Expression data from Drosophila melanogaster err mutant animals vs. wild type animals at a mid-second instar larval time

Cancer cells utilize a unique form of aerobic glycolysis, called the Warburg effect, to efficiently produce the macromolecules required for proliferation. Here we show that a metabolic program related to the Warburg effect is used during normal Drosophila development and regulated by the fly ortholog of the Estrogen-Related Receptor (ERR) family of nuclear receptors. dERR null mutants die as second instar larvae with abnormally low ATP levels, diminished triacylglyceride stores, and elevated levels of circulating sugars. Metabolomic profiling revealed that the pathways affected in these mutants correspond to those used in the Warburg effect. The expression of active dERR protein in mid-embryogenesis triggers a coordinate switch in gene expression that drives a metabolic program supporting the dramatic growth that occurs during larval development. This study suggests that mammalian ERR family members may promote cancer by directing a metabolic state that supports proliferation. Drosophila larvae were staged at a mid-second instar time point and hand sorted for developmental progression. Individual pools of isogenic animals were collected for each replicate. Three replcates were assayed for each genotype. The two genotypes assayed were a control wild type strain (w1118) and a transheteroallelic combination of err mutant alleles (err1/err2). Labled RNA was then hybridized onto Affymetrix microarrays.