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Peer-reviewedCC BYScience

Surface immune signaling unlocks NLR activation through mRNA alternative splicing

  • Chuyun Gao1
  • Xi Meng1
  • X S Chen1
  • Leiyun Yang1
  • Tarhan Ibrahim2
  • AmirAli Toghani3
  • Enoch Lok Him Yuen2
  • Nick Moritz Eilmann2
  • Freddie J. King2
  • Kangping Li1
  • Luyao Wang1
  • Biying Sun1
3 more authors
  • Yuanchao Wang1
  • Tolga O. Bozkurt2
  • Suomeng Dong1
  1. 1State 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 of Education), College of Plant Protection, Nanjing Agricultural University, Nanjing, China
  2. 2Department of Life Sciences, Imperial College London, London, UK
  3. 3The Sainsbury Laboratory, University of East Anglia, Norwich Research Park, UK
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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.

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Cite

BibTeXRIS
BibTeX
@article{gao2026surface,
  title = {{Surface immune signaling unlocks NLR activation through mRNA alternative splicing}},
  author = {Chuyun Gao and Xi Meng and X S Chen and Leiyun Yang and Tarhan Ibrahim and AmirAli Toghani and Enoch Lok Him Yuen and Nick Moritz Eilmann and Freddie J. King and Kangping Li and Luyao Wang and Biying Sun and Yuanchao Wang and Tolga O. Bozkurt and Suomeng Dong},
  journal = {Science},
  year = {2026},
  month = jul,
  doi = {10.1126/science.adx9929},
  url = {https://doi.org/10.1126/science.adx9929},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Surface immune signaling unlocks NLR activation through mRNA alternative splicing
AU  - Chuyun Gao
AU  - Xi Meng
AU  - X S Chen
AU  - Leiyun Yang
AU  - Tarhan Ibrahim
AU  - AmirAli Toghani
AU  - Enoch Lok Him Yuen
AU  - Nick Moritz Eilmann
AU  - Freddie J. King
AU  - Kangping Li
AU  - Luyao Wang
AU  - Biying Sun
AU  - Yuanchao Wang
AU  - Tolga O. Bozkurt
AU  - Suomeng Dong
PY  - 2026
DA  - 2026/07/02
JO  - Science
DO  - 10.1126/science.adx9929
UR  - https://doi.org/10.1126/science.adx9929
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.
SN  - 0036-8075
SN  - 0193-4511
SN  - 1095-9203
ER  -