Current address: Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge CB2 3EA, UK.
The role of calcium in ABA-induced gene expression and stomatal movements
Article first published online: 23 DEC 2001
The Plant Journal
Volume 26, Issue 3, pages 351–362, May 2001
How to Cite
Webb, A. A. R., Larman, M. G., Montgomery, L. T., Taylor, J. E. and Hetherington, A. M. (2001), The role of calcium in ABA-induced gene expression and stomatal movements. The Plant Journal, 26: 351–362. doi: 10.1046/j.1365-313X.2001.01032.x
- Issue published online: 23 DEC 2001
- Article first published online: 23 DEC 2001
- Received 30 November 2000; revised 26 February 2001; accepted 6 March 2001.
- abscisic acid;
- guard cells;
- gene expression.
There is much interest in the transduction pathways by which abscisic acid (ABA) regulates stomatal movements (ABA-turgor signalling) and by which this phytohormone regulates the pattern of gene expression in plant cells (ABA-nuclear signalling). A number of second messengers have been identified in both the ABA-turgor and ABA-nuclear signalling pathways. A major challenge is to understand the architecture of ABA-signalling pathways and to determine how the ABA signal is coupled to the appropriate response. We have investigated whether separate Ca2+-dependent and -independent ABA-signalling pathways are present in guard cells. Our data suggest that increases in [Ca2+]i are a common component of the guard cell ABA-turgor and ABA-nuclear signalling pathways. The effects of Ca2+ antagonists on ABA-induced stomatal closure and the ABA-responsive CDeT6-19 gene promoter suggest that Ca2+ is involved in both ABA-turgor signalling and ABA-nuclear signalling in guard cells. However, the sensitivity of these pathways to alterations in the external calcium concentration differ, suggesting that the ABA-nuclear and ABA-turgor signalling pathways are not completely convergent. Our data suggest that whilst Ca2+-independent signalling elements are present in the guard cell, they do not form a completely separate Ca2+-independent ABA-signalling pathway.