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

ABA 2 (GCA2) 的生长控制，钙振荡的中央调节剂

• 批准号: 71800568
• 负责人: Professor Dr. Erwin Grill
• 金额: --
• 依托单位: Lehrstuhl für Botanik
• 依托单位国家: 德国
• 项目类别: Research Units
• 财政年份: 2008
• 资助国家: 德国
• 起止时间: 2007-12-31 至 2017-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/71800568?language=en
• 关键词: Growth; Control; ABA; GCA2; central

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.

Ca2+ 在植物激素脱落酸 (ABA) 信号通路中的整合目前尚不清楚。阐明这个过程是我们研究的中心目标。我们的分析重点是含有钙调蛋白结构域的蛋白激酶 GCA2，该蛋白已被定性为 Ca2+ 结合蛋白。 ABA 不敏感突变体 gca2-1 的特征表明该基因座在 ABA、CO2、Ca2+ 和过氧化氢整合中发挥作用。不同信号的共同点是它们调节 ABA 响应途径，导致 ABA 依赖性基因表达和蒸腾控制。因此，这些信号似乎很早就整合到 ABA 转导中，位于或接近 ABA 受体。事实上，GCA2 与 ABA 受体成分和直接相关的蛋白激酶相互作用。对 GCA2 作用和调节的更深入了解提供了进入一个令人着迷但研究很少的研究领域的机会，即整合外源和内源 (ABA) 信号的分子机制。我们在该研究领域看到了长期的科学挑战。更具体地说，我们在这个项目中探究GCA2基因座是否受到拟南芥生态型中的自然选择及其生理后果的影响。在这种情况下，我们对分子机制感兴趣，即 GCA2-ABA 受体成分通过蛋白质相互作用和磷酸化状态相互作用。该研究包括已知 GCA2 靶标和相互作用成分的表征以及新靶标和相互作用成分的鉴定。 ABA 反应调节剂和转录因子 ABF2 将成为该研究的焦点，它是 Ca2+ 依赖性蛋白激酶的中心靶点。在共同努力中，我们计划可视化细胞 Ca2+ 释放并模拟 Ca2+ 依赖性 ABF2 调节。总之，该研究与其他项目部分一起将为将 Ca2+ 信号整合到 ABA 反应途径的分子机制提供新的见解。