An oomycete effector subverts host vesicle trafficking to channel starvation-induced autophagy to the pathogen interface

卵菌效应器破坏宿主囊泡运输,将饥饿诱导的自噬引导至病原体界面

阅读:6
作者:Pooja Pandey #, Alexandre Y Leary #, Yasin Tumtas, Zachary Savage, Bayantes Dagvadorj, Cian Duggan, Enoch Lh Yuen, Nattapong Sanguankiattichai, Emily Tan, Virendrasinh Khandare, Amber J Connerton, Temur Yunusov, Mathias Madalinski, Federico Gabriel Mirkin, Sebastian Schornack, Yasin Dagdas, Sophien

Abstract

Eukaryotic cells deploy autophagy to eliminate invading microbes. In turn, pathogens have evolved effector proteins to counteract antimicrobial autophagy. How adapted pathogens co-opt autophagy for their own benefit is poorly understood. The Irish famine pathogen Phytophthora infestans secretes the effector protein PexRD54 that selectively activates an unknown plant autophagy pathway that antagonizes antimicrobial autophagy at the pathogen interface. Here, we show that PexRD54 induces autophagosome formation by bridging vesicles decorated by the small GTPase Rab8a with autophagic compartments labeled by the core autophagy protein ATG8CL. Rab8a is required for pathogen-triggered and starvation-induced but not antimicrobial autophagy, revealing specific trafficking pathways underpin selective autophagy. By subverting Rab8a-mediated vesicle trafficking, PexRD54 utilizes lipid droplets to facilitate biogenesis of autophagosomes diverted to pathogen feeding sites. Altogether, we show that PexRD54 mimics starvation-induced autophagy to subvert endomembrane trafficking at the host-pathogen interface, revealing how effectors bridge distinct host compartments to expedite colonization.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。