Surface immune signaling unlocks NLR activation through mRNA alternative splicing.

Authors

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

Published in

Science (New York, N.Y.). Volume 393. Issue 6806. Pages 65-70. Jul 02, 2026. Epub Jul 02, 2026.

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.

PMID:
42391383
Bibliographic data and abstract were imported from PubMed on 03 Jul 2026.

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