A splicing checkpoint couples surface and intracellular plant immunity

Abstract Plant immunity operates through two interconnected layers. Pattern-triggered immunity (PTI) is initiated by cell-surface pattern-recognition receptors, whereas effector-triggered immunity (ETI) is executed by intracellular nucleotide-binding leucine-rich repeat (NLR) receptors. The two layers are known to potentiate one another, yet how a signal perceived at the plasma membrane is relayed to prime an intracellular NLR has remained unclear. In a recent study, Gao et al. (2026) show that the potato late blight resistance protein Rpi-vnt1.1 carries a self-imposed restraint, an autoinhibitory N-terminal extension encoded by an intron-retained mRNA isoform. Pathogen perception, acting through PTI, shifts the balance of alternative splicing towards an isoform that lacks this extension, producing a resistosome-competent receptor that the Phytophthora infestans effector AVRvnt1 can then activate. This work defines pre-mRNA alternative splicing as a checkpoint that couples surface and intracellular immunity, and points to a broadly conserved and engineerable mode of NLR control.