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. 2018 Aug 10;16(8):e2005886. doi: 10.1371/journal.pbio.2005886

Fig 10. BMAL1- and REV-ERB-dependent programming of muscle metabolism.

Fig 10

Our integration of multiple “–omics” datasets indicates that the muscle clock may modulate diurnal fuel selection in anticipation of the feeding phase by direct BMAL1-dependent activation of genes promoting neutral lipid storage (Dgat2) and metabolic efficiency (Coq10b) while coordinating REV-ERB-mediated repression of a network of genes involved in lipid metabolism (Plin5, Acsl1, Ucp3, Pdk4) and muscle protein turnover (MuRF-1, Atrogin-1, polyubiquitin-C, Snat2). Muscle clock disruption causes loss of BMAL1-dependent activation and REV-ERB-dependent repression of target genes, resulting in a state of metabolic inefficiency characterized by increased lipid mobilization and oxidation and in increased protein turnover. BMAL1, brain and muscle ARNT-like protein 1; HDAC3, histone deacetylase 3; NCoR1, nuclear receptor corepressor 1; RORE, ROR response element.