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Fig. 4 | Clinical Epigenetics

Fig. 4

From: Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy

Fig. 4

Epigenetic regulation of the quiescent and proliferative state of SCs. a In QSC and during self-renewal, the PAX7 promoter is active, holding permissive chromatin marks through the TrxG activity, while MYF5/MYOD expression is repressed despite containing both permissive and repressive marks, including H3K4me3 (TrxG) and H3K27me3 (PRC2, YY1-EZH2 complex), respectively. Repression of MYF5 and MYOD is also induced by SUV39H1 (H3K9me2/3) and by removal of acetylation marks carried by HDACs. Furthermore, note that MYOD expression is repressed by ID, SIR2 as well as MEF2 and SUV4-20H1/H2 (H4K20me2/3). The MYOG gene expression is inactivated via the cooperative action of PRC2 and HDACs. b In proliferating myoblasts, CARM1 targets and methylates PAX7 protein, which facilitates recruitment of TrxG to the MYF5 promoter. In addition, PRC2 and HDACs are removed from the MYOD promoter, which enables binding of TrxG, PCAF-p300/CBP, SRF and phosphorylated MEF2 as well as the SWI/SNF complex that induces chromatin relaxation and MYOD transcription. Also note that at this stage of myogenesis, phosphorylated MYOD as well as SUV39H1 halt expression of MYOG in addition to PRC2 and HDACs

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