西湖大学柴继杰小组研究出通过修饰的宿主蛋白复合物平衡植物辅助NLR的激活。2025年2月12日出版的《自然》发表了这项成果。
小组进一步表明,抑制性NRG1家族成员NRG1C在与第二信使激活的EDS1-SAG101结合方面有效地优于NRG1A。这些发现揭示了NRG1A通过识别修饰的宿主EDS1-SAG101复合物而激活的机制,以及NRG1C通过隔离激活的EDS1-SAG101而抑制NRG1A的机制,从而揭示了中心植物免疫应答系统的激活和约束。
据悉,核苷酸结合的富亮氨酸重复序列(NLR)受体通过感应病原体效应在植物免疫中发挥重要作用。在拟南芥中,某些传感器NLR作为NADase催化第二信使的产生,这可以通过增强疾病易感性来识别。1(EDS1)及其伴侣衰老相关基因101 (SAG101),激活辅助NLRN需求基因1 (NRG1) 。低温电镜结构显示,第二信使激活的EDS1-SAG101主要与NRG1A富含亮氨酸的重复结构域接触,介导诱导EDS1-SAG101 - NRG1A复合物的形成。结构比较表明,第二信使的结合诱导EDS1-SAG101的构象变化,这些变化被NRG1A识别,导致其变构激活。
附:英文原文
Title: Balanced plant helper NLR activation by a modified host protein complex
Author: Huang, Shijia, Wang, Junli, Song, Ridan, Jia, Aolin, Xiao, Yu, Sun, Yue, Wang, Lin, Mahr, Dennis, Wu, Zhongshou, Han, Zhifu, Li, Xin, Parker, Jane E., Chai, Jijie
Issue&Volume: 2025-02-12
Abstract: Nucleotide-binding leucine-rich repeat (NLR) receptors play crucial roles in plant immunity by sensing pathogen effectors. In Arabidopsis, certain sensor NLRs function as NADases to catalyse the production of second messengers, which can be recognized by enhanced disease susceptibility1 (EDS1) with its partner senescence-associated gene101 (SAG101), to activate helper NLRN requirement gene1 (NRG1). A cryoelectron microscopy structure shows that second-messenger-activated EDS1–SAG101 mainly contacts the leucine-rich repeat domain of NRG1A to mediate the formation of an induced EDS1–SAG101–NRG1A complex. Structural comparisons show that binding of a second messenger induces conformational changes in EDS1–SAG101, which are recognized by NRG1A, leading to its allosteric activation. We further show that an inhibitory NRG1 family member, NRG1C, efficiently outcompetes NRG1A for binding to second-messenger-activated EDS1–SAG101. These findings uncover mechanisms for NRG1A activation through its recognition of a modified host EDS1–SAG101 complex, and NRG1A inhibition by NRG1C through sequestration of the activated EDS1–SAG101, thus shedding light on the activation and constraint of a central plant immune response system.
DOI: 10.1038/s41586-024-08521-7
Source: https://www.nature.com/articles/s41586-024-08521-7
Nature:《自然》,创刊于1869年。隶属于施普林格·自然出版集团,最新IF:69.504
官方网址:http://www.nature.com/
投稿链接:http://www.nature.com/authors/submit_manuscript.html