The ArabidopsisTNL immune receptor BNT1 localizes to the plastid envelope and is required for the flg22‐induced resistance against Pseudomonas

SUMMARY Precise localization and trafficking of plant immune receptors are critical for their function. We identify the TNL‐class nucleotide‐binding leucine‐rich repeat receptor (NLR) BURNOUT1 (BNT1) from Arabidopsis thaliana as localized to plastids, key organelles for plant immunity. Alternative transcription start site usage generates two isoforms of BNT1: BNT1.2, which is targeted to the plastid envelope via an N‐terminal signal‐anchored mechanism, and BNT1.1, which resides in the cytoplasm. Moreover, BNT1.2 is predominantly expressed in epidermal cells, where it localizes to the so‐called sensory plastids. Functional analysis revealed that bnt1 mutants exhibit compromised PAMP‐triggered immunity (PTI) responses, including impaired callose deposition and reduced flg22‐induced resistance to Pseudomonas syringae pv. tomato , while flg22‐induced apoplastic reactive oxygen species production remains unaffected. Notably, only the plastid‐localized BNT1.2 isoform is required for these PTI responses. Our findings reveal a role for NLRs in regulating PTI responses from plastids and highlight these organelles as key hubs for signal(s) integration during plant–pathogen interactions.