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 ionotropic glutamate receptor genes in Arabidopsis thaliana (AtGluR2). This gene was found to alter Ca²⁺ utilization when overexpressed in A. thaliana. These transgenic plants displayed symptoms of Ca²⁺ deficiency, including browning and death of the shoot apex, necrosis of leaf tips, and deformation of leaves. Supplementation with Ca²⁺ alleviated these phenotypes. Overall levels of Ca²⁺ in tissues of control plants were not significantly different from those of transgenic plants, suggesting that overexpression of the AtGluR2 gene did not affect Ca²⁺ 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 hypersensitivity was ameliorated by supplementation with Ca²⁺. The results showed 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 conducting vessels. This suggests that AtGluR2 encodes a functional channel that unloads Ca²⁺ from the xylem vessels. The results together suggest that appropriate expression of the AtGluR2 protein may play critical roles in Ca²⁺ nutrition by controlling the ion allocation among different Ca²⁺ sinks both during normal development and during adaptation to ionic stresses.