Contribution of the Shigella flexneri Sit, Iuc, and Feo Iron Acquisition Systems to Iron Acquisition In Vitro and in Cultured Cells

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Abstract
Shigella flexneri possesses multiple iron acquisition systems, including proteins involved in the synthesis and uptake of siderophores and the Feo system for ferrous iron utilization. We identified an additional S . flexneri putative iron transport gene, sitA , in a screen for S . flexneri genes that are induced in the eukaryotic intracellular environment. sitA was present in all Shigella species and in most enteroinvasive Escherichia coli strains but not in any other E . coli isolates tested. The sit locus consists of four genes encoding a potential ABC transport system. The deduced amino acid sequence of the S . flexneri sit locus was homologous to the Salmonella enterica serovar Typhimurium Sit and Yersinia pestis Yfe systems, which mediate both manganese and iron transport. The S . flexneri sit promoter was repressed by either iron or manganese, and the iron repression was partially dependent upon Fur. A sitA :: cam mutation was constructed in S . flexneri . The sitA mutant showed reduced growth, relative to the wild type, in Luria broth containing an iron chelator but formed wild-type plaques on Henle cell monolayers, indicating that the sitA mutant was able to acquire iron and/or manganese in the host cell. However, mutants defective in two of these iron acquisition systems ( sitA iucD , sitA feoB , and feoB iucD ) formed slightly smaller plaques on Henle cell monolayers. A strain carrying mutations in sitA , feoB , and iucD did not form plaques on Henle cell monolayers.