{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T20:07:10Z","timestamp":1791317230672,"version":"4.3.1"},"reference-count":38,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2009,10,1]],"date-time":"2009-10-01T00:00:00Z","timestamp":1254355200000},"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":[[2009,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            We investigated the role of the 58-kDa FTT0918 protein in the iron metabolism of\n            <jats:italic>Francisella tularensis<\/jats:italic>\n            . The phenotypes of SCHU S4, a prototypic strain of\n            <jats:italic>F. tularensis<\/jats:italic>\n            subsp.\n            <jats:italic>tularensis<\/jats:italic>\n            , and the \u0394FTT0918 and \u0394\n            <jats:italic>fslA<\/jats:italic>\n            isogenic mutants were analyzed. The gene product missing in the \u0394\n            <jats:italic>fslA<\/jats:italic>\n            mutant is responsible for synthesis of a siderophore. When grown in broth with various iron concentrations, the two deletion mutants generally reached lower maximal densities than SCHU S4. The \u0394FTT0918 mutant, but not the \u0394\n            <jats:italic>fslA<\/jats:italic>\n            mutant, upregulated the genes of the\n            <jats:italic>F. tularensis<\/jats:italic>\n            siderophore locus (\n            <jats:italic>fsl<\/jats:italic>\n            ) operon even at high iron concentrations. A chrome azurol sulfonate plate assay confirmed siderophore production by all strains except the \u0394\n            <jats:italic>fslA<\/jats:italic>\n            strain. In a cross-feeding experiment using medium devoid of free iron, SCHU S4 promoted growth of the \u0394\n            <jats:italic>fslA<\/jats:italic>\n            strain but not of the \u0394FTT0918 strain. The sensitivity of SCHU S4 and the \u0394FTT0918 and \u0394\n            <jats:italic>fslA<\/jats:italic>\n            strains to streptonigrin demonstrated that the \u0394FTT0918 strain contained a smaller free intracellular iron pool and that the \u0394\n            <jats:italic>fslA<\/jats:italic>\n            strain contained a larger one than SCHU S4. In contrast to the marked attenuation of the \u0394FTT0918 strain, the \u0394\n            <jats:italic>fslA<\/jats:italic>\n            strain was as virulent as SCHU S4 in a mouse model. Altogether, the data demonstrate that the FTT0918 protein is required for\n            <jats:italic>F. tularensis<\/jats:italic>\n            to utilize iron bound to siderophores and that it likely has a role also in siderophore-independent iron acquisition. We suggest that the FTT0918 protein be designated Fe utilization protein A, FupA.\n          <\/jats:p>","DOI":"10.1128\/iai.00702-09","type":"journal-article","created":{"date-parts":[[2009,8,4]],"date-time":"2009-08-04T16:07:37Z","timestamp":1249402057000},"page":"4429-4436","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":53,"title":["The 58-Kilodalton Major Virulence Factor of\n            <i>Francisella tularensis<\/i>\n            Is Required for Efficient Utilization of Iron"],"prefix":"10.1128","volume":"77","author":[{"given":"Helena","family":"Lindgren","sequence":"first","affiliation":[{"name":"Department of Clinical Microbiology, Clinical Bacteriology, and Laboratory for Molecular Infection Medicine Sweden, Umea\u030a University, SE-90185 Umea\u030a, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie","family":"Honn","sequence":"additional","affiliation":[{"name":"Department of Clinical Microbiology, Clinical Bacteriology, and Laboratory for Molecular Infection Medicine Sweden, Umea\u030a University, SE-90185 Umea\u030a, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Igor","family":"Golovlev","sequence":"additional","affiliation":[{"name":"Department of Clinical Microbiology, Clinical Bacteriology, and Laboratory for Molecular Infection Medicine Sweden, Umea\u030a University, SE-90185 Umea\u030a, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Konstantin","family":"Kadzhaev","sequence":"additional","affiliation":[{"name":"Department of Clinical Microbiology, Clinical Bacteriology, and Laboratory for Molecular Infection Medicine Sweden, Umea\u030a University, SE-90185 Umea\u030a, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wayne","family":"Conlan","sequence":"additional","affiliation":[{"name":"National Research Council Canada, Institute for Biological Sciences, Ottawa, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anders","family":"Sjo\u0308stedt","sequence":"additional","affiliation":[{"name":"Department of Clinical Microbiology, Clinical Bacteriology, and Laboratory for Molecular Infection Medicine Sweden, Umea\u030a University, SE-90185 Umea\u030a, 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