eIF4A, a target of siRNA derived from rice stripe virus, negatively regulates antiviral autophagy by interacting with ATG5 in Nicotiana benthamiana
文献类型： 外文期刊
作者： Zhang, Xiangxiang 1 ; Yin, Yueyan 1 ; Su, Yunhe 1 ; Jia, Zhaoxing 1 ; Jiang, Liangliang 1 ; Lu, Yuwen 1 ; Zheng, Hongy 1 ;
作者机构： 1.Ningbo Univ, Inst Plant Virol, State Key Lab Managing Biot & Chem Threats Qual &, Ningbo, Peoples R China
2.Yunnan Agr Univ, Plant Protect Coll, Kunming, Yunnan, Peoples R China
3.Zhejiang Acad Agr Sci, Inst Virol & Biotechnol, Key Lab Biotechnol Plant Protect, Minist Agr & Zhejiang Prov, Hangzhou, Peoples R China
期刊名称：PLOS PATHOGENS （ 影响因子：6.823； 五年影响因子：7.455 ）
ISSN： 1553-7366
年卷期： 2021 年 17 卷 9 期
页码：
收录情况： SCI
摘要： Autophagy is induced by viral infection and has antiviral functions in plants, but the underlying mechanism is poorly understood. We previously identified a viral small interfering RNA (vsiRNA) derived from rice stripe virus (RSV) RNA4 that contributes to the leaf-twisting and stunting symptoms caused by this virus by targeting the host eukaryotic translation initiation factor 4A (eIF4A) mRNA for silencing. In addition, autophagy plays antiviral roles by degrading RSV p3 protein, a suppressor of RNA silencing. Here, we demonstrate that eIF4A acts as a negative regulator of autophagy in Nicotiana benthamiana. Silencing of NbeIF4A activated autophagy and inhibited RSV infection by facilitating autophagic degradation of p3. Further analysis showed that NbeIF4A interacts with NbATG5 and interferes with its interaction with ATG12. Overexpression of NbeIF4A suppressed NbATG5-activated autophagy. Moreover, expression of vsiRNA-4A, which targets NbeIF4A mRNA for cleavage, induced autophagy by silencing NbeIF4A. Finally, we demonstrate that eIF4A from rice, the natural host of RSV, also interacts with OsATG5 and suppresses OsATG5-activated autophagy, pointing to the conserved function of eIF4A as a negative regulator of antiviral autophagy. Taken together, these results reveal that eIF4A negatively regulates antiviral autophagy by interacting with ATG5 and that its mRNA is recognized by a virus-derived siRNA, resulting in its silencing, which induces autophagy against viral infection.
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