The transcriptional TOR and AMPK target sugarbabe regulates amino acid and lipid catabolism. Torsten Buelow, Katrin Riemschoss, Ingo Zinke, Michael J. Pankratz. Molecular Brain Physiology and Behavior, LIMES Institute, University of Bonn, 53115 Bonn, Germany.

   Varying availability and composition of food make it necessary for organisms to adapt their metabolism in order to find a balance between growth, maintenance and autophagy. Two key sensors gathering information about the internal nutrient resources are the protein kinases TOR (target of rapamycin) and AMPK (AMP-activated protein kinase). These sensors form a signaling network that combines energy status and amino acid availability.Over the last decade, much knowledge has been gained on the regulation of these metabolic core components. Far less is known about the genetic program and its components downstream to these key sensors that coordinate basic biochemical processes. The nutrient dependent transcription factor sugarbabe is expressed in the fat body and gut of Drosophila larvae, and is strongly upregulated upon amino acid starvation but not complete starvation. Here we show that sugarbabe is a transcriptional target of TOR and AMPK signaling and mediates metabolic adaptation to nutrient conditions by repressing genes of both amino acid and lipid catabolism. We altered TOR and AMPK activity by genetic and pharmaceutical means and found sugarbabe to be repressed by both protein kinases, leading to derepression of its target genes. Our results show an example where nutrient information is processed from its sensors to transcription factors that control specific biochemical pathways.