美国华盛顿大学Zheng, Ning课题组宣布他们开发出水杨酸对植物免疫的转录激活作用。2026年9月16日，国际知名学术期刊《自然》发表了这一成果。

植物防御激素水杨酸（SA）通过其受体NPR1（病程相关基因非表达子1）发出信号，触发系统获得性抗性，导致广泛的转录重编程。然而，NPR1感知SA并激活转录的分子机制仍未得到解决。在此，研究人员表明，SA稳定NPR1的SA结合结构域（SBD），并通过变构作用促进其与MED15A（Mediator复合体的一个亚基）的相互作用。利用NPR1邻近组和AlphaFold结构预测，研究人员鉴定出NPR1与MED15A的激酶诱导结构域相互作用（KIX）结构域之间的直接相互作用。他们表明，重组NPR1以SA依赖的方式招募MED15A，并且MED15A的结合反过来增强NPR1对SA的亲和力。冷冻电镜和氢-氘交换质谱揭示，SA和MED15A KIX结构域通过不同的界面稳定NPR1-SBD的SA结合核心，从而协同增强NPR1-SBD形成三元复合物的能力。研究人员进一步证明，NIMIN1——SA-NPR1通路的抑制因子——通过与MED15A竞争相同的NPR1-SBD对接位点，并通过变构阻断激素结合，从而拮抗SA信号传导。与先前确立MED15A在SA信号传导中关键作用的遗传学证据一致，研究人员的发现为SA如何在植物免疫反应中促进转录激活这一长期存在的问题提供了机制上的解答。

附：英文原文

Title: Transcriptional activation of plant immunity by salicylic acid

Author: Zhang, Songwen, Gish, Madeline, Li, Huan, Hinds, Thomas R., Mao, Haibin, Cornell, Moira, Silvetti, Massi, Klucas, Sydney, Vorauer, Clint, Mundorff, Charlie C., Yadav, Smita, Guttman, Miklos, Zheng, Ning

Issue&Volume: 2026-09-16

Abstract: The plant defence hormone salicylic acid (SA) triggers systemic acquired resistance by signalling through its receptor, NON-EXPRESSOR OF PATHOGENESIS-RELATED GENE 1 (NPR1), leading to widespread transcriptional reprogramming1,2. However, the molecular mechanism by which NPR1 senses SA and activates transcription remains unresolved. Here we show that SA stabilizes the SA-binding domain (SBD) of NPR1 and allosterically promotes its interaction with MED15A, a subunit of the Mediator complex. Leveraging the NPR1 proxiome and AlphaFold structural predictions, we identify a direct interaction between NPR1 and the kinase-inducible domain interacting (KIX) domain of MED15A. We show that recombinant NPR1 recruits MED15A in an SA-dependent manner, and that MED15A binding reciprocally enhances the affinity of NPR1 for SA. Cryo-electron microscopy and hydrogen–deuterium exchange mass spectrometry reveal that SA and the MED15A KIX domain cooperatively potentiate NPR1-SBD for ternary complex formation by stabilizing its SA-binding core via separate interfaces. We further demonstrate that NIMIN1, a repressor of the SA–NPR1 pathway, antagonizes SA signalling by competing with MED15A for the same NPR1-SBD docking site and allosterically blocking hormone binding. In line with previous genetic evidence establishing a critical role of MED15A in SA signalling, our findings provide a mechanistic resolution to the longstanding question of how SA promotes transcriptional activation during plant immune responses.

DOI: 10.1038/s41586-026-11021-5

Source: https://www.nature.com/articles/s41586-026-11021-5