Structures of two core subunits of the bacterial type IV secretion system,, VirB8 from Brucella suis and ComB10 from Helicobacter pylori
Structures of two core subunits of the bacterial type IV secretion system,, VirB8 from Brucella suis and ComB10 from Helicobacter pylori
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DOI：
10.1073/pnas.0408927102
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发表时间：
2005-03-22
影响因子：
11.1
通讯作者：
Waksman, G
中科院分区：
文献类型：
--
作者：
Terradot, L;Bayliss, R;Waksman, G
IV型分泌系统（T4 SSs）是革兰氏阴性菌中常用的分泌机制。它们用于感染人类、动物或植物细胞以及传播抗生素耐药性。T4 SS装置跨越细菌的两个膜，并且通常由12种蛋白质组成，以典型的根癌土壤杆菌T4 SS的蛋白质命名为VirB 1 -11和VirD 4。VirB 8/VirB 10的周质核心复合物在结构和功能上将系统的细胞质NTPases与其外膜和菌毛组分连接。在这里，我们提出的晶体结构的布鲁氏菌病的病原体猪的病毒B8，和ComB 10，幽门螺杆菌的病毒B10同源物，胃溃疡的病原体。VirB 8和科里的结构类似于已知的折叠，尽管具有其各自家族特有的和保守的新的二级结构修饰。这两种蛋白质都像晚餐一样结晶，提供了关于它们自我关联的详细预测。这些结构作出了重大贡献的剧目T4 SS组件结构，并将作为跳板，为未来的功能和蛋白质-蛋白质相互作用的研究，通过使用基于知识的定点突变和缺失突变。
Type IV secretion systems (T4SSs) are commonly used secretion machineries in Gram-negative bacteria. They are used in the infection of human, animal, or plant cells and the propagation of antibiotic resistance. The T4SS apparatus spans both membranes of the bacterium and generally is composed of 12 proteins, named VirB1-11 and VirD4 after proteins of the canonical Agrobacterium tumefaciens T4SS. The periplasmic core complex of VirB8/VirB10 structurally and functionally links the cytoplasmic NTPases of the system with its outer membrane and pilus components. Here we present crystal structures of VirB8 of Brucella suis, the causative agent of brucellosis, and ComB10, a VirB10 homolog of Helicobacter pylori, the causative agent of gastric ulcers. The structures of VirB8 and Cori resemble known folds, albeit with novel secondary-structure modifications unique to and conserved within their respective families. Both proteins crystallized as dinners, providing detailed predictions about their self associations. These structures make a substantial contribution to the repertoire of T4SS component structures and will serve as springboards for future functional and protein-protein interaction studies by using knowledge-based site-directed and deletion mutagenesis.