(A) YY1 controls the activation of SCs by acting as a switch of metabolic reprogramming. In Ctrl SCs, its expression is increased during SC activation upon injury induced muscle damage and it transcriptionally suppresses mitochondrial gene expression through direct binding to their TSS regions together with PRC2 repressive complex. Meanwhile, it also stabilizes Hif1α protein to facilitate its trans-activating of glycolytic genes. As a result, successful activation of glycolytic pathways occurs, allowing SCs to activate and proliferation to drive the repairing of the damaged muscle. When YY1 is deleted in the YY1iKO mouse, Hif1α level is decreased due to protein destabilization, leading to a reduction in glycolytic gene expression and glycolytic rate. Meanwhile, although the expression of mitochondrial genes is up-regulated, OXPHOS could not be increased likely because of reduced flow of pyruvate substrate into mitochondria. As a result of the inhibited metabolic reprogramming, SC activation is repressed and the regeneration is compromised. Quiescent SCs are defined by expression of Pax7 and lack of MyoD expression (Pax7+MyoD-), activated and proliferating myoblasts by the concomitant expression of Pax7 and MyoD (Pax7+MyoD+), differentiating myocytes by expression of MyoG (Pax7-MyoG+), and differentiated myotubes are marked by expression of Myosin heavy chain (MyHC). Error bars represent s.d.'s of the mean. Student's t-test (two-sided): *P<0.05, **P<0.01, ***P<0.001. 