A plant RNA virus activates selective autophagy in a UPR-dependent manner to promote virus infection

文献类型: 外文期刊

第一作者: Li, Fangfang

作者: Li, Fangfang;Zhang, Changwei;Tang, Ziwei;Zhang, Lingrui;Dai, Zhaoji;Lyu, Shanwu;Li, Yinzi;Wang, Aiming;Li, Fangfang;Zhang, Changwei;Lyu, Shanwu;Hou, Xilin;Tang, Ziwei;Zhang, Lingrui;Dai, Zhaoji;Bernards, Mark

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关键词: autophagy; potyvirus; RNA-dependent RNA polymerase (RdRp); tonoplast; turnip mosaic virus (TuMV); unfolded protein response (UPR); vacuole; virus replication complex (VRC)

期刊名称:NEW PHYTOLOGIST ( 影响因子:10.151; 五年影响因子:10.475 )

ISSN: 0028-646X

年卷期: 2020 年 228 卷 2 期

页码:

收录情况: SCI

摘要: Autophagy is an evolutionarily conserved pathway in eukaryotes that delivers unwanted cytoplasmic materials to the lysosome/vacuole for degradation/recycling. Stimulated autophagy emerges as an integral part of plant immunity against intracellular pathogens. In this study, we used turnip mosaic virus (TuMV) as a model to investigate the involvement of autophagy in plant RNA virus infection. The small integral membrane protein 6K2 of TuMV, known as a marker of the virus replication site and an elicitor of the unfolded protein response (UPR), upregulates the selective autophagy receptor geneNBR1in a UPR-dependent manner. NBR1 interacts with TuMV NIb, the RNA-dependent RNA polymerase of the virus replication complex (VRC), and the autophagy cargo receptor/adaptor protein ATG8f. The NIb/NBR1/ATG8f interaction complexes colocalise with the 6K2-stained VRC. Overexpression of NBR1 or ATG8f enhances TuMV replication, and deficiency of NBR1 or ATG8f inhibits virus infection. In addition, ATG8f interacts with the tonoplast-specific protein TIP1 and the NBR1/ATG8f-containing VRC is enclosed by the TIP1-labelled tonoplast. In TuMV-infected cells, numerous membrane-bound viral particles are evident in the vacuole. Altogether these results suggest that TuMV activates and manipulates UPR-dependent NBR1-ATG8f autophagy to target the VRC to the tonoplast to promote viral replication and virion accumulation.

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