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

Ca2+在植物激素脱落酸（ABA）信号通路中的整合在很大程度上尚不清楚。阐明这一过程是我们研究的中心目标。我们的分析集中在钙调素结构域含有蛋白激酶GCA2，已被表征为Ca2+结合蛋白。ABA不敏感突变体gca2-1的特征表明该基因位点在ABA、CO2、Ca2+和过氧化氢的整合中起作用。不同信号的共同之处在于，它们调节ABA反应通路，导致ABA依赖基因表达和蒸腾控制。因此，这些信号似乎很早就被整合到ABA转导中，在ABA受体处或附近。事实上，GCA2与ABA受体组分和直接相关的蛋白激酶相互作用。对GCA2的作用和调控有了更深入的了解，就有机会进入一个令人着迷但研究较少的研究领域，即整合外源和内源（ABA）信号的分子机制。在这个研究领域，我们看到了长期的科学挑战。更具体地说，我们在这个项目中追求的问题是，GCA2位点是否受到自然选择的拟南芥生态型及其生理后果。在这种情况下，我们对分子机制感兴趣，即GCA2-ABA受体组分通过蛋白质相互作用和磷酸化状态的相互作用。该研究包括已知的表征和鉴定新的GCA2靶点和相互作用成分。ABA反应调节因子和转录因子ABF2将是研究的焦点，它作为Ca2+依赖性蛋白激酶的中心靶点出现。在共同努力下，我们计划可视化细胞Ca2+释放并模拟Ca2+依赖的ABF2调节。总之，该研究与其他项目部分将为将Ca2+信号整合到ABA反应途径的分子机制提供新的见解。

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.