vanZ, a member of the VanA glycopeptide resistance gene cluster, confers resistance to lipoglycopeptide antibiotics independent of cell wall precursor modification by the vanHAX genes. Orthologs of vanZ are present in the genomes of many clinically relevant bacteria, including Enterococcus faecium and Streptococcus pneumoniae; however, vanZ genes are absent in Staphylococcus aureus. Here, we show that the expression of enterococcal vanZ paralogs in S. aureus increases the minimal inhibitory concentrations of lipoglycopeptide antibiotics teicoplanin, dalbavancin, oritavancin and new teicoplanin pseudoaglycone derivatives. The reduction in the binding of fluorescently labeled teicoplanin to the cells suggests the mechanism of VanZ-mediated resistance. In addition, using a genomic vanZ gene knockout mutant of S. pneumoniae, we have shown that the ability of VanZ proteins to compromise the activity of lipoglycopeptide antibiotics by reducing their binding is a more general feature of VanZ-superfamily proteins.

中文翻译：

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VanZ减少了脂糖肽抗生素与金黄色葡萄球菌和肺炎链球菌细胞的结合。

VanZ是VanA糖肽耐药性基因簇的成员，赋予对脂糖肽抗生素的耐药性，而不受vanHAX基因对细胞壁前体的修饰。vanZ的直系同源基因存在于许多临床相关细菌的基因组中，包括粪肠球菌和肺炎链球菌。但是，金黄色葡萄球菌中不存在vanZ基因。在这里，我们显示肠球菌vanZ旁系同源物在金黄色葡萄球菌中的表达增加了脂肽抗生素抗生素替考拉宁，达巴万星，奥利万星和新的替考拉宁伪糖苷配基的最小抑菌浓度。荧光标记的替考拉宁与细胞结合的减少表明VanZ介导的抗性机制。此外，使用肺炎链球菌的基因组vanZ基因敲除突变体，