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OsMAPK6使一种锌指蛋白OsLIC磷酸化,以促进下游的OsWRKY30,从而增强水稻对白叶枯病和条斑病的抗性。

OsMAPK6 phosphorylates a zinc finger protein OsLIC to promote downstream OsWRKY30 for rice resistance to bacterial blight and leaf streak.

作者信息

Wang Lihan, Chen Jie, Zhao Yuqin, Wang Shiping, Yuan Meng

机构信息

National Key Laboratory of Crop Genetic Improvement, National Center of Plant Gene Research (Wuhan), Hubei Hongshan Laboratory, Huazhong Agricultural University, Wuhan, 430070, China.

出版信息

J Integr Plant Biol. 2022 May;64(5):1116-1130. doi: 10.1111/jipb.13249. Epub 2022 Apr 19.

Abstract

Rice OsLIC encoding a CCCH zinc finger transcription factor plays an important role in immunity. However, the immune signaling pathways that OsLIC-involved and the underlying mechanisms that OsLIC-conferred resistance against pathogens are largely unclear. Here, we show that OsLIC, as a substrate for OsMAPK6, negatively regulates resistance to Xanthomonas oryzae pv. oryzae (Xoo) and X. oryzae pv. oryzicola (Xoc) by directly suppressing OsWRKY30 transcription. Biochemical assays showed that OsLIC bound to OsWRKY30 promoter and suppressed its transcription. Genetic assays confirmed that the osilc knockout mutants and OsWRKY30-overexpressing plants exhibited enhanced resistance to Xoo and Xoc, knocking out OsWRKY30 in the oslic mutants attenuated the resistance against bacterial pathogens. OsMAPK6 physically interacted with and phosphorylated OsLIC leading to decreased OsLIC DNA-binding activity, therefore, overexpression of OsLIC partially suppressed OsMAPK6-mediated rice resistance. In addition, both OsMAPK6-phosphorylated activation of OsLIC and phosphorylation-mimic OsLIC had reduced DNA-binding activity towards OsWRKY30 promoter, thereby promoting OsWRKY30 transcription. Collectively, these results reveal that OsMAPK6-mediated phosphorylation of OsLIC positively regulates rice resistance to Xoo and Xoc by modulating OsWRKY30 transcription, suggesting that OsMAPK6-OsLIC-OsWRKY30 module is an immune signaling pathway in response to the bacterial pathogens.

摘要

水稻中编码CCCH锌指转录因子的OsLIC在免疫中发挥重要作用。然而,OsLIC参与的免疫信号通路以及OsLIC赋予对病原体抗性的潜在机制在很大程度上尚不清楚。在此,我们表明,作为OsMAPK6的底物,OsLIC通过直接抑制OsWRKY30转录来负向调节对水稻白叶枯病菌(Xanthomonas oryzae pv. oryzae,Xoo)和水稻细菌性条斑病菌(X. oryzae pv. oryzicola,Xoc)的抗性。生化分析表明,OsLIC与OsWRKY30启动子结合并抑制其转录。遗传学分析证实,osilc敲除突变体和OsWRKY30过表达植株对Xoo和Xoc表现出增强的抗性,在oslic突变体中敲除OsWRKY30减弱了对细菌病原体的抗性。OsMAPK6与OsLIC发生物理相互作用并使其磷酸化,导致OsLIC的DNA结合活性降低,因此,OsLIC的过表达部分抑制了OsMAPK6介导的水稻抗性。此外,OsMAPK6磷酸化激活的OsLIC和磷酸化模拟的OsLIC对OsWRKY30启动子的DNA结合活性均降低,从而促进OsWRKY30转录。总的来说这些结果揭示,OsMAPK6介导的OsLIC磷酸化通过调节OsWRKY30转录正向调控水稻对Xoo和Xoc的抗性,表明OsMAPK6-OsLIC-OsWRKY30模块是一条响应细菌病原体的免疫信号通路。

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