1. Involvement of putative glutamate receptors in plant defence signaling and NO production.
- Author
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Vatsa P, Chiltz A, Bourque S, Wendehenne D, Garcia-Brugger A, and Pugin A
- Subjects
- Algal Proteins pharmacology, Calcium metabolism, Cell Culture Techniques, Excitatory Amino Acid Agonists pharmacology, Excitatory Amino Acid Antagonists pharmacology, Fungal Proteins, Glutamic Acid metabolism, Glutamic Acid pharmacology, Glutamic Acid physiology, Immunity, Innate, Nicotiana cytology, Nicotiana metabolism, Calcium Signaling, Nitric Oxide metabolism, Plant Proteins metabolism, Receptors, Glutamate metabolism, Nicotiana immunology
- Abstract
Ionotropic glutamate receptors (iGluRs) are non-selective cation channels permeable to calcium, present in animals and plants. In mammals, glutamate is a well-known neurotransmitter and recently has been recognized as an immunomodulator. As animals and plants share common mechanisms that govern innate immunity with calcium playing a key role in plant defence activation, we have checked the involvement of putative iGluRs in plant defence signaling. Using tobacco cells, we first provide evidence supporting the activity of iGluRs as calcium channels and their involvement in NO production as reported in animals. Thereafter, iGluRs were shown to be activated in response to cryptogein, a well studied elicitor of defence response, and partly responsible for cryptogein-induced NO production. However, other cryptogein-induced calcium-dependent events including anion efflux, H(2)O(2) production, MAPK activation and hypersensitive response (HR) did not depend on iGluRs indicating that different calcium channels regulate different processes at the cell level. We have also demonstrated that cryptogein induces efflux of glutamate in the apoplast by exocytosis. Taken together, our results demonstrate for the first time, an involvement of a putative iGluR in plant defence signaling and NO production, by mechanisms that show homology with glutamate mode of action in mammals., (Copyright © 2011 Elsevier Masson SAS. All rights reserved.)
- Published
- 2011
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