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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\n                    <jats:italic toggle=\"yes\">Phytophthora infestans<\/jats:italic>\n                    effector AVRvnt1, enabling resistosome assembly and immune signaling. The widespread conservation of N-terminal extensions in coiled coil\u2013type NLRs points to a common regulatory mechanism in preventing potential autoactivation while preserving pathogen sensitivity.\n                  <\/jats:p>","DOI":"10.1126\/science.adx9929","type":"journal-article","created":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T18:04:19Z","timestamp":1783015459000},"page":"65-70","update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":7,"title":["Surface immune signaling unlocks NLR activation through mRNA alternative splicing"],"prefix":"10.1126","volume":"393","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6116-0011","authenticated-orcid":true,"given":"Chuyun","family":"Gao","sequence":"first","affiliation":[{"name":"State Key Laboratory of Agricultural and Forestry Biosecurity, Sanya Institute of Nanjing Agricultural University, The Key Laboratory of Integrated Management of Crop Diseases and Pests (Ministry 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