Arabidopsis mutants resistant to S(+)-beta-methyl-alpha, beta-diaminopropionic acid, a cycad-derived glutamate receptor agonist

Ionotropic glutamate receptors (iGluRs) are ligand-gated ion channels that are the predominant neuroreceptors in the mammalian brain. Genes with high sequence similarity to animal iGluRs have been identified in Arabidopsis. T o understand the role of Arabidopsis glutamate receptor-like (AK;LR) genes in plants, we have taken a pharmacological approach by examining the effect s of BMAA [S(+)-beta -methyl-alpha, beta -diaminopropionic acid], a cycad-d erived iGluR agonist, on Arabidopsis morphogenesis. When applied to Arabido psis seedlings, BMAA caused a 2- to 3-fold increase in hypocotyl elongation and inhibited cotyledon opening during early seedling development. The eff ect of BMAA on hypocotyl elongation is light specific. Furthermore, BMAA ef fects on early morphogenesis of Arabidopsis can be reversed by the simultan eous application of glutamate, the native iGluR agonist in animals. To dete rmine the targets of BMAA action in Arabidopsis, a genetic screen was devis ed to isolate Arabidopsis mutants with a BMAA insensitive morphology (bim). When grown in the light on BMAA, bim mutants exhibited short hypocotyls co mpared with wild type. bim mutants were grouped into three classes based on their morphology when grown in the dark in the absence of BMAA. Class-I bi m mutants have a normal, etiolated morphology, similar to wild-type plants. Class-II bim mutants have shorter hypocotyls and closed cotyledons when gr own in the dark. Class-III bim mutants have short hypocotyls and open cotyl edons when grown in the dark, resembling the previously characterized const itutively photomorphogenic mutants (cop, det, Jus, and shy). Further analys is of the bim mutants should help define whether plant-derived iGluR agonis ts target glutamate receptor signaling pathways in plants.