ABSTRACT
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.
