Calcium network control of nutrient and metabolite transport

钙网络控制营养物和代谢物运输

• 批准号: 71800676
• 负责人: Professor Dr. Rainer Hedrich
• 金额: --
• 依托单位: Lehrstuhl für Botanik I: Molekulare Pflanzenphysiologie und Biophysik
• 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 2016-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/71800676?language=en
• 关键词: Calcium; network; control; nutrient; metabolite

The picture of fast ABA-signalling leading to the Ca2+-dependent activation of S-type anion channels in guard cells is quite detailed by now. However, the majority of collected data is of a qualitative nature and therefore not sufficient to mathematically model fast ABA-signalling in guard cells so far.Thus within the proposed project we intend to i) decompose and quantify the calcium signal itself, ii) the activity and affinity of signal-decoding protein kinases, the iii) abundance of and stoichiometry between ABA-signalling components. Furthermore, we will address the following key questions: iv) How do the individual signalling components influence each other? v) What are the spatio-temporal events that occur during ABA-dependent closure? vi) How do kinases with different Ca2+ affinities encode Ca2+ signals and thereby fine-tune the activity of anion channels? The collection of these quantitative data together with mathematical modeling will proof or disproof our current notion of fast ABA-signalling in guard cells and will come up with new predictions and in turn experiments on ABA-induced stomatal closure.

快速ABA信号导致保卫细胞中S型阴离子通道的Ca 2+依赖性激活的图片现在相当详细。然而，大多数收集的数据是定性的性质，因此不足以在保卫细胞中快速ABA信号的数学模型到目前为止，因此，在拟议的项目中，我们打算i）分解和量化钙信号本身，ii）信号解码蛋白激酶的活性和亲和力，iii）ABA信号组分之间的丰度和化学计量。此外，我们将解决以下关键问题：iv）各个信号组件如何相互影响？v）在依赖ABA的闭合期间发生的时空事件是什么？vi）具有不同Ca2+亲和力的激酶如何编码Ca2+信号，从而微调阴离子通道的活性？这些定量数据的收集与数学建模将证明或反驳我们目前的概念，快速ABA信号在保卫细胞，并将提出新的预测，进而实验ABA诱导气孔关闭。