Inactivation of β-1,3-glucan synthase-like 5 confers broad-spectrum resistance to Plasmodiophora brassicae pathotypes in cruciferous plants

文献类型： 外文期刊

第一作者： Wu, Yupo

作者： Wu, Yupo;Zhao, Chuanji;Zhang, Yi;Shen, Cuicui;Zhang, Yuanyuan;Zhang, Xiong;Gao, Lixia;Zeng, Lingyi;Ke, Qinglin;Qin, Li;Liu, Fan;Huang, Junyan;Ren, Li;Liu, Yueying;Cheng, Hongtao;Tong, Chaobo;Hu, Qiong;Cheng, Xiaohui;Liu, Shengyi;Liu, Lijiang;Gao, Lixia;Wei, Yangdou

作者机构：

期刊名称：NATURE GENETICS （ 影响因子：29.0； 五年影响因子：37.4 ）

ISSN： 1061-4036

年卷期： 2025 年

页码：

收录情况： SCI

摘要： Clubroot disease, caused by the obligate intracellular rhizarian protist Plasmodiophora brassicae, is devastating to cruciferous crops worldwide. Widespread field P. brassicae pathotypes frequently overcome the pathotype-specific resistance of modern varieties, posing a challenge for durable control of this disease. Here a genome-wide association study of 3 years of data comprising field clubroot phenotyping of 244 genome-resequenced Brassica napus accessions identified a strong association of beta-1,3-glucan synthase-like 5 (GSL5) with clubroot susceptibility. GSL5 was evolutionarily conserved, and inactivation of GSL5 by genome editing in Arabidopsis, B. napus, Brassicarapa and Brassica oleracea conferred broad-spectrum, high-level resistance to P. brassicae pathotypes without yield penalties in B. napus. GSL5 inactivation derepressed the jasmonic acid-mediated immunity during P. brassicae secondary infection, and this immune repression was possibly reinforced through stabilization of GSL5 by a P. brassicae effector, facilitating clubroot susceptibility. Our study provides durable resistance resources for cruciferous clubroot disease control and insights into plant resistance against intracellular eukaryotic phytopathogens.

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