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Updated: Jul 4, 2026
09:04
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
Surface immune signaling unlocks NLR activation through mRNA alternative splicing
Chuyun Gao1, Xi Meng1, Xianchu Chen1
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.
Science (New York, N.Y.)
|July 2, 2026
Summary
Plant immune signaling uses mRNA splicing to control NLR immune receptor activation, preventing autoimmunity while maintaining pathogen defense. This mechanism ensures proper immune responses against pathogens like Phytophthora infestans.
Area of Science:
- Plant immunity
- Molecular plant-pathogen interactions
- Genetics
Background:
- Plants possess pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) to fight pathogens.
- Coordination of PTI and ETI, and prevention of autoimmunity, are not fully understood.
Purpose of the Study:
- To investigate the regulatory mechanism linking surface immune signaling to nucleotide-binding leucine-rich repeat (NLR) immune receptor activation.
- To understand how plants prevent autoimmunity while maintaining pathogen sensitivity.
Main Methods:
- Identified an inhibitory N-terminal prodomain in the potato resistance protein Rpi-vnt1.1.
- Investigated the role of mRNA splicing in regulating Rpi-vnt1.1 activation.
- Analyzed the interaction between PTI signaling, Rpi-vnt1.1 splicing, and effector AVRvnt1 recognition.
Main Results:
- The Rpi-vnt1.1 N-terminal prodomain inhibits resistosome formation, preventing autoactivation.
- Pathogen perception triggers PTI signaling, inducing alternative splicing of Rpi-vnt1.1 mRNA to remove the inhibitory prodomain.
- Spliced Rpi-vnt1.1 is primed for activation by the Phytophthora infestans effector AVRvnt1, leading to resistosome assembly and immune signaling.
Conclusions:
- PTI signaling regulates NLR activation via mRNA splicing, controlling autoactivation and pathogen sensitivity.
- Conserved N-terminal extensions in NLRs suggest a common regulatory mechanism for immune receptor activation.
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