Overexpression of the AtGluR2 gene encoding an arabidopsis homolog of mammalian glutamate receptors impairs calcium utilization and sensitivity to ionic stress in transgenic plants

We have identified a homolog of the mammalian iono-tropic glutamate recepto r genes in Arabidopsis thaliana (AtGluR2). This gene was found to alter Ca2 + utilization when overexpressed in A. thaliana. These transgenic plants di splayed symptoms of Ca2+ deficiency, including browning and death of the sh oot apex, necrosis of leaf tips, and deformation of leaves. Supplementation with Ca2+ alleviated these phenotypes. Overall levels of Ca2+ in tissues o f control plants were not significantly different from those of transgenic plants, suggesting that overexpression of the AtGluR2 gene did not affect C a2+ uptake. However, the relative growth yield as a function of Ca2+ levels revealed that the critical deficiency content of Ca2+ in transgenic plants was three times higher than that of control plants. The transgenic plants also exhibited hypersensitivity to Na+ and K+ ionic stresses. The ion hyper sensitivity was ameliorated by supplementation with Ca2+. The results showe d that overexpression of the AtGluR2 gene caused reduced efficiency of Ca2 utilization in the transgenic plants. The promoter of the AtGluR2 gene was active in vascular tissues, particularly in cells adjacent to the conducti ng vessels. This suggests that AtGluR2 encodes a functional channel that un loads Ca2+ from the xylem vessels. The results together suggest that approp riate expression of the AtGluR2 protein may play critical roles in Ca2+ nut rition by controlling the ion allocation among different Ca2+ sinks both du ring normal development and during adaptation to ionic stresses.