The Potyvirus Silencing Suppressor Protein VPg Mediates Degradation of SGS3 via Ubiquitination and Autophagy Pathways
The Potyvirus Silencing Suppressor Protein VPg Mediates Degradation of SGS3 via Ubiquitination and Autophagy Pathways
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DOI：
10.1128/jvi.01478-16
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发表时间：
2017-01-01
影响因子：
5.4
通讯作者：
Wang, Aiming
中科院分区：
文献类型：
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作者：
Cheng, Xiaofei;Wang, Aiming
RNA沉默是动植物的一种先天抗病毒免疫反应。为了对抗这种宿主免疫反应，病毒已经进化出一种有效的策略，通过表达RNA沉默的病毒抑制物(VSR)来保护自己。大多数马铃薯Y病毒编码两个VSR，辅助成分-蛋白酶(HCPro)和病毒基因组连锁蛋白(VPG)。前者的分子生物学特征已经很好，但VPG如何发挥其在抑制RNA沉默中的作用尚不清楚。在本研究中，我们发现芜菁花叶病毒(TuMV)感染导致基因沉默抑制因子3(SGS3)水平降低，SGS3是RNA沉默途径的关键组成部分，在双链RNA合成中发挥作用，以产生病毒衍生的小干扰RNA(VsiRNA)。我们还证明了在11个TuMV编码的病毒蛋白中，VPG是唯一与SGS3相互作用的蛋白。我们进一步提出的证据表明，VPG的单独表达，独立于病毒感染，足以诱导SGS3及其亲密伙伴RNA依赖的RNA聚合酶6(RDR6)的降解。此外，我们发现VPG介导的SGS3的降解通过20S泛素-蛋白酶体和自噬途径发生。综上所述，我们的数据表明VPG介导的SGS3的降解在抑制VPg沉默方面发挥了作用。重要的马铃薯Y病毒是已知的植物病毒中最大的一组，造成世界上许多重要农业作物的重大损失。为了确定感染，马铃薯Y病毒必须克服宿主的抗病毒沉默反应。一种名为VPG的病毒蛋白已被证明在这一过程中发挥了作用，但它是如何发挥作用的尚不清楚。本文发现芜菁花叶病毒(TuMV)的VPG蛋白是一种马铃薯Y病毒，它与宿主蛋白SGS3相互作用，SGS3是RNA沉默途径中的关键蛋白。此外，这种相互作用导致SGS3及其相互作用和功能伙伴RDR6的降解，RDR6是RNA沉默途径的另一个重要组成部分。我们还确定了VPG介导的SGS3降解所招募的细胞途径。因此，这项工作揭示了VPG破坏宿主抗病毒RNA沉默以促进病毒感染的可能机制。
RNA silencing is an innate antiviral immunity response of plants and animals. To counteract this host immune response, viruses have evolved an effective strategy to protect themselves by the expression of viral suppressors of RNA silencing (VSRs). Most potyviruses encode two VSRs, helper component-proteinase (HCPro) and viral genome-linked protein (VPg). The molecular biology of the former has been well characterized, whereas how VPg exerts its function in the suppression of RNA silencing is yet to be understood. In this study, we show that infection by Turnip mosaic virus (TuMV) causes reduced levels of suppressor of gene silencing 3 (SGS3), a key component of the RNA silencing pathway that functions in double-stranded RNA synthesis for virus-derived small interfering RNA (vsiRNA) production. We also demonstrate that among 11 TuMV-encoded viral proteins, VPg is the only one that interacts with SGS3. We furthermore present evidence that the expression of VPg alone, independent of viral infection, is sufficient to induce the degradation of SGS3 and its intimate partner RNA-dependent RNA polymerase 6 (RDR6). Moreover, we discover that the VPg-mediated degradation of SGS3 occurs via both the 20S ubiquitin-proteasome and autophagy pathways. Taken together, our data suggest a role for VPg-mediated degradation of SGS3 in suppression of silencing by VPg.IMPORTANCE Potyviruses represent the largest group of known plant viruses and cause significant losses of many agriculturally important crops in the world. In order to establish infection, potyviruses must overcome the host antiviral silencing response. A viral protein called VPg has been shown to play a role in this process, but how it works is unclear. In this paper, we found that the VPg protein of Turnip mosaic virus (TuMV), which is a potyvirus, interacts with a host protein named SGS3, a key protein in the RNA silencing pathway. Moreover, this interaction leads to the degradation of SGS3 and its interacting and functional partner RDR6, which is another essential component of the RNA silencing pathway. We also identified the cellular pathways that are recruited for the VPg-mediated degradation of SGS3. Therefore, this work reveals a possible mechanism by which VPg sabotages host antiviral RNA silencing to promote virus infection.