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 Householder, T. C.
Right arrow Articles by Clark, V. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Householder, T. C.
Right arrow Articles by Clark, V. L.

 Previous Article  |  Next Article 

Journal of Bacteriology, January 1999, p. 541-551, Vol. 181, No. 2
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

cis- and trans-Acting Elements Involved in Regulation of aniA, the Gene Encoding the Major Anaerobically Induced Outer Membrane Protein in Neisseria gonorrhoeae

Tracey C. Householder,1 Wesley A. Belli,1,dagger Sarah Lissenden,2 Jeffrey A. Cole,2 and Virginia L. Clark1,*

Department of Microbiology and Immunology, School of Medicine and Dentistry, University of Rochester, Rochester, New York 14642,1 and School of Biochemistry, University of Birmingham, Birmingham B15 2TT, United Kingdom2

Received 13 August 1998/Accepted 6 November 1998

AniA (formerly Pan1) is the major anaerobically induced outer membrane protein in Neisseria gonorrhoeae. AniA has been shown to be a major antigen in patients with gonococcal disease, and we have been studying its regulation in order to understand the gonococcal response to anaerobiosis and its potential role in virulence. This study presents a genetic analysis of aniA regulation. Through deletion analysis of the upstream region, we have determined the minimal promoter region necessary for aniA expression. This 130-bp region contains a sigma 70-type promoter and an FNR (fumarate and nitrate reductase regulator protein) binding site, both of which are absolutely required for anaerobic expression. Also located in the minimal promoter region are three T-rich direct repeats and several potential NarP binding sites. This 80-bp region is required for induction by nitrite. By site-directed mutagenesis of promoter sequences, we have determined that the transcription of aniA is initiated only from the sigma 70-type promoter. The gearbox promoter, previously believed to be the major promoter, does not appear to be active during anaerobiosis. The gonococcal FNR and NarP homologs are involved in the regulation of aniA, and we demonstrate that placing aniA under the control of the tac promoter compensates for the inability of a gonococcal fnr mutant to grow anaerobically.


* Corresponding author. Mailing address: Department of Microbiology and Immunology, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642. Phone: (716) 275-3154. Fax: (716) 473-9573. E-mail: Ginny_Clark{at}urmc.rochester.edu.

dagger Present address: Astra Pharmaceuticals, L.P., Rochester, NY 14623.


Journal of Bacteriology, January 1999, p. 541-551, Vol. 181, No. 2
0021-9193/99/$04.00+0
Copyright © 1999, 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 © 1999 by the American Society for Microbiology. All rights reserved.