[摘要]：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 Ca(2+) levels. In plants, knowledge about the signalling events leading to Ca(2+) influx and on the molecular identity of the channels involved is scarce. We used a transgenic Arabidopsis thaliana line stably expressing the luminescent aequorin Ca(2+) biosensor to monitor pharmacological interference with Ca(2+) 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 Ca(2+)-transport processes in plants and animals we found strong evidence for a prominent role of amino acid-controlled Ca(2+) fluxes, probably through iGluR (ionotropic glutamate receptor)like channels. Interference with amino acid-mediated Ca(2+) 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, elf 18 and chitin recognition involves apoplastic Ca(2+) influx via iGluR-like channels.
