Staphylococcus aureus sortase mutants defective in the display of surface proteins and in the pathogenesis of animal infections
Staphylococcus aureus sortase mutants defective in the display of surface proteins and in the pathogenesis of animal infections
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DOI：
10.1073/pnas.080520697
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发表时间：
2000-05-09
影响因子：
11.1
通讯作者：
Schneewind, O
中科院分区：
文献类型：
--
作者：
Mazmanian, SK;Liu, G;Schneewind, O
许多革兰氏阳性细菌将它们的表面粘附素共价地拴在细胞壁的肽聚糖上。我们发现金黄色葡萄球菌的表面蛋白通过分选酶与细胞壁相连，分选酶在一个保守的LPXTG基序上切割多肽。缺乏分选酶的金黄色葡萄球菌突变体不能加工和显示表面蛋白，并且在建立感染方面存在缺陷。因此，克拉姆阳性细菌的细胞壁包膜代表了在细菌感染发病过程中负责与宿主环境相互作用的表面细胞器。
Many Gram-positive bacteria covalently tether their surface adhesins to the cell wall peptidoglycan. We find that surface proteins of Staphylococcus aureus are linked to the cell wall by sortase, an enzyme that cleaves polypeptides at a conserved LPXTG motif. S. aureus mutants lacking sortase fail to process and display surface proteins and are defective in the establishment of infections. Thus, the cell wall envelope of Cram-positive bacteria represents a surface organelle responsible for interactions with the host environment during the pathogenesis of bacterial infections.