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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.

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.
Published ahead of print on 16 March 2009.
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