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A Viral RNA Silencing Suppressor Modulates Reactive Oxygen Species Levels to Induce the Autophagic Degradation of Dicer-Like and Argonaute-Like Proteins

文献类型： 外文期刊

作者： Zhai, Shiyu 1 ; Pang, Tianxing 1 ; Peng, Shiyu 1 ; Zou, Shenshen 3 ; Deng, Zhiping 4 ; Suzuki, Nobuhiro 5 ; Kang, Zhensheng 1 ; Andika, Ida Bagus 1 ; Sun, Liying 1 ;

作者机构： 1.Northwest A&F Univ, State Key Lab Crop Stress Biol Arid Areas, Yangling 712100, Shaanxi, Peoples R China

2.Northwest A&F Univ, Coll Plant Protect, Yangling 712100, Shaanxi, Peoples R China

3.Shandong Agr Univ, Coll Plant Protect, Dept Plant Pathol, Tai An 271002, Peoples R China

4.Zhejiang Acad Agr Sci, Inst Virol & Biotechnol, Hangzhou 310021, Zhejiang, Peoples R China

5.Okayama Univ, Inst Plant Sci & Resources, Kurashiki 7100046, Japan

6.Northwest A&F Univ, Inst Future Agr, Yangling 712100, Shaanxi, Peoples R China

关键词： argonaute; autophagic degradation; cryphonectria hypovirus 1; dicer; reactive oxygen species; RNA silencing suppressor

期刊名称：ADVANCED SCIENCE （ 影响因子：14.1； 五年影响因子：15.6 ）

ISSN：

年卷期： 2025 年

页码：

收录情况： SCI

摘要： Mounting evidence indicates that viruses exploit elevated reactive oxygen species (ROS) levels to promote replication and pathogenesis, yet the mechanistic underpinnings of this viral strategy remain elusive for many viral systems. This study uncovers a sophisticated viral counter-defense mechanism in the Cryphonectria hypovirus 1 (CHV1)-Fusarium graminearum system, where the viral p29 protein subverts host redox homeostasis to overcome antiviral responses. That p29 directly interacts with and inhibits the enzymatic activity of fungal NAD(P)H-dependent FMN reductase 1 (FMR1), leading to increased ROS accumulation and subsequent autophagy activation is demonstrated. Strikingly, this ROS-induced autophagy selectively targets for degradation two core antiviral RNA silencing components against CHV1 in F. graminearum, Dicer-like 2 (DCL2) and Argonaute-like 1 (AGL1), thereby compromising the host's primary antiviral defense system. Genetic analysis confirms this coordinated hijacking of host machineries, as CHV1 shows enhanced accumulation in the FMR1 knockout and reduced accumulation in autophagy-deficient fungal strains. This work reveals a tripartite interplay among oxidative stress, autophagy, and RNA silencing that CHV1 manipulates through p29 multifunctional activity. These findings provide a model for how viruses coordinately regulate distinct host defense systems to optimize infection.

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