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Nat Commun. 2019 Oct 22;10(1):4810. doi: 10.1038/s41467-019-12781-7.

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

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Department of Microbiology and Cell Science, University of Florida, Gainesville, FL, 32611, USA.
Department of Plant Pathology, University of Florida, Gainesville, FL, 32611, USA.
Citrus Research and Education Center, University of Florida, 700 Experiment Station Road, Lake Alfred, FL, 33850, USA.
Interdisciplinary Center for Biotechnology Research, University of Florida, Gainesville, FL, 32610, USA.
National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, 27709, USA.
Department of Microbiology and Cell Science, University of Florida, Gainesville, FL, 32611, USA.


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.

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