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

  1. Chenggang Wang
  2. Mingqi Zhou
  3. Xudong Zhang
  4. Jin Yao
  5. Yanping Zhang
  6. Zhonglin Mou  Is a corresponding author
  1. University of Florida, United States
  2. GlaxoSmithKline, United States
Research Article
  • Cited 14
  • Views 2,449
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Cite this article as: eLife 2017;6:e25474 doi: 10.7554/eLife.25474

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.

Article and author information

Author details

  1. Chenggang Wang

    Department of Microbiology and Cell Science, University of Florida, Gainesville, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Mingqi Zhou

    Department of Microbiology and Cell Science, University of Florida, Gainesville, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-4605-5467
  3. Xudong Zhang

    Department of Microbiology and Cell Science, University of Florida, Gainesville, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. Jin Yao

    Target Sciences, GlaxoSmithKline, King of Prussia, United States
    Competing interests
    The authors declare that no competing interests exist.
  5. Yanping Zhang

    Interdisciplinary Center for Biotechnology Research, University of Florida, Gainesville, United States
    Competing interests
    The authors declare that no competing interests exist.
  6. 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.
    ORCID icon "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.

Reviewing Editor

  1. Thorsten Nürnberger, University of Tubingen, Germany

Publication history

  1. Received: January 25, 2017
  2. Accepted: July 18, 2017
  3. Accepted Manuscript published: July 19, 2017 (version 1)
  4. Version of Record published: August 17, 2017 (version 2)

Copyright

© 2017, Wang et al.

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.

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