近日，南京农业大学
在这项研究中，该课题组研究人员揭示了表面免疫信号通过mRNA剪接解锁核苷酸结合富亮氨酸重复（NLR）免疫受体激活的调控机制。研究小组在马铃薯晚疫病抗性蛋白Rpi-vnt1.1中发现了一个N端原域，该原域抑制抗性体的形成，阻止了该NLR的潜在自激活。在病原体感知后，PTI信号诱导Rpi-vnt1.1 mRNA的选择性剪接，去除该抑制元件。这引发了Rpi-vnt1.1被疫霉菌效应物AVRvnt1激活，使抵抗体组装和免疫信号传导成为可能。盘绕型NLRs中n端延伸的广泛保存表明，在保持病原体敏感性的同时，防止潜在的自激活存在一种共同的调节机制。
据介绍，植物通过激活模式触发免疫（PTI）和效应触发免疫（ETI）来对抗病原体。然而，这些系统如何协调免疫激活，同时防止自身免疫仍然知之甚少。
附：英文原文
Title: Surface immune signaling unlocks NLR activation through mRNA alternative splicing
Author: Chuyun Gao, Xi Meng, Xianchu Chen, Leiyun Yang, Tarhan Ibrahim, AmirAli Toghani, Enoch Lok Him Yuen, Nick Eilmann, Freddie King, Kangping Li, Luyao Wang, Biying Sun, Yuanchao Wang, Tolga Osman Bozkurt, Suomeng Dong
Issue&Volume: 2026-07-02
Abstract: Plants activate pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) to combat pathogens. However, how these systems coordinate immune activation while preventing autoimmunity remains poorly understood. In this study, we uncovered a regulatory mechanism in which surface immune signaling unlocks nucleotide-binding leucine-rich repeat (NLR) immune receptor activation through mRNA splicing. We identified an N-terminal prodomain in the potato late blight resistance protein Rpi-vnt1.1 that inhibits resistosome formation, preventing potential autoactivation of this NLR. Upon pathogen perception, PTI signaling induced alternative splicing of Rpi-vnt1.1 mRNA, removing this inhibitory element. This primed Rpi-vnt1.1 for activation by the Phytophthora infestans effector AVRvnt1, enabling resistosome assembly and immune signaling. The widespread conservation of N-terminal extensions in coiled coil–type NLRs points to a common regulatory mechanism in preventing potential autoactivation while preserving pathogen sensitivity.
DOI: adx9929
Source: https://www.science.org/doi/10.1126/science.adx9929