BioProject

3 ventricles from E18.5 male mice were pooled for each array. Three arrays per genotype. More...

3 ventricles from E18.5 male mice were pooled for each array. Three arrays per genotype. Title: ERRγ Directs and Maintains the Transition to Oxidative Metabolism in the Post-Natal Heart Abstract: At birth the heart undergoes a critical metabolic switch to transition from a predominant dependence on carbohydrates during fetal life to a greater dependence on postnatal oxidative metabolism. This remains the principle metabolic state throughout life; although pathologic conditions such as heart failure and cardiac hypertrophy reactivate components of the fetal genetic program to increase carbohydrate utilization. Disruption of the ERRγ gene, which is expressed at high levels in the fetal and postnatal mouse heart, blocks this switch resulting in lactatemia, electrocardiographic (ECG) abnormalities and death during the first week of life. Genomic ChIP-on-chip and expression analysis at E18.5 clearly identifies ERRγ as both a direct and indirect regulator of a nuclear-encoded mitochondrial genetic network that coordinates the postnatal metabolic transition. These findings reveal an unexpected and essential molecular genetic component of the oxidative metabolic gene program in the heart and highlight ERRγ in the study of cardiac hypertrophy and failure. Keywords: ChIP-on-chip, electrocardiography, fetal gene program, OXPHOS, PGC-1a, sodium current, Single time point (E18.5) to compare genotype differences Overall design: Fetal mice were collected by caesarean secation. Hearts were stored in RNALater (Qiagen) Less...