Figure 3.

p53 binds to the myogenin promoter and regulates its transcription in response to genotoxic stress. (a) Schematics of putative p53 or p63 response elements (REs) on the mouse and human myogenin promoter with p53 and p63 ChIP-seq profiles,^{41, 46} respectively. Arrow: transcription start site (TSS); Myog or MYOG: myogenin gene; bg: background signal. (b) Protein or RNA expression kinetics of p53 and myogenin from 2 to 96 h post IR in C2C12 myoblasts maintained under either growth or differentiation condition. (c) ChIP analysis of p53 binding to mouse myogenin 2560 site at 6 and 48 h post IR in C2C12 myoblasts maintained under either growth or differentiation condition. ChIP background was measured by binding of the p53 antibody to a gene desert region. p53 enrichment on the p21 promoter, p21, served as a positive control. ns, not significant; *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001. (d) ChIP analysis of p53 binding to the human myogenin promoter. ChIP was performed with an anti-ER antibody of RD cells ectopically expressing ER fusion of the control, p53, or p53^R245W. p53^R245W is the mouse equivalent of human p53^R248W expressed in RD cells and is defective in DNA binding. Fold enrichment relative to the control is shown as bold numbers on the top of each bracket. ChIP background was measured by binding of the ER-fusion proteins to a gene desert region. p53 enrichment on the p21 promoter, p21, served as a positive control