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芜菁花叶病毒拮抗病毒沉默抑制子 HCpro 的选择性自噬。

Turnip Mosaic Virus Counteracts Selective Autophagy of the Viral Silencing Suppressor HCpro.

机构信息

Department of Plant Biology, Uppsala BioCenter, Swedish University of Agricultural Sciences (SLU) and Linnean Center for Plant Biology, 75007 Uppsala, Sweden.

Molecular Cancer Research Group, Institute of Medical Biology, University of Tromsø - The Arctic University of Norway, 9037 Tromsø, Norway.

出版信息

Plant Physiol. 2018 Jan;176(1):649-662. doi: 10.1104/pp.17.01198. Epub 2017 Nov 13.

Abstract

Autophagy is a conserved intracellular degradation pathway and has emerged as a key mechanism of antiviral immunity in metazoans, including the selective elimination of viral components. In turn, some animal viruses are able to escape and modulate autophagy for enhanced pathogenicity. Whether host autophagic responses and viral countermeasures play similar roles in plant-virus interactions is not well understood. Here, we have identified selective autophagy as antiviral pathway during plant infection with turnip mosaic virus (TuMV), a positive-stranded RNA potyvirus. We show that the autophagy cargo receptor NBR1 suppresses viral accumulation by targeting the viral RNA silencing suppressor helper-component proteinase (HCpro), presumably in association with virus-induced RNA granules. Intriguingly, TuMV seems to antagonize NBR1-dependent autophagy during infection by the activity of distinct viral proteins, thereby limiting its antiviral capacity. We also found that NBR1-independent bulk autophagy prevents premature plant death, thus extending the lifespan of virus reservoirs and particle production. Together, our study highlights a conserved role of selective autophagy in antiviral immunity and suggests the evolvement of viral protein functions to inhibit autophagy processes, despite a potential trade-off in host survival.

摘要

自噬是一种保守的细胞内降解途径,已成为真核生物抗病毒免疫的关键机制,包括对病毒成分的选择性消除。反过来,一些动物病毒能够逃避并调节自噬以增强致病性。宿主自噬反应和病毒对策在植物-病毒相互作用中是否发挥相似的作用,目前还不太清楚。在这里,我们已经确定在植物感染芜菁花叶病毒(TuMV)时,自噬是一种抗病毒途径,TuMV 是一种正链 RNA 马铃薯 Y 病毒科病毒。我们表明,自噬货物受体 NBR1 通过靶向病毒 RNA 沉默抑制辅助蛋白酶(HCpro)来抑制病毒积累,可能与病毒诱导的 RNA 颗粒有关。有趣的是,TuMV 似乎通过不同病毒蛋白的活性拮抗 NBR1 依赖性自噬,从而限制其抗病毒能力。我们还发现,NBR1 非依赖性批量自噬可防止植物过早死亡,从而延长病毒库和颗粒产生的寿命。总之,我们的研究强调了选择性自噬在抗病毒免疫中的保守作用,并表明病毒蛋白功能的进化抑制了自噬过程,尽管这可能对宿主生存造成潜在的权衡。

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