IAI FigSearch
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 Sengupta, N.
Right arrow Articles by Chowdhury, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sengupta, N.
Right arrow Articles by Chowdhury, R.

 Previous Article  |  Next Article 

Infection and Immunity, October 2003, p. 5583-5589, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5583-5589.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The Global Regulator ArcA Modulates Expression of Virulence Factors in Vibrio cholerae

Nilanjan Sengupta,{dagger} Kalidas Paul, and Rukhsana Chowdhury*

Biophysics Division, Indian Institute of Chemical Biology, Calcutta 700 032, India

Received 24 March 2003/ Returned for modification 2 June 2003/ Accepted 8 July 2003

A Vibrio cholerae arcA mutant was constructed and used to examine the role of the global anaerobiosis response regulator ArcA in the expression of virulence factors in this important human pathogen. In V. cholerae, expression of the major virulence factors cholera toxin (CT) and toxin-coregulated pilus (TCP) is regulated by the transcriptional activator ToxT. toxT expression, in turn, is controlled by the transmembrane DNA binding proteins ToxR and TcpP. In the V. cholerae arcA mutant, although ToxR and TcpP were unaffected, Northern blot and reverse transcription-PCR analyses indicated that the expression of toxT was significantly decreased with concomitant reduction in the expression of CT and TCP. CT and TCP expression was completely restored in the V. cholerae arcA mutant strain by expressing a cloned toxT gene in the mutant. These results suggest that ArcA functions as a positive regulator of toxT expression under both aerobic and anaerobic conditions, although as expected, the effect was more pronounced during anaerobic growth. This was reflected in a reduction of virulence of the V. cholerae arcA mutant strain in the infant mouse cholera model.

* Corresponding author. Mailing address: Biophysics Division, Indian Institute of Chemical Biology, 4 Raja S. C. Mullick Rd., Calcutta 700 032, India. Phone: 91 33 473 0350. Fax: 91 33 473 5197. E-mail: rukhsana{at}iicb.res.in.

Editor: A. D. O'Brien

{dagger} Present address: Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Fla.

Infection and Immunity, October 2003, p. 5583-5589, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5583-5589.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2003 by the American Society for Microbiology. All rights reserved.