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Plant Physiol, December 2000, Vol. 124, pp. 1615-1624

Arabidopsis Mutants Resistant to S(+)-beta -Methyl-alpha , beta -Diaminopropionic Acid, a Cycad-Derived Glutamate Receptor Agonist1

Eric D. Brenner, Nora Martinez-Barboza, Alexandra P. Clark, Quail S. Liang, Dennis W. Stevenson, and Gloria M. Coruzzi*

Department of Biology, New York University, New York, New York 10003 (E.D.B., A.P.C., Q.S.L., G.M.C.); Department of Biology, City University of New York, New York, New York 10016 (N.M.-B.); and New York Botanical Garden, Bronx, New York 10458 (D.W.S.)

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. To understand the role of Arabidopsis glutamate receptor-like (AtGLR) genes in plants, we have taken a pharmacological approach by examining the effects of BMAA [S(+)-beta -methyl-alpha , beta -diaminopropionic acid], a cycad-derived iGluR agonist, on Arabidopsis morphogenesis. When applied to Arabidopsis seedlings, BMAA caused a 2- to 3-fold increase in hypocotyl elongation and inhibited cotyledon opening during early seedling development. The effect of BMAA on hypocotyl elongation is light specific. Furthermore, BMAA effects on early morphogenesis of Arabidopsis can be reversed by the simultaneous application of glutamate, the native iGluR agonist in animals. To determine the targets of BMAA action in Arabidopsis, a genetic screen was devised to isolate Arabidopsis mutants with a BMAA insensitive morphology (bim). When grown in the light on BMAA, bim mutants exhibited short hypocotyls compared 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 bim mutants have a normal, etiolated morphology, similar to wild-type plants. Class-II bim mutants have shorter hypocotyls and closed cotyledons when grown in the dark. Class-III bim mutants have short hypocotyls and open cotyledons when grown in the dark, resembling the previously characterized constitutively photomorphogenic mutants (cop, det, fus, and shy). Further analysis of the bim mutants should help define whether plant-derived iGluR agonists target glutamate receptor signaling pathways in plants.

1 This work was supported by the National Institutes of Health (grant no. GM32877 to G.C.), the National Institutes of Health postdoctoral fellowship (to E.B.), and a Humana fellowship from the City University of New York (to N.M.).

* Corresponding author; e-mail gloria.coruzzi{at}nyu.edu; fax 212-995-4204.

© 2000 American Society of Plant Physiologists


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