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

Abstract

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