Pax7 remodels the chromatin landscape in skeletal muscle stem cells
Fig 6
Induced accessibility of Pax7 binding sites associated with the formation of novel Pax7-specific enhancers.
(A) mESC do not exhibit features of enhancers seen in myogenic precursors, and sites bound by MyoD in myoblasts are Pax7-specific as they lack chromatin accessibility in mESC. Histone modifications (H3K27Ac, H3K4me1, H3K4me3) and chromatin accessibility in myotubes (MT) differentiated from either iPax7 cells or C2C12 cells share similar patterns. MB from C2C12 with and without Flag control (Cntrl) also exhibit similar histone modification patterns. (B) Venn diagram depicting the number of shared and unique peaks with the indicated histone modifications at Pax7 binding sites (as defined in Dox-treated iPax7 cells) in control (MB Cntrl) and Pax7 expressing (MB Pax7) C2C12 cells. (C) Accessibility at Pax7 sites changes upon Pax7 expression in C2C12. Bar graph showing the quantification of accessible Pax7 binding sites with associated histone modifications at these sites in C2C12 control versus cells ectopically expressing Pax7. (D) Schematic showing the percentage of sites marked with individual histone modifications (as indicated) at known Pax7 binding sites in control C2C12 cells that undergo a novel conversion to an enhancer signature after Pax7 expression in C2C12 myoblasts.