(A) Schematic of muscle injury experiments and FACS isolation of MuSCs. Tamoxifen was administered for 5 consecutive days to induce recombination, followed by BaCl₂ (or vehicle) administration to induce muscle injury. Dendra2⁺DAPI^– MuSCs were collected at 2 days post injury (dpi). In vehicle-treated muscle, quiescent (CD34⁺) MuSCs (QSCs) were harvested. In injured muscle, activated (CD34^–) MuSCs (ASCs) were harvested. (B) Representative snapshots of MyoD binding at the MyoG and Mef2a genes in 2-dpi QSCs and ASCs. Identified peaks in the proximity of the transcriptional start site are indicated by red boxes. (C) Venn diagram of MyoG- and MyoD-bound genes in 2-dpi ASCs. Genes were compared with a list of known mitochondrial regulators (Supplemental Table 1). (D) Representative snapshots of MyoD binding at the Pgc-1β gene in 2-dpi QSCs and ASCs. (E) Representative snapshots of MyoD and MyoG binding at the Pgc-1α gene in 2-dpi QSCs and ASCs. (F) Mouse 3T3-L1 fibroblasts were transfected with empty vector (pQC-empty) or MyoD-expressing vector (pQC-MyoD) and assessed by Western blotting 48 hours after transfection for the indicated targets. Histone 2B (H2B) is shown as a loading control. Molecular weight markers (in kDa) are indicated. (G) Pgc-1α and Pgc-1β mRNA levels (normalized to β2-microglobulin) assessed by qRT-PCR in wild-type QSCs and ASCs at 2 dpi. Statistical significance was assessed using 2-tailed t tests with adjustments for multiple comparisons (G). For each ChIP-seq data set, 3 biological replicates were analyzed. Box-and-whisker plots indicate median (horizontal line) and interquartile ranges (bounds of the box) from the indicated number of biological replicates; whiskers were plotted using Tukey’s method.