Premium
De‐regulated expression of the plant glutamate receptor homolog AtGLR3.1 impairs long‐term Ca 2+ ‐programmed stomatal closure
Author(s) -
Cho Daeshik,
Kim Sun A.,
Murata Yoshiyuki,
Lee Sangmee,
Jae SeulKi,
Nam Hong Gil,
Kwak June M.
Publication year - 2009
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2009.03789.x
Subject(s) - guard cell , microbiology and biotechnology , arabidopsis , cytosol , biology , biophysics , glutamate receptor , chemistry , receptor , biochemistry , gene , mutant , enzyme
Summary Cytosolic Ca 2+ ([Ca 2+ ] cyt ) mediates diverse cellular responses in both animal and plant cells in response to various stimuli. Calcium oscillation amplitude and frequency control gene expression. In stomatal guard cells, [Ca 2+ ] cyt has been shown to regulate stomatal movements, and a defined window of Ca 2+ oscillation kinetic parameters encodes necessary information for long‐term stomatal movements. However, it remains unknown how the encrypted information in the cytosolic Ca 2+ signature is decoded to maintain stomatal closure. Here we report that the Arabidopsis glutamate receptor homolog AtGLR3.1 is preferentially expressed in guard cells compared to mesophyll cells. Furthermore, over‐expression of AtGLR3.1 using a viral promoter resulted in impaired external Ca 2+ ‐induced stomatal closure. Cytosolic Ca 2+ activation of S‐type anion channels, which play a central role in Ca 2+ ‐reactive stomatal closure, was normal in the AtGLR3.1 over‐expressing plants. Interestingly, AtGLR3.1 over‐expression did not affect Ca 2+ ‐induced Ca 2+ oscillation kinetics, but resulted in a failure to maintain long‐term ‘Ca 2+ ‐programmed’ stomatal closure when Ca 2+ oscillations containing information for maintaining stomatal closure were imposed. By contrast, prompt short‐term Ca 2+ ‐reactive closure was not affected in AtGLR3.1 over‐expressing plants. In wild‐type plants, the translational inhibitor cyclohexamide partially inhibited Ca 2+ ‐programmed stomatal closure induced by experimentally imposed Ca 2+ oscillations without affecting short‐term Ca 2+ ‐reactive closure, mimicking the guard cell behavior of the AtGLR3.1 over‐expressing plants. Our results suggest that over‐expression of AtGLR3.1 impairs Ca 2+ oscillation‐regulated stomatal movements, and that de novo protein synthesis contributes to the maintenance of long‐term Ca 2+ ‐programmed stomatal closure.