A lectin receptor kinase as a potential sensor for extracellular nicotinamide adenine dinucleotide in Arabidopsis thaliana

Abstract
Data availability
Article and author information
Metrics

Abstract

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.

Data availability

The following data sets were generated

1. Wang C
2. Zhou M
3. Zhang X
4. Yao J
5. Zhang Y
6. Mou Z
(2016) Microarray analysis of exogenous NAD+-induced transcriptome changes in Arabidopsis thaliana
Publicly available at the NCBI Gene Expression Omnibus (accession no: GSE76568).

https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76568

The following previously published data sets were used

1. Wang Y
2. Zhang Y
3. Yao J
4. Sun Y
5. Mou Z
(2012) Microarray analysis of Atelp2, npr1 and wild type (Col-0) infected with the avirulent bacterial pathogen Pst DC3000/avrRpt2
Publicly available at the NCBI Gene Expression Omnibus (accession no: GSE38986).

https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE38986

Article and author information

Author details

Chenggang Wang

Department of Microbiology and Cell Science, University of Florida, Gainesville, United States

Competing interests
The authors declare that no competing interests exist.
Mingqi Zhou

Department of Microbiology and Cell Science, University of Florida, Gainesville, United States

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-4605-5467
Xudong Zhang

Department of Microbiology and Cell Science, University of Florida, Gainesville, United States

Competing interests
The authors declare that no competing interests exist.
Jin Yao

Target Sciences, GlaxoSmithKline, King of Prussia, United States

Competing interests
The authors declare that no competing interests exist.
Yanping Zhang

Interdisciplinary Center for Biotechnology Research, University of Florida, Gainesville, United States

Competing interests
The authors declare that no competing interests exist.
Zhonglin Mou

Department of Microbiology and Cell Science, University of Florida, Gainesville, United States

For correspondence
zhlmou@ufl.edu

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0003-0243-4905

Funding

National Science Foundation (IOS-0842716)

Zhonglin Mou

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Copyright

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.