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Journal of Experimental Botany 2007 58(12):3249-3262; doi:10.1093/jxb/erm172
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© 2007 The Author(s).
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. This paper is available online free of all access charges (see http://jxb.oxfordjournals.org/open_access.html for further details)

RESEARCH PAPER

Involvement of calcium signalling in dormancy release of grape buds

Xuequn Pang1,2, Tamar Halaly2, Omer Crane2, Tsvicka Keilin2, Alexandra Keren-Keiserman2, Aliza Ogrodovitch2, David Galbraith3 and Etti Or2,*

1College of Life Science, South China Agricultural University, Guangzhou, 510642, PR China
2Department of Fruit Tree Sciences, Institute of Plant Sciences, Agricultural Research Organization, the Volcani Center, Bet Dagan 50250, Israel
3Department of Plant Sciences and Bios Institute, University of Arizona, Tucson, AZ 85721, USA

* To whom correspondence should be addressed. E-mail: vhettior{at}agri.gov.il

Artificial induction of grape bud dormancy release by hydrogen cyanamide (HC) serves as a reliable model system to explore the events occurring shortly after the induction of dormancy release. Recently, a group of genes with remarkable differences in expression level between HC-treated and control buds was identified. The identification of several calcium signalling-related genes within that group raised the hypothesis of the involvement of Ca2+ signalling in grape bud dormancy release. Therefore, the effects of HC treatment on the expression profiles of several calcium sensors, the effect of the plasma membrane calcium channel blocker LaCl3 and the calcium chelator EGTA on HC-induced and chilling-induced bud-break, and the effect of HC application on calcium-dependent protein phosphorylation activities in the bud tissue were studied. Here the HC-induced expression of Ca2+-ATPase is described, indicating that this treatment might evoke an increase in [Ca2+]cyt. Similar induction was confirmed for calmodulin, calmodulin-binding protein, and calcium-dependent protein kinase (CDPK). Both LaCl3 and EGTA blocked the inducing effect of HC on bud-break, and their inhibitory effects were removed by supplying exogenous Ca2+. Calcium-dependent histone phosphorylation was up to 70% higher in HC-treated buds. Endogenous protein phosphorylation assays detected four proteins exhibiting increased phosphorylation following HC treatment, of which two were phosphorylated in a calcium-dependent manner. One of these, a 47 kDa protein, presented strong and Ca2+-dependent phosphorylation only in HC-treated buds. The potential role of CDPK in the phosphorylation of this protein was supported by an immunoprecipitation assay. The data suggest, for the first time, that calcium signalling is involved in the mechanism of bud dormancy release.

Key words: Bud dormancy, calcium signalling, heat shock, hydrogen cyanamide, Vitis

Received 17 December 2006; Revised 7 June 2007 Accepted 25 June 2007


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