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一种质外体真菌效应蛋白破坏玉米凝集素受体激酶1(ZmLecRK1)的N-糖基化,诱导其降解以抑制玉米的抗病性。

An apoplastic fungal effector disrupts N-glycosylation of ZmLecRK1, inducing its degradation to suppress disease resistance in maize.

作者信息

Liu Chuang, Chen Junbin, Li Zhenju, Zhang Zhen, Luan Yuyang, Liu Hui, Liu Hongtian, Huang Jianhua, Zhu Wangsheng

机构信息

State Key Laboratory of Maize Bio-breeding, College of Plant Protection, Ministry of Agriculture and Rural Affairs, Key Laboratory of Surveillance and Management for Plant Quarantine Pests, China Agricultural University, Beijing, People's Republic of China.

John Innes Centre, Norwich, UK.

出版信息

Nat Plants. 2025 Sep 12. doi: 10.1038/s41477-025-02112-8.

DOI:10.1038/s41477-025-02112-8
PMID:40940425
Abstract

Pathogens deploy effectors to suppress host immune responses and enable successful colonization in plants. While apoplastic effectors have major roles in pathogenicity, whether and how they directly attack extracellular immune receptors remains unclear. Here we identify an apoplastic effector FgLPMO9A from the fungal pathogen Fusarium graminearum that directly inhibits maize immune receptor ZmLecRK1-mediated resistance. FgLPMO9A belongs to the polysaccharide monooxygenase family, which depolymerizes polysaccharides. Deletion of FgLPMO9A attenuates F. graminearum virulence on maize, but this defect is fully rescued in the zmlecrk1 mutants. FgLPMO9A interacts with the extracellular S-domain of ZmLecRK1 and disrupts N-glycosylation at the N341 site, thereby promoting ZmLecRK1 degradation via the NBR1-mediated autophagy pathway. Notably, the ZmLecRK1 variant with the N341Q substitution confers enhanced resistance to F. graminearum in maize. We demonstrate that F. graminearum dampens maize immunity by deploying an apoplastic effector to induce extracellular immune receptor degradation.

摘要

病原体通过分泌效应蛋白来抑制宿主的免疫反应,从而在植物中成功定殖。虽然质外体效应蛋白在致病性中起主要作用,但它们是否以及如何直接攻击细胞外免疫受体仍不清楚。在这里,我们从真菌病原体禾谷镰刀菌中鉴定出一种质外体效应蛋白FgLPMO9A,它直接抑制玉米免疫受体ZmLecRK1介导的抗性。FgLPMO9A属于多糖单加氧酶家族,可使多糖解聚。缺失FgLPMO9A会减弱禾谷镰刀菌对玉米的毒力,但在zmlecrk1突变体中这种缺陷完全得到挽救。FgLPMO9A与ZmLecRK1的细胞外S结构域相互作用,并破坏N341位点的N-糖基化,从而通过NBR1介导的自噬途径促进ZmLecRK1的降解。值得注意的是,具有N341Q替代的ZmLecRK1变体赋予玉米对禾谷镰刀菌更强的抗性。我们证明,禾谷镰刀菌通过分泌一种质外体效应蛋白来诱导细胞外免疫受体降解,从而削弱玉米的免疫力。

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本文引用的文献

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Natural variations of maize ZmLecRK1 determine its interaction with ZmBAK1 and resistance patterns to multiple pathogens.
玉米 ZmLecRK1 的自然变异决定了它与 ZmBAK1 的相互作用以及对多种病原体的抗性模式。
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