: analysis of nsrR and fnr single and nsrR fnr double mutants carrying an aniA promoter lacZ fusion indicate that the role of NsrR is to prevent FNR-dependent aniA expression under aerobic conditions, indicating that FNR in N. meningitidis retains considerable activity aerobically.

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