Ecdysone and 20-hydroxyecdysone are not required to activate glycolytic gene expression in embryos.

Many of the enzymes involved in carbohydrate metabolism are coordinately up-regulated approximately midway through embryogenesis. Previous studies have demonstrated that this metabolic transition is controlled by the Estrogen-Related Receptor (dERR), which is stabilized and activated immediately prior to onset of glycolytic gene expression. The mechanisms that promote dERR activity, however, are poorly understood and other transcriptional regulators could control this metabolic transition, independent of dERR. In this regard, the steroid hormone 20-hydroxyecdysone (20E) represents an intriguing candidate for regulating glycolytic gene expression in embryos - not only does the embryonic 20E pulse immediately precede transcriptional up-regulation of glycolytic metabolism, but 20E is also known to promote gene expression. Here I test the hypothesis that embryonic 20E signaling is required to activate glycolytic gene expression. Using developmental northern blots, I demonstrate that the transcriptional up-regulation of glycolytic genes during embryogenesis still occurs in mutants, which are unable to synthesize either ecdysone or 20E. My finding indicates that ecdysone and 20E signaling are not required for this mid-embryonic metabolic transition.