Liu Chengyu, Han Li-Bo, Wen Yanhong, Lu Chuner, Deng Boqian, Liu Zixuan, Deng Xianya, Shen Ningning, Tang Dingzhong, Li Yuan-Bao
State Key Laboratory of Agricultural and Forestry Biosecurity, Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, Plant Immunity Center, Fujian Agriculture and Forestry University, Fuzhou, Fujian, 350002, China.
School of Future Technology, Fujian Agriculture and Forestry University, Fuzhou, Fujian, 350002, China.
New Phytol. 2025 Apr;246(1):280-297. doi: 10.1111/nph.20440. Epub 2025 Feb 13.
Rice blast disease caused by Magnaporthe oryzae poses a severe threat to rice production. To counteract M. oryzae, plants synthesize jasmonate (JA) and lignin, two primary defense-related metabolites, to initiate defense programs. However, the mechanism through which M. oryzae modulates JA- and lignin-mediated plant immunity remains unclear. In this study, a novel M. oryzae effector, MoBys1, was identified as being involved in pathogenesis. Knockout of MoBys1 in M. oryzae significantly reduced its infection ability. Conversely, overexpression of MoBys1 in rice impaired the rice defense response. MoBys1 localizes to the plant cytoplasm and nucleus and interacts with rice cinnamyl alcohol dehydrogenase 2 (OsCAD2), an enzyme that catalyzes lignin biosynthesis. While OsCAD2 mutants exhibited weakened defenses, overexpression lines demonstrated enhanced resistance, highlighting the critical role of OsCAD2 in blast resistance. Furthermore, OsCAD2 functions as a transcription factor regulating a wide range of biological processes, including JA and lignin signaling pathways. The interaction between MoBys1 and OsCAD2 promotes OsCAD2 degradation, leading to reduced lignin and JA accumulation. These findings uncover a novel counter-defense mechanism by which M. oryzae employs the effector MoBys1 to degrade OsCAD2 and suppress host defense-related metabolite accumulation during infection.
由稻瘟病菌引起的稻瘟病对水稻生产构成严重威胁。为了对抗稻瘟病菌，植物合成茉莉酸（JA）和木质素这两种主要的与防御相关的代谢产物，以启动防御程序。然而，稻瘟病菌调节JA和木质素介导的植物免疫的机制仍不清楚。在本研究中，一种新的稻瘟病菌效应因子MoBys1被鉴定为参与致病过程。在稻瘟病菌中敲除MoBys1显著降低了其感染能力。相反，在水稻中过表达MoBys1会损害水稻的防御反应。MoBys1定位于植物细胞质和细胞核，并与水稻肉桂醇脱氢酶2（OsCAD2）相互作用，OsCAD2是一种催化木质素生物合成的酶。虽然OsCAD2突变体表现出较弱的防御能力，但过表达系表现出增强的抗性，突出了OsCAD2在抗稻瘟病中的关键作用。此外，OsCAD2作为一种转录因子，调节包括JA和木质素信号通路在内的广泛生物过程。MoBys1与OsCAD2之间的相互作用促进了OsCAD2的降解，导致木质素和JA积累减少。这些发现揭示了一种新的反防御机制，即稻瘟病菌利用效应因子MoBys1在感染过程中降解OsCAD2并抑制宿主防御相关代谢产物的积累。
