Turnip mosaic virus P1 suppresses JA biosynthesis by degrading cpSRP54 that delivers AOCs onto the thylakoid membrane to facilitate viral infection
文献类型： 外文期刊
作者： Ji, Mengfei 1 ; Zhao, Jinping 3 ; Han, Kelei 2 ; Cui, Weijun 1 ; Wu, Xinyang 1 ; Chen, Binghua 2 ; Lu, Yuwen 2 ; Peng, Jiejun 2 ; Zheng, Hongying 2 ; Rao, Shaofei 2 ; Wu, Guanwei 2 ; Chen, Jianping 1 ; Yan, Fei 2 ;
作者机构： 1.Zhejiang Univ, Coll Agr & Biotechnol, Hangzhou, Peoples R China
2.Ningbo Univ, Inst Plant Virol, State Key Lab Managing Biot & Chem Threats Qual &, Ningbo, Peoples R China
3.Zhejiang Acad Agr Sci, Inst Virol & Biotechnol, Key Lab Biotechnol Plant Protect MOA & Zhejiang P, Hangzhou, Peoples R China
期刊名称：PLOS PATHOGENS （ 影响因子：7.464； 五年影响因子：7.913 ）
ISSN： 1553-7366
年卷期： 2021 年 17 卷 12 期
页码：
收录情况： SCI
摘要： Jasmonic acid (JA) is a crucial hormone in plant antiviral immunity. Increasing evidence shows that viruses counter this host immune response by interfering with JA biosynthesis and signaling. However, the mechanism by which viruses affect JA biosynthesis is still largely unexplored. Here, we show that a highly conserved chloroplast protein cpSRP54 was downregulated in Nicotiana benthamiana infected by turnip mosaic virus (TuMV). Its silencing facilitated TuMV infection. Furthermore, cpSRP54 interacted with allene oxide cyclases (AOCs), key JA biosynthesis enzymes, and was responsible for delivering AOCs onto the thylakoid membrane (TM). Interestingly, TuMV P1 protein interacted with cpSRP54 and mediated its degradation via the 26S proteosome and autophagy pathways. The results suggest that TuMV has evolved a strategy, through the inhibition of cpSRP54 and its delivery of AOCs to the TM, to suppress JA biosynthesis and enhance viral infection. Interaction between cpSRP54 and AOCs was shown to be conserved in Arabidopsis and rice, while cpSRP54 also interacted with, and was degraded by, pepper mild mottle virus (PMMoV) 126 kDa protein and potato virus X (PVX) p25 protein, indicating that suppression of cpSRP54 may be a common mechanism used by viruses to counter the antiviral JA pathway.
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