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

• Published in: PLoS pathogens Vol. 16; no. 8; p. e1008801
• Main Authors: 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, Wang, Haiyang, Liu, Yuqiang, Wan, Jianmin
• Format: Journal Article
• Language: English
• Published: San Francisco Public Library of Science 31.08.2020; Public Library of Science (PLoS)
• Subjects: Acid resistance; Agricultural production; Biology and Life Sciences; Botanical research; Brassinosteroids; Breeding; Crop diseases; Crop science; Crosstalk; Disease resistance; Disease resistance (Plants); Diseases and pests; Engineering and Technology; Genes; Genetic engineering; Genetics; Germplasm; Infections; Jasmonates; Jasmonic acid; Laboratories; MicroRNAs; Molecular modelling; Pathogens; Pesticides; Phosphorylation; Physiological aspects; Plant breeding; Research and Analysis Methods; Rice; Signal transduction; Signaling; Steroids (Organic compounds); Viral diseases; Viruses; China; Beijing China
• ISSN: 1553-7374; 1553-7366; 1553-7374
• DOI: 10.1371/journal.ppat.1008801

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 in OsMYC2 (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.