植物学报 ›› 2019, Vol. 54 ›› Issue (5): 547-549.doi: 10.11983/CBB19166

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ZmFBL41 Chang7-2: 玉米抗纹枯病的关键利器

李伟滔,贺闽,陈学伟()   

  1. 四川农业大学西南作物基因资源发掘与利用国家重点实验室(筹), 水稻研究所, 成都 611130
  • 收稿日期:2019-08-27 接受日期:2019-09-17 出版日期:2019-09-01 发布日期:2019-01-01
  • 通讯作者: 陈学伟 E-mail:xwchen88@163.com

Discovery of ZmFBL41 Chang7-2 as A Key Weapon against Banded Leaf and Sheath Blight Resistance in Maize

Li Weitao,He Min,Chen Xuewei()   

  1. Rice Research Institute, State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, Chengdu 611130, China
  • Received:2019-08-27 Accepted:2019-09-17 Online:2019-09-01 Published:2019-01-01
  • Contact: Chen Xuewei E-mail:xwchen88@163.com

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摘要：

由真菌Rhizoctonia solani引起的纹枯病严重危害玉米(Zea mays)和水稻(Oryza sativa)等作物的安全生产。R. solani的宿主范围广且抗源少, 加之相关的抗性机制研究有限, 导致纹枯病的危害长期得不到有效控制。近期, 中国科学家通过对318份玉米自交系进行全基因组关联分析, 筛选到1个与纹枯病抗性相关的、编码F-box结构域蛋白的候选基因ZmFBL41 (GRMZM2G109140)。ZmFBL41蛋白是SCF (SKP1-Cullin-F-box) E3泛素连接酶复合体的一员, 能介导复合体对肉桂醇脱氢酶ZmCAD的降解, 从而降低木质素的积累, 使玉米易感纹枯病。玉米抗病自交系Chang7-2中, 蛋白ZmFBL41 Chang7-2因2个关键氨基酸的变异, 不能结合并降解底物ZmCAD, 使木质素含量增加, 从而提高玉米对纹枯病的抗性。该研究率先揭示了SCF复合体可通过降解肉桂醇脱氢酶来调控植物免疫反应的新型分子机制, 为提高玉米及其它作物对纹枯病的抗性提供了重要理论依据和基因资源。

关键词: 植物免疫, SKP1-Cullin-F-box, 木质素, 纹枯病, 玉米, 水稻

Abstract:

The fungal pathogen Rhizoctonia solani causes banded leaf and sheath blight (BLSB) in maize (Zea mays) and sheath blight (ShB) in rice (Oryza sativa). R. solani has a wide range of host and severely threatens crop production. The lack of resistant resources against BLSB and the poor understanding of disease resistance mechanism hamper the development of effective approaches to control this fungal disease. Recently, Chinese scientists have made a breakthrough discovery that an F-box protein ZmFBL41 mediates the proteasomal degradation of cinnamyl-alcohol dehydrogenase ZmCAD to regulate BLSB and ShB disease resistance. By genome-wide association analysis, GRMZM2G 109140 (ZmFBL41) was identified as a major QTL candidate gene associated with BLSB disease resistance. ZmFBL41 protein is a member of SKP1-Cullin-F-box (SCF) E3 ubiquitin ligase complex which mediates the degradation of ZmCAD, thus reducing the accumulation of lignin and rendering maize more susceptible to R. solani. Interestingly, in the maize inbred line Chang7-2, the natural variation on two amino acids in ZmFBL41 Chang7-2 results in resistance against BLSB. Mechanistically, ZmFBL41 Chang7-2 fails to interact with and degrade its substrate ZmCAD, leading to the accumulation of lignin, which consequently enhances maize resistance. This study not only discovers a novel molecular mechanism underlying disease resistance of maize against R. solani, but also provides important theoretical basis and genetic resources for breeding maize and other crops with improved disease resistance.

Key words: plant immunity, SKP1-Cullin-F-box, lignin, banded leaf and sheath blight, maize, rice

图1

ZmFBL41介导的纹枯病抗性 ZmFBL41与ZmSKP1-1互作形成SCF复合体, 通过26S蛋白酶体降解底物ZmCAD, 减少木质素的积累, 从而使玉米易感纹枯病。而ZmFBL41Chang7-2因其中2个关键氨基酸位点变异(E214G, S217R), 不能结合并降解底物ZmCAD, 从而引起木质素积累, 使玉米对纹枯病的抗性增强。"

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