Metabolic adaptation of phosphate-starved plants - Functional analyses of novel-type, intracellular phosphatases of the the HAD superfamily

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The availability of phosphorus (P) has a profound impact on plant metabolism and productivity. Low inorganic phosphate availability triggers metabolic responses to maintain intracellular phosphate homeostasis in plants. Plants respond to exogenous P limitation with tightly controlled strategies to reprioritize metabolic phosphate consumption and remobilization pathways and to maximize the acquisition from the environment. This project is dedicated to functional plant strategies of intracellular phosphate mobilization by novel-type phosphatases which belong to the Haloacid Dehalogenase (HAD) superfamily. The respective genes are up-regulated by Pi starvation in a highly specific manner. Our recent discovery of the enzymatic properties of AtPECP1 and AtPPsPase1 which are phosphoethanolamine/phosphocholine and pyrophosphate-specific phosphatases, respectively, suggests functional roles in lipid and carbohydrate metabolism. It is the goal of the proposed work to elucidate how the gene products contribute to acclimatory responses to low P availability. Arabidopsis wild-type plants and transgenic lines completely compromised or enhanced in enzyme function will be supplied with different Pi concentrations and physiological, morphological and biochemical responses will be recorded. Changes in the pattern of lipid degradation products and distinct primary intermediates such as phosphorylated and UDP-activated sugars will be analyzed quantitatively using methods based on mass spectrometry. The engineered proteins will be tested for functionality in mutant complementation assays. Nutritional stress-induced transcriptional changes triggered by AtPPsPase1 action will be investigated by a microarray approach. Quantitative RT-PCR will be used to delineate the impact of regulatory factors of the Pi starvation response. The spatio-temporal expression of AtPECP1 and ATPPsPase1 by promoter-driven reporter genes are directed at testing Pi-dependent source-sink-relations.