The C4 Protein of TbLCYnV Promotes SnRK1 β2 Degradation Via the Autophagy Pathway to Enhance Viral Infection in N. benthamiana

文献类型： 外文期刊

第一作者： Li, Xinquan

作者： Li, Xinquan;Zhao, Min;Yang, Wanyi;Zhou, Xueping;Xie, Yan;Zhou, Xueping

作者机构：

关键词： SnRK1; NbSnRK1 beta 2; TbLCYnV C4; interaction; degradation; autophagy pathway

期刊名称：VIRUSES-BASEL （ 影响因子：4.7； 五年影响因子：4.8 ）

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年卷期： 2024 年 16 卷 2 期

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收录情况： SCI

摘要： Geminiviruses are a group of single-stranded DNA viruses that have developed multiple strategies to overcome host defenses and establish viral infections. Sucrose nonfermenting-1-related kinase 1 (SnRK1) is a key regulator of energy balance in plants and plays an important role in plant development and immune defenses. As a heterotrimeric complex, SnRK1 is composed of a catalytic subunit alpha (SnRK1 alpha) and two regulatory subunits, beta and gamma. Previous studies on SnRK1 in plant defenses against microbial pathogens have mainly focused on SnRK1 alpha. In this study, we validated the interaction between the C4 protein encoded by tobacco leaf curl Yunnan virus (TbLCYnV) and the regulatory subunit beta of Nicotiana benthamiana SnRK1, i.e., NbSnRK1 beta 2, and identified that the Asp22 of C4 is critical for TbLCYnV C4-NbSnRK1 beta 2 interactions. NbSnRK1 beta 2 silencing in N. benthamiana enhances susceptibility to TbLCYnV infection. Plants infected with viral mutant TbLCYnV (C4(D22A)), which contains the mutant version C4 (D22A) that is incapable of interacting with NbSnRK1 beta 2, display milder symptoms and lower viral accumulation. Furthermore, we discovered that C4 promotes NbSnRK1 beta 2 degradation via the autophagy pathway. We herein propose a model by which the geminivirus C4 protein causes NbSnRK1 beta 2 degradation via the TbLCYnV C4-NbSnRK1 beta 2 interaction to antagonize host antiviral defenses and facilitates viral infection and symptom development in N. benthamiana.

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