MYOD Remodeling of the Genome Architecture during Myogenic Conversion of Somatic Cells

We provide here an unprecedented analysis of the three-dimensional re-organization of the genome during cellular reprograming of one cell type into another by the ectopic expression of one single transcription factor. By integrating Hi-C analysis with ChIPseq-based detection of MYOD genome-wide binding and RNAseq profiling of gene expression, we discovered that MYOD causes profound alterations in the high order chromatin structure during fibroblast reprogramming into skeletal muscle cells. We also used CTCF ChIPSeq in IMR90 GSE31477 (GSM935404); CTCF ChIPSeq in human myoblasts (hMB) GSE29611 (GSM733762); CTCF ChIPSeq human myotubes (hMT) GSE29611 (GSM733783); H3K27Ac in IMR90 GSE43070 (GSM1055818); H3K27Ac in hMB GSE29611 (GSM733755); H3K27Ac in hMT GSE29611 (GSM733666) Same number of reads was used for H3K27Ac ChIP comparison. ChIPSeq p300 IMR90 GSE43070 (GSM1055812). We also used RNASeq from GSE90895 (GSM2417196, GSM2417197, GSM2417198, GSM2417204, GSM2417203) Integration of RNASeq, ChIPSeq and HiC experiments to characterize the 3D regulatory mechanisms for the myogenic conversion of fibrobalsts. For this project we used CTCF ChIPSeq in IMR90 GSE31477 (GSM935404); CTCF ChIPSeq in human myoblasts (hMB) GSE29611 (GSM733762); CTCF ChIPSeq human myotubes (hMT) GSE29611 (GSM733783); H3K27Ac in IMR90 GSE43070 (GSM1055818); H3K27Ac in hMB GSE29611 (GSM733755); H3K27Ac in hMT GSE29611 (GSM733666) Same number of reads was used for H3K27Ac ChIP comparison. We also used RNASeq from GSE90895 (GSM2417196, GSM2417197, GSM2417204, GSM2417203)