{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T13:05:29Z","timestamp":1780578329073,"version":"3.54.1"},"reference-count":63,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2009,5,1]],"date-time":"2009-05-01T00:00:00Z","timestamp":1241136000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The\n            <jats:italic>sit<\/jats:italic>\n            -encoded iron transport system is present within pathogenicity islands in all\n            <jats:italic>Shigella<\/jats:italic>\n            spp. and some pathogenic\n            <jats:italic>Escherichia coli<\/jats:italic>\n            strains. The islands contain numerous insertion elements and sequences with homology to bacteriophage genes. The\n            <jats:italic>Shigella flexneri sit<\/jats:italic>\n            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\n            <jats:italic>sit<\/jats:italic>\n            region is inherently unstable, yet\n            <jats:italic>sit<\/jats:italic>\n            genes are maintained in all of the clinical isolates tested. Characterization of the\n            <jats:italic>sitABCD<\/jats:italic>\n            genes in\n            <jats:italic>S. flexneri<\/jats:italic>\n            indicates that they encode a ferrous iron transport system, although the genes are induced aerobically. The\n            <jats:italic>sit<\/jats:italic>\n            genes provide a competitive advantage to\n            <jats:italic>S. flexneri<\/jats:italic>\n            growing within epithelial cells, and a\n            <jats:italic>sitA<\/jats:italic>\n            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\n            <jats:italic>sitA<\/jats:italic>\n            mutant was able to infect the mice and induce a protective immune response but was avirulent compared to its wild-type parent strain.\n          <\/jats:p>","DOI":"10.1128\/iai.00064-09","type":"journal-article","created":{"date-parts":[[2009,3,17]],"date-time":"2009-03-17T00:54:04Z","timestamp":1237251244000},"page":"1992-1999","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":40,"title":["Genetics and Virulence Association of the\n            <i>Shigella flexneri<\/i>\n            Sit Iron Transport System"],"prefix":"10.1128","volume":"77","author":[{"given":"Carolyn R.","family":"Fisher","sequence":"first","affiliation":[{"name":"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"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicola M. 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