Potyvirus RNA沉默抑制因子VPg通过泛素化和自噬途径来介SGS3降解
发表在JV上的关于植物病毒的文章。进一步明确了病毒蛋白参与寄主的自噬途径。
The Potyviral Silencing Suppressor Protein VPg Mediates Degradation of SGS3 via Ubiquitination and Autophagy PathwaysXiaofei Cheng and Aiming Wang*
RNA silencing is an innate antiviral immunity of plants and animals. To counteract this host immune response, viruses have evolved an effective strategy to protect themselves by expression of viral suppressors of RNA silencing (VSRs). Most potyviruses encode two VSRs, the helper component-proteinase (HC-Pro) and the viral genome-linked protein (VPg). The molecular biology of the former has been well characterized, whereas how VPg exerts its function in RNA silencing suppression is yet to be understood. In this study, we show that infection by Turnip mosaic virus (TuMV) causes the reduced level of SUPPRESSOR OF GENE SILENCING3 (SGS3), a key component of the RNA silencing pathway that functions in double-stranded RNA synthesis for virus-derived siRNA (vsiRNA) production. We also demonstrate that among 11 TuMV-encoded viral proteins, VPg is the only one that interacts with SGS3. We further present evidence that expression of VPg alone, independent of viral infection, is sufficient to induce the degradation of SGS3 and its intimate partner, RNA-DEPENDENT RNA POLYMERASE6 (RDR6). Moreover, we discover that the VPg-mediated degradation of SGS3 is via both the 20S ubiquitin-proteasome and autophagy pathways. Taken together, our data suggest a role for VPg-mediated degradation of SGS3 in silencing suppression by VPg.
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IMPORTANCE Potyviruses represent the largest group of known plant viruses and cause significant losses in many agriculturally important crops in the world. In order to establish their infections, potyviruses must overcome 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.http://jvi.asm.org/content/early/2016/10/14/JVI.01478-16.abstract
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