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 Google Scholar
Google Scholar
Right arrow Articles by Fisher, C. R.
Right arrow Articles by Payne, S. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fisher, C. R.
Right arrow Articles by Payne, S. M.

 Previous Article  |  Next Article 

Infection and Immunity, May 2009, p. 1992-1999, Vol. 77, No. 5
0019-9567/09/$08.00+0     doi:10.1128/IAI.00064-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Genetics and Virulence Association of the Shigella flexneri Sit Iron Transport System {triangledown}

Carolyn R. Fisher,1 Nicola M. L. L. Davies,1 Elizabeth E. Wyckoff,1 Zhengyu Feng,1 Edwin V. Oaks,2 and Shelley M. Payne1*

Section of Molecular Genetics and Microbiology, Institute for Cellular and Molecular Biology, 1 University Station A5000, The University of Texas at Austin, Austin, Texas 78712,1 Department of Enteric Infections/DCD&I, Walter Reed Army Institute of Research, Silver Spring, Maryland 20910-75002

Received 18 January 2009/ Returned for modification 16 February 2009/ Accepted 5 March 2009

The sit-encoded iron transport system is present within pathogenicity islands in all Shigella spp. and some pathogenic Escherichia coli strains. The islands contain numerous insertion elements and sequences with homology to bacteriophage genes. The Shigella flexneri sit genes can be lost as a result of deletion within the island. The formation of deletions was dependent upon RecA and occurred at relatively high frequency. This suggests that the sit region is inherently unstable, yet sit genes are maintained in all of the clinical isolates tested. Characterization of the sitABCD genes in S. flexneri indicates that they encode a ferrous iron transport system, although the genes are induced aerobically. The sit genes provide a competitive advantage to S. flexneri growing within epithelial cells, and a sitA mutant is outcompeted by the wild type in cultured epithelial cells. The Sit system is also required for virulence in a mouse lung model. The sitA mutant was able to infect the mice and induce a protective immune response but was avirulent compared to its wild-type parent strain.


* Corresponding author. Mailing address: The University of Texas at Austin, Molecular Genetics & Microbiology, 1 University Station A5000, Austin, TX 78712-0162. Phone: (512) 471-9258. Fax: (512) 471-7088. E-mail: payne{at}mail.utexas.edu

{triangledown} Published ahead of print on 16 March 2009.

Editor: A. J. Bäumler


Infection and Immunity, May 2009, p. 1992-1999, Vol. 77, No. 5
0019-9567/09/$08.00+0     doi:10.1128/IAI.00064-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.