Science (New York, N.Y.) · 2026
Surface immune signaling unlocks NLR activation through mRNA alternative splicing.
СтатьяНазвание и аннотация: Перевод в очереди
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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
Аннотация
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.