Extracellular pyridine nucleotides trigger plant systemic immunity through a lectin receptor kinase/BAK1 complex

Systemic acquired resistance (SAR) is a long-lasting broad-spectrum plant immunity induced by mobile signals produced in the local leaves where the initial infection occurs. Although multiple structurally unrelated signals have been proposed, the mechanisms responsible for perception of these signals in the systemic leaves are unknown. Here, we show that exogenously applied nicotinamide adenine dinucleotide (NAD + ) moves systemically and induces systemic immunity. We demonstrate that the lectin receptor kinase (LecRK), LecRK-VI.2, is a potential receptor for extracellular NAD + (eNAD + ) and NAD + phosphate (eNADP + ) and plays a central role in biological induction of SAR. LecRK-VI.2 constitutively associates with BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 (BAK1) in vivo. Furthermore, BAK1 and its homolog BAK1-LIKE1 are required for eNAD(P) + signaling and SAR, and the kinase activities of LecR-VI.2 and BAK1 are indispensable to their function in SAR. Our results indicate that eNAD + is a putative mobile signal, which triggers SAR through its receptor complex LecRK-VI.2/BAK1 in Arabidopsis thaliana . Systemic signals allows plants to mount immune responses in sites that are distal from the local infection site. Here, the authors provide evidence that nicotinamide adenine dinucleotide (NAD + ) is a potential systemic signal that induces immunity via the lectin receptor kinase LecRK-VI.2 and BAK1.