• 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 gene NBR1 in 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.

中文翻译：

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植物RNA病毒以UPR依赖性方式激活选择性自噬，从而促进病毒感染。

• 自噬是真核生物中进化上保守的途径，其将不需要的细胞质物质递送至溶酶体/真空，以进行降解/再循环。刺激的自噬已成为植物抵抗细胞内病原体免疫力的组成部分。
• 在这项研究中，我们使用芜菁花叶病毒（TuMV）作为模型来研究自噬在植物RNA病毒感染中的参与。
• TuMV的小整体膜蛋白6K2被称为病毒复制位点的标记和未折叠蛋白应答（UPR）的引发剂，它上调了选择性自噬受体基因NBR1以依赖UPR的方式。NBR1与TuMV NIb，病毒复制复合体（VRC）的RNA依赖性RNA聚合酶以及自噬货物受体/衔接蛋白ATG8f相互作用。NIb / NBR1 / ATG8f相互作用复合体与6K2染色的VRC共同定位。NBR1或ATG8f的过表达增强了TuMV复制，而NBR1或ATG8f的缺乏则抑制了病毒感染。此外，ATG8f与液泡膜特异性蛋白TIP1相互作用，并且含有NBR1 / ATG8f的VRC被TIP1标记的液泡膜包围。在TuMV感染的细胞中，液泡中明显有许多膜结合的病毒颗粒。
• 总而言之，这些结果表明TuMV激活并操纵了依赖UPR的NBR1-ATG8f自噬，从而将VRC靶向液泡膜以促进病毒复制和病毒体积累。