Nitrogen is an essential nutrient for development and growth of plants. Nitrogen use efficiency (NUE), the yield of grain per unit of N available in the soil, is a limiting factor for yield in crops. The Target of Rapamycin (TOR) kinase is a central regulator for growth, conserved in all eukaryotes. Its input consists of several environmental cues, such as nutrient availability and internal metabolic status. An important antagonist of TOR is the SNF-related kinase 1 (SnRK1), a stress related kinase. A link was proposed between TOR inactivity and nitrogen starvation, as is already shown in yeast and mammalian cells. We will elucidate the crosstalk between TOR and its antagonist, using the understanding to improve the NUE in maize. We will use an assay showing the phosphorylation status of a direct target of TOR, ATG13, as a readout for the TOR activity in differential N conditions. Quantitative phosphoproteomics, a method showing differential phosphorylation, will be performed in N shift experiments - in absence and presence of TOR inhibitors - to find targets of TOR activity for the nitrogen pathway. The pathway upstream of these kinases will be further investigated by identifying direct interactions. Validation will be done with an in vitro kinase assay and phenotypically, using mutant and overexpressing lines under low and high N conditions. We aim to find phenotypes that will produce a high yield, growing on lower nitrogen concentrations then are now applied to the field.