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 Domenech, P.
Right arrow Articles by Barry, C. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Domenech, P.
Right arrow Articles by Barry, C. E., III

 Previous Article  |  Next Article 

Journal of Bacteriology, January 2009, p. 477-485, Vol. 191, No. 2
0021-9193/09/$08.00+0     doi:10.1128/JB.01132-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

BacA, an ABC Transporter Involved in Maintenance of Chronic Murine Infections with Mycobacterium tuberculosis{triangledown}

Pilar Domenech,1,{dagger} Hajime Kobayashi,2 Kristin LeVier,2 Graham C. Walker,2 and Clifton E. Barry III1*

Tuberculosis Research Section, Laboratory of Clinical Infectious Disease, National Institute of Allergy and Infectious Disease, 33 North Drive, Bethesda, Maryland 20892,1 Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 021392

Received 12 August 2008/ Accepted 31 October 2008

BacA is an inner membrane protein associated with maintenance of chronic infections in several diverse host-pathogen interactions. To understand the function of the bacA gene in Mycobacterium tuberculosis (Rv1819c), we insertionally inactivated this gene and analyzed the resulting mutant for a variety of phenotypes. BacA deficiency in M. tuberculosis did not affect sensitivity to detergents, acidic pH, and zinc, indicating that there was no global compromise in membrane integrity, and a comprehensive evaluation of the major lipid constituents of the cell envelope failed to reveal any significant differences. Infection of mice with this mutant revealed no impact on establishment of infection but a profound effect on maintenance of extended chronic infection and ultimate outcome. As in alphaproteobacteria, deletion of BacA in M. tuberculosis led to increased bleomycin resistance, and heterologous expression of the M. tuberculosis BacA homolog in Escherichia coli conferred sensitivity to antimicrobial peptides. These results suggest a striking conservation of function for BacA-related proteins in transport of a critical molecule that determines the outcome of the host-pathogen interaction.

* Corresponding author. Mailing address: Tuberculosis Research Section, Laboratory of Clinical Infectious Diseases, Building 33, Room 2W20D, 33 North Drive, Bethesda, MD 20892. Phone: (301) 435-7509. Fax: (301) 480-5712. E-mail: cbarry{at}niaid.nih.gov

{triangledown} Published ahead of print on 7 November 2008.

{dagger} Present address: Research Institute of the McGill University Health Centre, 1650 Cedar Avenue, Montreal, Quebec H3G 1A4, Canada.

Journal of Bacteriology, January 2009, p. 477-485, Vol. 191, No. 2
0021-9193/09/$08.00+0     doi:10.1128/JB.01132-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Marlow, V. L., Haag, A. F., Kobayashi, H., Fletcher, V., Scocchi, M., Walker, G. C., Ferguson, G. P. (2009). Essential Role for the BacA Protein in the Uptake of a Truncated Eukaryotic Peptide in Sinorhizobium meliloti. J. Bacteriol. 191: 1519-1527 [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»