JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Anjum, M. F.
Right arrow Articles by Moir, J. W. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Anjum, M. F.
Right arrow Articles by Moir, J. W. B.
Journal of Bacteriology, June 2002, p. 2987-2993, Vol. 184, No. 11
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.11.2987-2993.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Nitric Oxide Metabolism in Neisseria meningitidis

Muna F. Anjum,1,{dagger} Tânia M. Stevanin,1,2* Robert C. Read,2 and James W. B. Moir1

Department of Molecular Biology and Biotechnology, University of Sheffield, Western Bank, Sheffield S10 2TN,1 Division of Genomic Medicine, University of Sheffield Medical School, Sheffield S10 2RX, United Kingdom2

Received 31 January 2002/ Accepted 7 March 2002

Neisseria meningitidis, the causative agent of meningococcal disease in humans, is likely to be exposed to nitrosative stress during natural colonization and disease. The genome of N. meningitidis includes the genes aniA and norB, predicted to encode nitrite reductase and nitric oxide (NO) reductase, respectively. These gene products should allow the bacterium to denitrify nitrite to nitrous oxide. We show that N. meningitidis can support growth microaerobically by the denitrification of nitrite via NO and that norB is required for anaerobic growth with nitrite. NorB and, to a lesser extent, the cycP gene product cytochrome c' are able to counteract toxicity due to exogenously added NO. Expression of these genes by N. meningitidis during colonization and disease may confer protection against exogenous or endogenous nitrosative stress.


* Corresponding author. Mailing address: Division of Genomic Medicine, University of Sheffield, Medical School, Beech Hill Rd., Sheffield S10 2RX, United Kingdom. Phone: 44 (0) 114-271-2968. Fax: 44 (0) 114-273-9926. E-mail: T.Stevanin{at}sheffield.ac.uk.

{dagger} Present address: Veterinary Laboratories Agency (Weybridge), Department of Bacterial Diseases, New Haw, Addlestone, Surrey KT15 3NB, United Kingdom.


Journal of Bacteriology, June 2002, p. 2987-2993, Vol. 184, No. 11
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.11.2987-2993.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 2002 by the American Society for Microbiology. All rights reserved.