Nicotinamide adenine dinucleotide (NAD+) participates in intracellular and extracellular signaling events unrelated to metabolism. In animals, purinergic receptors are required for extracellular NAD+ (eNAD+) to evoke biological responses, indicating that eNAD+ may be sensed by cell-surface receptors. However, the identity of eNAD+-binding receptors still remains elusive. Here, we identify a lectin receptor kinase (LecRK), LecRK-I.8, as a potential eNAD+ receptor in Arabidopsis. The extracellular lectin domain of LecRK-I.8 binds NAD+ with a dissociation constant of 436.5 104.8 nM, although much higher concentrations are needed to trigger in vivo responses. Mutations in LecRK-I.8 inhibit NAD+-induced immune responses, whereas overexpression of LecRK-I.8 enhances the Arabidopsis response to NAD+. Furthermore, LecRK-I.8 is required for basal resistance against bacterial pathogens, substantiating a role for eNAD+ in plant immunity. Our results demonstrate that lectin receptors can potentially function as eNAD+-binding receptors and provide direct evidence for eNAD+ being an endogenous signaling molecule in plants.
Microarray analysis of exogenous NAD+-induced transcriptome changes in Arabidopsis thalianaPublicly available at the NCBI Gene Expression Omnibus (accession no: GSE76568).
Microarray analysis of Atelp2, npr1 and wild type (Col-0) infected with the avirulent bacterial pathogen Pst DC3000/avrRpt2Publicly available at the NCBI Gene Expression Omnibus (accession no: GSE38986).
- Zhonglin Mou
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
- Thorsten Nürnberger, University of Tubingen, Germany
© 2017, Wang et al.
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