Rice stripe virus suppresses jasmonic acid-mediated resistance by hijacking brassinosteroid signaling pathway in rice

文献类型： 外文期刊

第一作者： Hu, Jinlong

作者： Hu, Jinlong;Huang, Jie;Xu, Haosen;Wang, Yongsheng;Li, Chen;Wen, Peizheng;You, Xiaoman;Zhang, Xiao;Pan, Gen;Li, Qi;Zhang, Hongliang;He, Jun;Wu, Hongming;Jiang, Ling;Liu, Yuqiang;Wan, Jianmin;Wang, Haiyang;Wan, Jianmin

作者机构：

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： 2020 年 16 卷 8 期

页码：

收录情况： SCI

摘要： Author summary Brassinosteroids (BR) and jasmonic acid (JA) play critical roles in responding to various stresses. However, the roles of BR and JA, particularly, the crosstalk between these two phytohormones in viral resistance is still very limited. In this work, we found that both BR and JA positively regulate RSV resistance, and JA pathway is necessary for BR-mediated RSV resistance in rice. RSV infection significantly inhibits the BR signaling pathway and increases the accumulation of OsGSK2. OsGSK2 interacts with and phosphorylates OsMYC2, resulting in the degradation of OsMYC2 and suppression of the JA-mediated RSV resistance response to facilitate virus infection. These findings revealed the molecular mechanism of crosstalk between the BR and JA in response to virus infection and deepen our understanding about the mechanism of RSV resistance. Rice stripe virus (RSV) is one of the most destructive viral diseases affecting rice production. However, so far, only one RSV resistance gene has been cloned, the molecular mechanisms underlying host-RSV interaction are still poorly understood. Here, we show that increasing levels or signaling of brassinosteroids (BR) and jasmonic acid (JA) can significantly enhance the resistance against RSV. On the contrary, plants impaired in BR or JA signaling are more susceptible to RSV. Moreover, the enhancement of RSV resistance conferred by BR is impaired inOsMYC2(a key positive regulator of JA response) knockout plants, suggesting that BR-mediated RSV resistance requires active JA pathway. In addition, we found that RSV infection suppresses the endogenous BR levels to increase the accumulation of OsGSK2, a key negative regulator of BR signaling. OsGSK2 physically interacts with OsMYC2, resulting in the degradation of OsMYC2 by phosphorylation and reduces JA-mediated defense to facilitate virus infection. These findings not only reveal a novel molecular mechanism mediating the crosstalk between BR and JA in response to virus infection and deepen our understanding about the interaction of virus and plants, but also suggest new effective means of breeding RSV resistant crops using genetic engineering.

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