De-regulated expression of the plant glutamate receptor homolog AtGLR3.1 impairs long-term Ca2+-programmed stomatal closure
Article first published online: 2 FEB 2009
© 2009 The Authors. Journal compilation © 2009 Blackwell Publishing Ltd
The Plant Journal
Volume 58, Issue 3, pages 437–449, May 2009
How to Cite
Cho, D., Kim, S. A., Murata, Y., Lee, S., Jae, S.-K., Nam, H. G. and Kwak, J. M. (2009), De-regulated expression of the plant glutamate receptor homolog AtGLR3.1 impairs long-term Ca2+-programmed stomatal closure. The Plant Journal, 58: 437–449. doi: 10.1111/j.1365-313X.2009.03789.x
- Issue published online: 27 APR 2009
- Article first published online: 2 FEB 2009
- Received 24 October 2008; revised 11 December 2008; accepted 18 December 2008; published online 2 February 2009.
- anion channel;
- calcium oscillation;
- gene expression;
- glutamate receptor homolog;
- guard cells
Cytosolic Ca2+ ([Ca2+]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, [Ca2+]cyt has been shown to regulate stomatal movements, and a defined window of Ca2+ oscillation kinetic parameters encodes necessary information for long-term stomatal movements. However, it remains unknown how the encrypted information in the cytosolic Ca2+ 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 Ca2+-induced stomatal closure. Cytosolic Ca2+ activation of S-type anion channels, which play a central role in Ca2+-reactive stomatal closure, was normal in the AtGLR3.1 over-expressing plants. Interestingly, AtGLR3.1 over-expression did not affect Ca2+-induced Ca2+ oscillation kinetics, but resulted in a failure to maintain long-term ‘Ca2+-programmed’ stomatal closure when Ca2+ oscillations containing information for maintaining stomatal closure were imposed. By contrast, prompt short-term Ca2+-reactive closure was not affected in AtGLR3.1 over-expressing plants. In wild-type plants, the translational inhibitor cyclohexamide partially inhibited Ca2+-programmed stomatal closure induced by experimentally imposed Ca2+ oscillations without affecting short-term Ca2+-reactive closure, mimicking the guard cell behavior of the AtGLR3.1 over-expressing plants. Our results suggest that over-expression of AtGLR3.1 impairs Ca2+ oscillation-regulated stomatal movements, and that de novo protein synthesis contributes to the maintenance of long-term Ca2+-programmed stomatal closure.