Surface immune signaling unlocks NLR activation through mRNA alternative splicing

• 成果类型: Article
• 署名作者: Gao, Chuyun; Meng, Xi; Chen, Xianchu; Yang, Leiyun; Ibrahim, Tarhan; Toghani, AmirAli; Yuen, Enoch Lok Him; Eilmann, Nick; King, Freddie; Li, Kangping; Wang, Luyao; Sun, Biying; Wang, Yuanchao; Bozkurt, Tolga Osman; Dong, Suomeng
• 署名单位: Nanjing Agricultural University; Imperial College London; University of East Anglia; UK Research & Innovation (UKRI); Biotechnology and Biological Sciences Research Council (BBSRC)
• 刊物名称: SCIENCE
• ISSN/ISSBN: 0036-8075; 1095-9203
• DOI: 10.1126/science.adx9929
• 发表日期: 2026-07-02
• 页码: 65-70
• 关键词: structural basis; perception; ELICITOR; domain; SYSTEM

摘要

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.