title: Ionotropic glutamate receptor (iGluR)-like channels mediate MAMP-induced calcium influx in Arabidopsis thaliana.
abstract: Binding of specific microbial epitopes [MAMPs (microbe-associated molecular patterns)] to PRRs (pattern recognition receptors) and subsequent receptor kinase activation are key steps in plant innate immunity. One of the earliest detectable events after MAMP perception is a rapid and transient rise in cytosolic Ca2+ levels. In plants, knowledge about the signalling events leading to Ca2+ influx and on the molecular identity of the channels involved is scarce. We used a transgenic Arabidopsis thaliana line stably expressing the luminescent aequorin Ca2+ biosensor to monitor pharmacological interference with Ca2+ signatures following treatment with the bacterial peptide MAMPs flg22 and elf18, and the fungal carbohydrate MAMP chitin. Using a comprehensive set of compounds known to impede Ca2+-transport processes in plants and animals we found strong evidence for a prominent role of amino acid-controlled Ca2+ fluxes, probably through iGluR (ionotropic glutamate receptor)-like channels. Interference with amino acid-mediated Ca2+ fluxes modulates MAMP-triggered MAPK (mitogen-activated protein kinase) activity and affects MAMP-induced accumulation of defence gene transcripts. We conclude that the initiation of innate immune responses upon flg22, elf18 and chitin recognition involves apoplastic Ca2+ influx via iGluR-like channels.
authors.affiliation: Max-Planck Institute for Plant Breeding Research, Department of Plant-Microbe Interactions, Carl-von-Linné-Weg 10, 50829 Köln, Germany.
authors.forename: Mark
authors.initials: M
authors.lastname: Kwaaitaal
authors.forename: Rik
authors.initials: R
authors.lastname: Huisman
authors.forename: Jens
authors.initials: J
authors.lastname: Maintz
authors.forename: Anja
authors.initials: A
authors.lastname: Reinstädler
authors.forename: Ralph
authors.initials: R
authors.lastname: Panstruga
mesh_terms: D000331:Aequorin / Q000737:chemistry; D000496:Alloxan / Q000494:pharmacology; D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D001426:Bacterial Proteins / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects; D002686:Chitin / Q000494:pharmacology; D016048:Dideoxyadenosine / Q000494:pharmacology; D004110:Diltiazem / Q000494:pharmacology; D004789:Enzyme Activation; D004963:Estrenes / Q000494:pharmacology; D018506:Gene Expression Regulation, Plant; D007736:Kynurenic Acid / Q000494:pharmacology; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D009355:Neomycin / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D030821:Plants, Genetically Modified; D011760:Pyrrolidinones / Q000494:pharmacology; D058468:Receptors, Ionotropic Glutamate / Q000378:metabolism*; D051192:Receptors, Pattern Recognition; D036226:Seedlings / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D014158:Transcription, Genetic; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000378:metabolism; D014700:Verapamil / Q000494:pharmacology
chemical_list: D029681:Arabidopsis Proteins; D001426:Bacterial Proteins; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D004963:Estrenes; D011760:Pyrrolidinones; D058468:Receptors, Ionotropic Glutamate; D051192:Receptors, Pattern Recognition; C060229:1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; D002686:Chitin; D016048:Dideoxyadenosine; D000331:Aequorin; D000496:Alloxan; D014700:Verapamil; D020928:Mitogen-Activated Protein Kinases; D010738:Type C Phospholipases; D004110:Diltiazem; D007736:Kynurenic Acid; D009355:Neomycin; D009543:Nifedipine