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 Frota, C. C.
Right arrow Articles by Colston, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Frota, C. C.
Right arrow Articles by Colston, M. J.

 Previous Article  |  Next Article 

Infection and Immunity, September 2004, p. 5483-5486, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.5483-5486.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The AraC Family Transcriptional Regulator Rv1931c Plays a Role in the Virulence of Mycobacterium tuberculosis{dagger}

Cristiane C. Frota,{ddagger} K. G. Papavinasasundaram,§ Elaine O. Davis,* and M. Joseph Colston

Division of Mycobacterial Research, National Institute for Medical Research, London, United Kingdom

Received 9 March 2004/ Returned for modification 6 May 2004/ Accepted 8 June 2004

A Mycobacterium tuberculosis strain disrupted in the AraC homologue Rv1931c was isolated. The mutant strain exhibited reduced survival both in macrophages and in a mouse infection model, with survival being restored on complementation with the Rv1931c gene. These results suggest that Rv1931c regulates genes important for virulence of M. tuberculosis.

* Corresponding author. Mailing address: Division of Mycobacterial Research, National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, United Kingdom. Phone: 020 8816 2358. Fax: 020 8816 2564. E-mail: edavis{at}nimr.mrc.ac.uk.

{dagger} In memory of the late Jo Colston and Peter Jenner, for their support and many helpful discussions.

Editor: S. H. E. Kaufmann

{ddagger} Present address: Division of Medical Microbiology, Departamento de Patologia, Federal University of Ceara, Fortaleza-Ceara 60441-750, Brazil.

§ Present address: Department of Medicine, UBC Division of Infectious Diseases, Vancouver, BC V5Z 3J5, Canada.

Infection and Immunity, September 2004, p. 5483-5486, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.5483-5486.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Singh, A. K., Singh, B. N. (2009). Differential Expression of sigH Paralogs during Growth and under Different Stress Conditions in Mycobacterium smegmatis. J. Bacteriol. 191: 2888-2893 [Abstract] [Full Text]  
  • Casaz, P., Garrity-Ryan, L. K., McKenney, D., Jackson, C., Levy, S. B., Tanaka, S. K., Alekshun, M. N. (2006). MarA, SoxS and Rob function as virulence factors in an Escherichia coli murine model of ascending pyelonephritis. Microbiology 152: 3643-3650 [Abstract] [Full Text]  
  • Papavinasasundaram, K. G., Chan, B., Chung, J.-H., Colston, M. J., Davis, E. O., Av-Gay, Y. (2005). Deletion of the Mycobacterium tuberculosis pknH Gene Confers a Higher Bacillary Load during the Chronic Phase of Infection in BALB/c Mice. J. Bacteriol. 187: 5751-5760 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»