Liu Guangli, Du Youwei, Chen Minghui, Lu Yiming, Liu Lu, Yang Wenrui, Wang Shuanghong, Liang Xiaofei, Zhu Mingqi, Gleason Mark L, Hsiang Tom, Zhang Rong, Sun Guangyu
College of Plant Protection and State Key Laboratory of Crop Stress Resistance and High-efficiency Production, Northwest A&F University, Yangling, Shaanxi, 712100, China.
College of Horticulture, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Sci Adv. 2025 Jun 20;11(25):eadt7970. doi: 10.1126/sciadv.adt7970. Epub 2025 Jun 18.
fungi cause destructive diseases among a wide range of hosts worldwide. We found that effector CfEC92 from specifically binds ATP through an unidentified ATP-binding domain, leading to changes in the protein secondary structure. The residues Cys, Asn, and Cys were critical for ATP binding with CfEC92, and mutations at these sites impaired the ability to suppress host immunity. CfEC92 interacted with MdNDPK2, a negative immune regulator in apple. The CfEC92-ATP complex altered the conformation of MdNDPK2, enhancing its affinity for ATP, and further increasing its autophosphorylation and kinase activity. The activated MdNDPK2 phosphorylated MdMPK3 to suppress host immunity. Homology and functional tests showed that the CxNC motif was highly conserved among species, suggesting that CNC effectors represent a class of broad-spectrum virulence factors. Our findings revealed a mechanism by which effectors cooperate with helper ATP to promote target protein phosphorylation and suppress host immunity.
真菌在全球范围内的多种宿主中引发破坏性疾病。我们发现来自[具体真菌名称]的效应蛋白CfEC92通过一个未知的ATP结合结构域特异性结合ATP，导致蛋白质二级结构发生变化。半胱氨酸（Cys）、天冬酰胺（Asn）和半胱氨酸残基对于CfEC92与ATP的结合至关重要，这些位点的突变会损害其抑制宿主免疫的能力。CfEC92与苹果中的负免疫调节因子MdNDPK2相互作用。CfEC92-ATP复合物改变了MdNDPK2的构象，增强了其对ATP的亲和力，并进一步增加其自身磷酸化和激酶活性。活化的MdNDPK2使MdMPK3磷酸化以抑制宿主免疫。同源性和功能测试表明，CxNC基序在[相关真菌]物种中高度保守，这表明CNC效应蛋白代表一类广谱毒力因子。我们的研究结果揭示了一种机制，即[真菌]效应蛋白与辅助ATP协同作用，促进靶蛋白磷酸化并抑制宿主免疫。
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