肌动蛋白解聚因子
皮动蛋白
肌动蛋白
肌动蛋白细胞骨架
细胞生物学
液泡
Wiskott–Aldrich综合征蛋白
福氏志贺氏菌
效应器
生物
脂筏
微生物学
细胞骨架
细胞质
细胞
生物化学
信号转导
基因
大肠杆菌
作者
Sonja Kühn,John Bergqvist,Magdalena Gil,Camila Valenzuela,Laura Barrio,Stéphanie Lebreton,Chiara Zurzolo,Jost Enninga
出处
期刊:Cell Reports
[Elsevier]
日期:2020-05-01
卷期号:31 (6): 107638-107638
被引量:28
标识
DOI:10.1016/j.celrep.2020.107638
摘要
The enteroinvasive bacterium Shigella flexneri forces its uptake into non-phagocytic host cells through the translocation of T3SS effectors that subvert the actin cytoskeleton. Here, we report de novo actin polymerization after cellular entry around the bacterium-containing vacuole (BCV) leading to the formation of a dynamic actin cocoon. This cocoon is thicker than any described cellular actin structure and functions as a gatekeeper for the cytosolic access of the pathogen. Host CDC42, TOCA-1, N-WASP, WIP, the Arp2/3 complex, cortactin, coronin, and cofilin are recruited to the actin cocoon. They are subverted by T3SS effectors, such as IpgD, IpgB1, and IcsB. IcsB immobilizes components of the actin polymerization machinery at the BCV dependent on its fatty acyltransferase activity. This represents a unique microbial subversion strategy through localized entrapment of host actin regulators causing massive actin assembly. We propose that the cocoon promotes subsequent invasion steps for successful Shigella infection.
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