Calcium network control of nutrient and metabolite transport

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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.