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首页> 美国卫生研究院文献>Journal of Bacteriology >Requirement of Staphylococcus aureus ATP-Binding Cassette-ATPase FhuC for Iron-Restricted Growth and Evidence that It Functions with More than One Iron Transporter
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Requirement of Staphylococcus aureus ATP-Binding Cassette-ATPase FhuC for Iron-Restricted Growth and Evidence that It Functions with More than One Iron Transporter

机译：金黄色葡萄球菌ATP结合盒式ATPase FhuC对铁限制生长的要求及其与多种铁转运蛋白结合起作用的证据

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In Staphylococcus aureus, fhuCBG encodes an ATP-binding cassette (ABC) transporter that is required for the transport of iron(III)-hydroxamates; mutation of either fhuB or fhuG eliminates transport. In this paper, we describe construction and characterization of an S. aureus fhuCBG deletion strain. The ΔfhuCBG::ermC mutation not only resulted in a strain that was incapable of growth on iron(III)-hydroxamates as a sole source of iron but also resulted in a strain which had a profound growth defect in iron-restricted laboratory media. The growth defect was not a result of the inability to transport iron(III)-hydroxamates since S. aureus fhuG::Tn917 and S. aureus fhuD1::Km fhuD2::Tet mutants, which are also unable to transport iron(III)-hydroxamates, do not have similar iron-restricted growth defects. Complementation experiments demonstrated that the growth defect of the ΔfhuCBG::ermC mutant was the result of the inability to express FhuC and that this was the result of an inability to transport iron complexed to the S. aureus siderophore staphylobactin. Transport of iron(III)-staphylobactin is dependent upon SirA (binding protein), SirB (permease), and SirC (permease). S. aureus expressing FhuC with a Walker A K42N mutation could not utilize iron(III)-hydroxamates or iron(III)-staphylobactin as a sole source of iron, supporting the conclusion that FhuC, as expected, functions with FhuB, FhuG, and FhuD1 or FhuD2 to transport iron(III)-hydroxamates and is the “genetically unlinked” ABC-ATPase that functions with SirA, SirB, and SirC to transport iron(III)-staphylobactin. Finally, we demonstrated that the ΔfhuCBG::ermC strain had decreased virulence in a murine kidney abscess model.
机译：在金黄色葡萄球菌中，fhuCBG编码一个ATP结合盒（ABC）转运蛋白，这是铁（III）-羟肟酸铁转运所必需的。 fhuB或fhuG的突变消除了转运。在本文中，我们描述了金黄色葡萄球菌fhuCBG缺失菌株的构建和表征。 ΔfhuCBG:: ermC突变不仅导致菌株无法作为唯一铁源在异羟肟酸铁（III）上生长，而且导致菌株在铁受限的实验室培养基中具有严重的生长缺陷。自金黄色葡萄球菌fhuG :: Tn917和金黄色葡萄球菌fhuD1 :: Km fhuD2 :: Tet突变体以来，不能运输铁（III）的原因不是生长缺陷，而是因为不能运输铁（III）。 -异羟肟酸酯，没有类似的铁限制生长缺陷。补充实验表明，ΔfhuCBG:: ermC突变体的生长缺陷是由于无法表达FhuC的结果，而这是由于无法转运复合至金黄色葡萄球菌铁载体葡萄球菌素的铁的结果。铁（III）-葡萄球菌蛋白酶的转运依赖于SirA（结合蛋白），SirB（通透酶）和SirC（通透酶）。表达带有Walker A K42N突变的金黄色葡萄球菌不能利用异羟肟酸铁（III）或葡萄球菌铁（III）作为唯一的铁源，支持了这样的结论，即FhuC可以预期与FhuB，FhuG和FhuD1或FhuD2可以运输异羟肟酸铁（III），是与SirA，SirB和SirC起作用的“遗传上未连接的” ABC-ATPase，可以运输铁（III）-葡萄球菌素。最后，我们证明了在鼠肾脓肿模型中ΔfhuCBG:: ermC菌株的毒力降低。

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