一个细菌效应器揭示了引发异种的V-ATPase-ATG16L1轴
Yue Xu1, Ping Zhou2, Sen Cheng3
1College of Biological Sciences, China Agricultural University, 100094 Beijing, China; National Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Cell
|July 23, 2019
概括
研究人员发现沙门氏菌
科学领域:
- 细胞生物学
- 微生物学
- 免疫学
背景情况:
- 自食,特别是异食,是对细胞内细菌的重要宿主防御机制.
- 外食症的确切发病途径尚不完全理解.
- 细菌病原体已经发展出逃避宿主免疫反应的策略,包括自.
研究的目的:
- 为了确定抑制异种的细菌因素.
- 为了阐明宿主机器参与启动异食症.
- 了解细菌效应器如何干扰宿主防御机制.
主要方法:
- 进行了细菌转子子查,以确定阻断异种的沙门氏菌.
- 使用CRISPR选来识别异种的重要宿主因素.
- 使用生物化学测试和基因突变来研究蛋白质相互作用和功能领域.
主要成果:
- 鉴定了SopF,一种III型分泌系统 (T3SS) 效应剂,作为沙门氏菌异的强有力的抑制剂.
- 发现宿主V-ATPase和ATG16L1复合物在真空损伤时调解异的启动.
- 在V-ATPase中,SopF通过ADP-ribosylatingGln124阻止异食,防止ATG16L1的招募.
结论:
- V-ATPase-ATG16L1轴对细胞内病原体的自识别至关重要.
- 沙门氏菌SopF因子通过向宿主轴来抑制外食,促进细菌的增殖.
- 这项研究揭示了一种新的细菌免疫逃避机制和宿主防御的关键途径.
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