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 Chakraborty, S.
Right arrow Articles by Thanassi, D. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chakraborty, S.
Right arrow Articles by Thanassi, D. G.

 Previous Article  |  Next Article 

Infection and Immunity, July 2008, p. 2852-2861, Vol. 76, No. 7
0019-9567/08/$08.00+0     doi:10.1128/IAI.01726-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Type IV Pili in Francisella tularensis: Roles of pilF and pilT in Fiber Assembly, Host Cell Adherence, and Virulence {triangledown}

Subhra Chakraborty,1 Michael Monfett,1 Tamara M. Maier,2 Jorge L. Benach,1 Dara W. Frank,2 and David G. Thanassi1*

Center for Infectious Diseases, Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York 11794-5120,1 Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin 532262

Received 21 December 2007/ Returned for modification 28 January 2008/ Accepted 6 April 2008

Francisella tularensis, a highly virulent facultative intracellular bacterium, is the causative agent of tularemia. Genome sequencing of all F. tularensis subspecies revealed the presence of genes that could encode type IV pili (Tfp). The live vaccine strain (LVS) expresses surface fibers resembling Tfp, but it was not established whether these fibers were indeed Tfp encoded by the pil genes. We show here that deletion of the pilF putative Tfp assembly ATPase in the LVS resulted in a complete loss of surface fibers. Disruption of the pilT putative disassembly ATPase also caused a complete loss of pili, indicating that pilT functions differently in F. tularensis than in model Tfp systems such as those found in Pseudomonas aeruginosa and Neisseria spp. The LVS pilF and pilT mutants were attenuated for virulence in a mouse model of tularemia by the intradermal route. Furthermore, although absence of pili had no effect on the ability of the LVS to replicate intracellularly, the pilF and pilT mutants were defective for adherence to macrophages, pneumocytes, and hepatocytes. This work confirms that the surface fibers expressed by the LVS are encoded by the pil genes and provides evidence that the Francisella pili contribute to host cell adhesion and virulence.

* Corresponding author. Mailing address: 242 Center for Infectious Diseases, Stony Brook University, Stony Brook, NY 11794-5120. Phone: (631) 632-4549. Fax: (631) 632-4294. E-mail: david.thanassi{at}stonybrook.edu

{triangledown} Published ahead of print on 21 April 2008.

Editor: A. Camilli

Infection and Immunity, July 2008, p. 2852-2861, Vol. 76, No. 7
0019-9567/08/$08.00+0     doi:10.1128/IAI.01726-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Buchan, B. W., McCaffrey, R. L., Lindemann, S. R., Allen, L.-A. H., Jones, B. D. (2009). Identification of migR, a Regulatory Element of the Francisella tularensis Live Vaccine Strain iglABCD Virulence Operon Required for Normal Replication and Trafficking in Macrophages. Infect. Immun. 77: 2517-2529 [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»