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. Author manuscript; available in PMC: 2018 Jan 10.
Published in final edited form as: Cell Metab. 2016 Oct 20;25(1):86–92. doi: 10.1016/j.cmet.2016.09.010

Figure 1. Circadian clock controls oxygen consumption and anaerobic glycolysis through regulation of HIF1α.

Figure 1

(A) OCR from WT and Bmal1−/− C2C12 myotubes treated sequentially with oligomycin and FCCP (carbonyl cyanide-p-trifluoromethoxyphenylhydrazone) (n=9–10). (B) ECAR from intact WT and Bmal1−/− C2C12 myotubes treated sequentially with glucose and oligomycin (n=10). (C) Immunoblots of HIF1α and β-actin in WT vs Bmal1−/− (left) and Cry1/2+/− vs Cry1/2−/− (right) MEFs exposed for 14 hours to increasing doses of CoCl2 (0 μM and a dilution curve from 7.8 to 125 μM). (D) Immunoblots of HIF1α and β-actin following exposure to 1% O2 for indicated times in WT vs Bmal1−/− C2C12 myotubes. (E) Expression of HIF target genes in WT vs Bmal1−/− C2C12 myotubes exposed to 1% O2 for 6 hours (n=7–14). (F) Expression of HIF target genes in gastrocnemius muscle from adult life-inducible skeletal muscle Bmal1−/− mice (ACTA-rtTA-TRE-Cre;Bmalfx/fx) and controls (ACTA-rtTA-TRE-Cre and Bmalfx/fx) (n=4–5). (G) Relative luciferase activity of C212 myoblasts transfected with HRE-LUC and plasmids expressing circadian and HIF TFs (n=3). Data are represented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001. See also Figures S1–S2.