Suppression of Jasmonic Acid-Mediated Defense by Viral-Inducible MicroRNA319 Facilitates Virus Infection in Rice

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• 作者：Chao Zhang¹ ; ⁴ ; Zuomei Ding¹ ; ⁴ ; Kangcheng Wu¹ ; ⁴ ; Liang Yang¹ ; Yang Li¹ ; Zhen Yang¹ ; Shan Shi¹ ; Xiaojuan Liu¹ ; Shanshan Zhao² ; Zhirui Yang² ; Yu Wang² ; Luping Zheng¹ ; Juan Wei¹ ; Zhenguo Du¹ ; Aihong Zhang³ ; Hongqin Miao³ ; Yi Li² ; Zujian Wu¹ ; ^{wuzujian@126.com" class="auth_mail" title="E-mail the corresponding author} ; Jianguo Wu¹ ; ² ; ^{wujianguo81@126.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：miR319 ; rice ragged stunt virus ; RRSV ; TCP21 ; viral infection ; jasmonic acid
• 刊名：Molecular Plant
• 出版年：2016
• 出版时间：6 September 2016
• 年：2016
• 卷：9
• 期：9
• 页码：1302-1314
• 全文大小：1986 K

文摘

MicroRNAs (miRNAs) are pivotal modulators of plant development and host–virus interactions. However, the roles and action modes of specific miRNAs involved in viral infection and host susceptibility remain largely unclear. In this study, we show that Rice ragged stunt virus (RRSV) infection caused increased accumulation of miR319 but decreased expression of miR319-regulated TCP (TEOSINTE BRANCHED/CYCLOIDEA/PCF) genes, especially TCP21, in rice plants. Transgenic rice plants overexpressing miR319 or downregulating TCP21 exhibited disease-like phenotypes and showed significantly higher susceptibility to RRSV in comparison with the wild-type plants. In contrast, only mild disease symptoms were observed in RRSV-infected lines overexpressing TCP21 and especially in the transgenic plants overexpressing miR319-resistant TCP21. Both RRSV infection and overexpression of miR319 caused the decreased endogenous jasmonic acid (JA) levels along with downregulated expression of JA biosynthesis and signaling-related genes in rice. However, treatment of rice plants with methyl jasmonate alleviated disease symptoms caused by RRSV and reduced virus accumulation. Taken together, our results suggest that the induction of miR319 by RRSV infection in rice suppresses JA-mediated defense to facilitate virus infection and symptom development.