Yokota K, Kamio Y
Department of Molecular and Cell Biology, Graduate School of Agricultural Science, Tohoku University, Sendai, Japan.
Biosci Biotechnol Biochem. 2000 Dec;64(12):2744-7. doi: 10.1271/bbb.64.2744.
Staphylococcal bi-component cytotoxins, leukocidin (Luk), Panton-Valentine leukocidin (PVL), and gamma-hemolysin (Hlg) consist of LukF and LukS, LukF-PV and LukS-PV, and LukF and Hlg2, respectively, and Luk and Hlg share LukF. LukF-PV can not substitute for LukF for Hlg, despite 73% identity in amino acid sequence and close similarity in the 3-dimensional structure between them. Here, we demonstrated that the absence of hemolytic activity of LukF-PV in cooperation with Hlg2 is due to the failure of the binding of LukF-PV to human erythrocytes. We identified Y72 residue at the bottom of rim domain in LukF as the crucial residue for its binding, which is a prerequisite to the subsequent binding of Hlg2 to human erythrocytes. The data obtained showed that a mutant of LukF-PV in which T71 residue was replaced by the corresponding residue of LukF, Y72, endowed LukF-PV with the binding capability to human erythrocytes which was accompanied by its hemolytic activity in the presence of Hlg2.
葡萄球菌双组分细胞毒素，白细胞毒素（Luk）、杀白细胞素（PVL）和γ-溶血素（Hlg）分别由LukF和LukS、LukF-PV和LukS-PV、LukF和Hlg2组成，并且Luk和Hlg共享LukF。尽管LukF-PV与LukF在氨基酸序列上有73%的同一性且三维结构非常相似，但LukF-PV不能替代LukF与Hlg配合。在此，我们证明LukF-PV与Hlg2协同作用时缺乏溶血活性是由于LukF-PV无法与人红细胞结合。我们确定LukF边缘结构域底部的Y72残基是其结合的关键残基，这是随后Hlg2与人红细胞结合的先决条件。所得数据表明，将LukF-PV中的T71残基替换为LukF的相应残基Y72后，LukF-PV获得了与人红细胞的结合能力，并在Hlg2存在的情况下具有溶血活性。
