病原体蛋白 EspF(U) 通过模仿和多价值性劫持了actin聚合.
Nathan A Sallee1, Gonzalo M Rivera, John E Dueber
1Graduate Program in Chemistry and Chemical Biology, University of California, San Francisco, 600 16th Street, San Francisco, California 94158, USA.
Nature
|July 25, 2008
概括
肠道出血性大肠杆菌使用 EspF(U) 蛋白来触发宿主细胞中的行为基脚的形成. 这种蛋白质独特地模仿了一个内部的N-WASP元素,而不是CDC42,以激活细菌附着的actin聚合.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 肠道出血性大肠杆菌 (EHEC) 使用actin脚架进行肠道附着.
- 细菌蛋白 EspF(U) (TccP) 注射到宿主细胞中会诱导动因基脚的形成.
- EspF(U) 激活维斯科特-阿尔德里奇综合征蛋白 (WASP) 家庭的活性核子,通常由CDC42进行调节.
研究的目的:
- 阐明 EspF(U) 激活 N-WASP 的机制.
- 确定负责N-WASP相互作用的特定EspF(U) 动机.
- 了解 EspF(U) 如何利用宿主细胞机械进行细菌粘附.
主要方法:
- EspF的结构分析 (U) 重复.
- 在 EspF ((U)) 中识别N-WASP结合基因.
- 生物化学测试以测量活性蛋白聚合和N-WASP激活.
主要成果:
- 在 EspF(U) 重复中有一个17-氨基酸基因对N-WASP结合来说就足够了.
- EspF(U) 模仿了N-WASP的自身抑制元件,而不是自然激活剂CDC42.
- 通过协调N-WASP激活,多重的EspF(U) 重复增强了actin聚合功效.
结论:
- EHEC EspF(U) 通过破坏其自身抑制状态来激活N-WASP,提供一种新的病原体与宿主相互作用机制.
- 病原体已经设计了一个强大的actin聚合机器,使用简单的,重复的自身抑制片段.
- 这种机制允许选择性激活特定的细胞过程,促进细菌殖民.
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