Salmonella typhimurium encodes a putative iron transport system within thecentisome 63 pathogenicity island

Upon entry into the host, Salmonella enterica strains are presumed to encou nter on iron-restricted environment. Consequently, these bacteria have evol ved a variety of often-redundant high-affinity acquisition systems to obtai n iron in this restricted environment. We have identified an iron transport system that is encoded within the centisome 63 pathogenicity island of Sal monella typhimurium. The nucleotide composition of this locus is significan tly different from that of the rest of this pathogenicity island, suggestin g a different ancestry and a mosaic structure for this region of the S. typ himurium chromosome. This locus, designated sit, consists of four open read ing frames which encode polypeptides with extensive homology to the yfe ABC iron transport system of Yersinia pestis, as well as other ABC transporter s. The sitA gene encodes a putative periplasmic binding protein, sitB encod es an ATP-binding protein, and sitC and sitD encode two putative permeases (integral membrane proteins). This operon is capable of complementing the g rowth defect of the enterobactin-deficient Escherichia coil strain SAB11 in iron-restricted minimal medium. Transcription of the sit operon is repress ed under iron-rich growth conditions in a fur dependent manner. Introductio n of a sitBCD deletion into wild-type S. typhimurium resulted in no apparen t growth defect in either nutrient-rich or minimal medium and no measurable virulence phenotype. These results further support the existence of redund ant iron uptake systems in S. enterica.