GSE123901
Coordinated control of adiposity and growth by anti-anabolic kinase ERK7
Nutrient availability influences animal growth and metabolism. How starvation inhibits anabolic functions in vivo remains insufficiently  understood. Here we establish an atypical MAP kinase ERK7 as an inhibitor of growth and lipid anabolism with an essential role in the  physiological adaptation to starvation stress. Drosophila null mutants of ERK7 display accelerated growth rate and elevated triacylglycerol  (TAG) stores on rich diet. ERK7 inhibits TAG storage in the Drosophila fat body by negatively regulating the expression of the Gli-similar  transcription factor Sugarbabe. While displaying growth advantage on rich diet, ERK7 mutants fail to cease their growth during starvation  and are consequently starvation sensitive. ERK7 modulates the majority of the starvation-induced gene expression response in a genomewide  setting, influencing, for example, genes involved in insulin signaling and lipid metabolism. In conclusion, ERK7 regulates peripheral  nutrient sensing to control animal growth and lipid metabolism with respect to nutrient availability. Overall design: Control and ERK7 mutant flies starved and fed