@article{Gao:2026:10.1126/science.adx9929,
author = {Gao, C and Meng, X and Chen, X and Yang, L and Ibrahim, T and Toghani, A and Yuen, ELH and Eilmann, N and King, F and Li, K and Wang, L and Sun, B and Wang, Y and Bozkurt, TO and Dong, S},
doi = {10.1126/science.adx9929},
journal = {Science},
pages = {65--70},
title = {Surface immune signaling unlocks NLR activation through mRNA alternative splicing.},
url = {http://dx.doi.org/10.1126/science.adx9929},
volume = {393},
year = {2026}
}

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TY  - JOUR
AB  - 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.
AU  - Gao,C
AU  - Meng,X
AU  - Chen,X
AU  - Yang,L
AU  - Ibrahim,T
AU  - Toghani,A
AU  - Yuen,ELH
AU  - Eilmann,N
AU  - King,F
AU  - Li,K
AU  - Wang,L
AU  - Sun,B
AU  - Wang,Y
AU  - Bozkurt,TO
AU  - Dong,S
DO  - 10.1126/science.adx9929
EP  - 70
PY  - 2026///
SP  - 65
TI  - Surface immune signaling unlocks NLR activation through mRNA alternative splicing.
T2  - Science
UR  - http://dx.doi.org/10.1126/science.adx9929
UR  - https://www.ncbi.nlm.nih.gov/pubmed/42391383
VL  - 393
ER  - 

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