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

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 b...

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Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485985/
https://www.ncbi.nlm.nih.gov/pubmed/32866183
http://dx.doi.org/10.1371/journal.ppat.1008801
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author 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
author_facet 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
author_sort Hu, Jinlong
collection PubMed
description 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.
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spelling pubmed-74859852020-09-21 Rice stripe virus suppresses jasmonic acid-mediated resistance by hijacking brassinosteroid signaling pathway in rice 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 PLoS Pathog Research Article 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. Public Library of Science 2020-08-31 /pmc/articles/PMC7485985/ /pubmed/32866183 http://dx.doi.org/10.1371/journal.ppat.1008801 Text en © 2020 Hu et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
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
Rice stripe virus suppresses jasmonic acid-mediated resistance by hijacking brassinosteroid signaling pathway in rice
title Rice stripe virus suppresses jasmonic acid-mediated resistance by hijacking brassinosteroid signaling pathway in rice
title_full Rice stripe virus suppresses jasmonic acid-mediated resistance by hijacking brassinosteroid signaling pathway in rice
title_fullStr Rice stripe virus suppresses jasmonic acid-mediated resistance by hijacking brassinosteroid signaling pathway in rice
title_full_unstemmed Rice stripe virus suppresses jasmonic acid-mediated resistance by hijacking brassinosteroid signaling pathway in rice
title_short Rice stripe virus suppresses jasmonic acid-mediated resistance by hijacking brassinosteroid signaling pathway in rice
title_sort rice stripe virus suppresses jasmonic acid-mediated resistance by hijacking brassinosteroid signaling pathway in rice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485985/
https://www.ncbi.nlm.nih.gov/pubmed/32866183
http://dx.doi.org/10.1371/journal.ppat.1008801
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