Growth Control by ABA 2 (GCA2), a central regulator of calcium oscillations

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The integration of Ca2+ in the signal pathway of the phytohormone abscisic acid (ABA) is largely not understood. The elucidation of this process is a central goal of our studies. Our analysis focuses on the calmodulin-domain containing protein kinase GCA2 that has been characterized as a Ca2+-binding protein. The characterization of the ABA-insensitive mutant gca2-1 points to a role of this gene locus in the integration of ABA, CO2, Ca2+ and hydrogen peroxide. The different signals have in common that they regulate the ABA response pathway leading to both ABA-dependent gene expression and transpirational control. Hence, those signals seem to be integrated early into ABA transduction, at or close to the ABA receptor. Indeed, GCA2 interacts with ABA receptor components and directly associated protein kinases. A deeper understanding of GCA2 action and regulation offers the opportunity to gain access to a fascinating and yet poorly studied research field, namely the molecular mechanisms of integrating exogenous and endogenous (ABA) signals. We see in that research area our long-term scientific challenge. More specifically, we pursue in this project the question whether the GCA2 locus is subjected to natural selection among Arabidopsis ecotypes and the physiological consequences thereof. In this context, we are interested in the molecular mechanisms, i.e. the interplay of GCA2-ABA receptor components via protein interactions and phosphorylation status. The study includes the characterization of known and the identification of novel GCA2 targets and interaction components. The ABA response regulator and transcription factor ABF2 will be a focal point in the study, which emerges as a hub target of Ca2+-dependent protein kinases. In a joint effort, we plan to visualize cellular Ca2+-release and to model the Ca2+-dependent ABF2 regulation. In conclusion, the study together with other project parts will provide novel insights into the molecular mechanisms of integrating the Ca2+signal into ABA response pathways.