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首页> 外文期刊>Infection and immunity >The Metal Homeostasis Protein, Lsp, of Streptococcus pyogenes Is Necessary for Acquisition of Zinc and Virulence
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The Metal Homeostasis Protein, Lsp, of Streptococcus pyogenes Is Necessary for Acquisition of Zinc and Virulence

机译：化脓性链球菌的金属稳态蛋白Lsp是获取锌和毒力所必需的

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“Cluster 9” family lipoproteins function as ligand-binding subunits of ABC-type transporters in maintaining transition metal homeostasis and have been implicated in the virulence of several bacteria. While these proteins share high similarity, the specific metal that they recognize and whether their role in virulence directly involves metal homeostasis cannot be reliably predicted. We examined the cluster 9 protein Lsp of Streptococcus pyogenes and found that specific deletion of lsp produced mutants highly attenuated in a murine model of soft tissue infection. Under standard in vitro conditions, growth of the Lsp? mutant was indistinguishable from that of the wild type, but growth was defective under zinc-limited conditions. The growth defect could be complemented by plasmids expressing wild-type Lsp but not Lsp engineered to lack its putative lipidation residue. Furthermore, Zn2+ but not Mn2+ rescued Lsp? growth, implicating Zn2+ as the physiological ligand for Lsp. Mutation of residues in the putative Zn2+-binding pocket generated variants both hypo- and hyperresistant to zinc starvation, and both mutant classes displayed attenuated virulence. Together, these data suggest that Lsp is a ligand-binding component of an ABC-type zinc permease and that perturbation of zinc homeostasis inhibits the ability of S. pyogenes to cause disease in a zinc-limited host milieu.
机译：“ Cluster 9”家族脂蛋白在维持过渡金属稳态中起着ABC型转运蛋白的配体结合亚基的作用，并且与几种细菌的毒性有关。尽管这些蛋白质具有高度相似性，但不能可靠地预测它们识别的特定金属以及它们在毒力中的作用是否直接涉及金属稳态。我们检查了化脓性链球菌的簇9蛋白Lsp，发现 lsp 的特定缺失在软组织感染的小鼠模型中高度减毒了突变体。在标准的体外条件下，Lsp β突变体的生长与野生型没有区别，但在锌受限的条件下生长有缺陷。表达野生型Lsp的质粒可以弥补生长缺陷，但工程改造后的Lsp不能缺少假定的脂化残基。此外，Zn 2 + 而不是Mn 2 + 拯救了Lsp ？的生长，暗示Zn 2 + 具有生理意义。 Lsp的配体。假定的Zn 2 + 结合口袋中残基的突变产生了对锌饥饿的低抗性和高抗性的变体，并且两个突变体类别均显示出弱毒力。总之，这些数据表明Lsp是ABC型锌通透酶的配体结合成分，锌稳态的扰动抑制了 S的能力。化脓引起锌限制的宿主环境中的疾病。

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