ArticlePlant physiology2013
Glutamate receptor-like channel3.3 is involved in mediating glutathione-triggered cytosolic calcium transients, transcriptional changes, and innate immunity responses in Arabidopsis.
Article in Plant physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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54 citing papers in PubMed, 133 citations in OpenAlex.
- Glutathione induces trap closure for carnivory in Cape sundew.Science advances · 2026Article
- A maize mutant in the glutamate receptor-like dwarf13 is modified by cis-acting natural variation and a cornichon homolog.PLoS genetics · 2025Article
- Cysteine Signalling in Plant Pathogen Response.Plant, cell & environment · 2025Article
- The glutamate receptor-like GLR2.7 modulates insect egg-induced defense responses in Arabidopsis.The New phytologist · 2025Article
- Coordinated actions of NLR-assembled and glutamate receptor-like calcium channels in plant effector-triggered immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Regeneration and defense: unveiling the molecular interplay in plants.The New phytologist · 2025Review
- Structure and gating of kainate receptors.Frontiers in pharmacology · 2025Review
- Glutamate Receptor-like (GLR) Family inInternational journal of molecular sciences · 2024Article
- Involvement of GLR-mediated nitric oxide effects on ROS metabolism in Arabidopsis plants under salt stress.Journal of plant research · 2024Article
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- CaNature plants · 2024Article
- Genome-wide identification of the glutamate receptor-like gene family inPlant signaling & behavior · 2023Article
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- Why did glutamate, GABA, and melatonin become intercellular signalling molecules in plants?eLife · 2023Review
- Merging Signaling with Structure: Functions and Mechanisms of Plant Glutamate Receptor Ion Channels.Annual review of plant biology · 2023Review
- Genome-wide identification and expression analysis of the glutamate receptor gene family in sweet potato and its two diploid relatives.Frontiers in plant science · 2023Article
- Genes related to osmoregulation and antioxidation play important roles in the response ofFrontiers in plant science · 2023Article
- A glutamate receptor-like gene is involved in ABA-mediated growth control inPlant signaling & behavior · 2022Article
- Roles of Glutamate Receptor-Like Channels (GLRs) in Plant Growth and Response to Environmental Stimuli.Plants (Basel, Switzerland) · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tripeptide reduced glutathione (GSH; γ-glutamate [Glu]-cysteine [Cys]-glycine) is a major endogenous antioxidant in both animal and plant cells. It also functions as a neurotransmitter mediating communication among neurons in the central nervous system of animals through modulating specific ionotropic Glu receptors (GLRs) in the membrane. Little is known about such signaling roles in plant cells. Here, we report that transient rises in cytosolic calcium triggered by exogenous GSH in Arabidopsis (Arabidopsis thaliana) leaves were sensitive to GLR antagonists and abolished in loss-of-function atglr3.3 mutants. Like the GSH biosynthesis-defective mutant PHYTOALEXIN DEFICIENT2, atglr3.3 showed enhanced susceptibility to the bacterial pathogen Pseudomonas syringae pv tomato DC3000. Pathogen-induced defense marker gene expression was also decreased in atglr3.3 mutants. Twenty-seven percent of genes that were rapidly responsive to GSH treatment of seedlings were defense genes, most of which were dependent on functional AtGLR3.3, while GSH suppressed pathogen propagation through the AtGLR3.3-dependent pathway. Eight previously identified putative AtGLR3.3 ligands, GSH, oxidized glutathione, alanine, asparagine, Cys, Glu, glycine, and serine, all elicited the AtGLR3.3-dependent cytosolic calcium transients, but only GSH and Cys induced the defense response, with the Glu-induced AtGLR3.3-dependent transcription response being much less apparent than that triggered by GSH. Together, these observations suggest that AtGLR3.3 is required for several signaling effects mediated by extracellular GSH, even though these effects may not be causally related.
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