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

ABSTRACT: 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)

ORGANISM(S): Homo sapiens

PROVIDER: GSE98509 | GEO | 2019/09/10

REPOSITORIES: GEO

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MYOD Gene Expression Regulation during Myogenic Conversion of Fibroblasts

Project description:We provide here gene expression profile of IMR90 fibroblasts expressing or not MYOD culured in GM for 1 day or GM for 1 day and DM for 3 days

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A KAP1 phosphorylation switch controls MyoD function during skeletal muscle differentiation (ChIP-seq)

Project description:The transcriptional activator MyoD serves as a master controller of myogenesis. Often in partnership with Mef2, MyoD binds to the promoters of hundreds of muscle genes in proliferating myoblasts, yet activates these targets only upon receiving cues that launch differentiation. What regulates this off/on switch of MyoD function has been incompletely understood, although known to reflect the action of chromatin modifiers. Here, we identify KAP1/TRIM28 as a key regulator of MyoD function. In myoblasts, KAP1 is present with MyoD and Mef2 at many muscle genes, where it acts as a scaffold to recruit not only co-activators such as p300 and LSD1, but also co-repressors such as G9a and HDAC1, with promoter silencing as net outcome. Upon differentiation, MSK1-mediated phosphorylation of KAP1 releases the co-repressors from the scaffold, unleashing transcriptional activation by MyoD/Mef2 and their positive cofactors. Thus, our results reveal KAP1 as a previously unappreciated interpreter of cell signaling, which modulates the ability of MyoD to drive myogenesis. Kap1 and H3K9me3 ChIPseq in proliferating C2C12 cells

2015-02-02 | E-GEOD-62660 | biostudies-arrayexpress

Genome-wide maps of MyoD, MLL4 and histone modifications during MyoD-induced myogenesis in WT and MLL4-/- brown preadipocytes

Project description:Enhancers play a central role in cell-type-specific gene expression and are marked by H3K4me1/2. Active enhancers are further marked by H3K27ac. However, the methyltransferases responsible for the deposition of H3K4me1/2 on enhancers remain elusive. Furthermore, the functions of these methyltransferases on enhancers and associated cell-type-specific gene expression are poorly understood. Here, we identify MLL4 (KMT2D) as a major H3K4 mono- and di-methyltransferase in mammalian cells. Using adipogenesis and myogenesis as model systems, we show that MLL4 exhibits cell-type- and differentiation-stage-specific genomic binding and is predominantly localized on enhancers. MLL4 co-localizes with lineage-determining transcription factors (TFs) on active enhancers during differentiation. Deletion of MLL4 dramatically decreases H3K4me1/2 and H3K27ac on enhancers and leads to severe defects in cell-type-specific gene expression and cell differentiation. Finally, we provide evidence that lineage-determining TFs recruit and require MLL4 to establish enhancers critical for cell-type-specific gene expression. Together, these results identify MLL4 as an H3K4 mono-/di-methyltransferase required for enhancer activation during cell differentiation. ChIP-Seq of MyoD, MLL4 and histone modifications (H3K4me1, H3K4me3, and H3K27ac) in adenoviral GFP- or Cre-infected MLL3-/-;MLL4-flox/flox cells. Preadipocytes: brown preadipocytes before differentiation. D5 myocytes: 5 days after MyoD-induced myogenesis of brown preadipocytes.

2013-12-17 | E-GEOD-50465 | biostudies-arrayexpress

ChIP-seq of Active Histone Mark (H3K27ac) and Myogenic Regulatory Factors (MYF5 and MYOD) in Fusion Negative Rhabdomyosarcoma Cell Lines

Project description:We performed Chip-seq analysis of Myogenic Regulatory Transcription Factors (MYF5 and MYOD) in Fusion Negative Rhabdomyosarcoma cell lines. Endogenous MYF5/H3K27ac Chip-seq was performed in Rh18 cells and MYOD-H3K27ac Chip-seq was performed in RD cells, given that these cell lines express these proteins in a mutually-exclusive manner. Analysis revealed a common subset of enhancer and promoter regions bound by these transcription factors that are enriched for cell cycle regulation and embryonic muscle development pathways. Keywords: rhabdomyiosarcoma, Chip-seq, chromatin, Transcription factos, MYF5, MYOD

2016-12-20 | GSE84628 | GEO

Myogenesis MyoD

2006-12-13 | GSE6487 | GEO

Molecular profiling of Ctcf hemizygous mouse embryonic fibroblasts: HiC

Project description:CTCF is a highly conserved and ubiquitously expressed protein involved in several fundamental processes such as fine-tuning gene expression, imprinting, X-chromosome inactivation and 3D chromatin organisation. To understand the impact of differences in the concentration of CTCF abundance on these processes, we exploit a CTCF hemizygous mouse model with a stable reduction in the concentration of this protein. We derived independent primary lines of mouse embryonic fibroblasts (MEFs) from wildtype and CTCF-hemizygous mouse E13.5 embryos. For three biological replicates, cells were fixed in DMEM containing 2% fresh formaldehyde and incubated at room temperature for 10 min, quenched with 1M glycine for 5 min, and washed twice with ice cold PBS, before being flash-frozen at -80°C. Cross-linked cells were lysed, followed by chromatin HindIII digestion, biotinylataion, ligation, proteinase K treatment, DNA purification, sonication, end repair, biotin pull-down, adapter ligation, and PCR amplification. Pooled indexed libraries were sequenced on an Illumina HiSeq4000 to produce paired-end 150bp reads. On the same MEF lines we have performed RNAseq and ChIPseq for CTCF, H3K4me3 and H3K27ac.

2018-07-29 | E-MTAB-6262 | biostudies-arrayexpress

Architectural role of cell-fate-instructive transcription factor MyoD in orchestrating 3D genome organization in muscle cells.

Project description:Cell-type specific transcription factors play important roles in lineage specification whereas it is largely unknown whether and how they regulate context-specific 3D chromatin structure. Herein, we comprehensively mapped 3D chromatin organization in muscle cells and uncovered master transcription factor MyoD-mediated myogenic lineage specific chromatin structures in comparison with embryonic stem cells and neuronal cells. We discovered that MyoD is significantly enriched at loop anchor and mediate numerous chromatin loops without CTCF binding. Importantly, we found MyoD-involved interactions were dramatically disrupted when MyoD was absent, implying MyoD is an indispensable factor for loop regulation. Additionally, MyoD mediated shorter, weaker and more dynamic interactions, especially enhancer - enhancer and enhancer - promoter loops. Finally, MyoD mainly regulate cell type-specific contacts which were concomitant to muscle cell specific gene expression. Collectively, we utilized high resolution Hi-C data and genetic model to prove a master transcriptional factor govern lineage specific chromatin loops. We propose that MyoD-mediated interactions are a general feature of lineage specific transcriptional factors-regulated gene expression.

2021-05-01 | GSE157339 | GEO

Transcription profiling of mouse embryoic fibroblasts expressing wild type MyoD or its non-acetylatable version MyoD RRR to investigate how MyoD acetylation may contribute to differential gene activation.

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2007-11-15 | E-GEOD-6487 | biostudies-arrayexpress

Identification of ETO2 direct target genes through integration of transcriptomic (RNAseq) and chromatin binding location (ChIPseq)

Project description:Erythroid cell lines (HEL and K562) were conditionally invalidated for the ETO2 gene using the CRISPR/Cas9 system. Gene expression profiling (RNAseq) and chromatin immunoprecipitation followed by high-throughput sequencing (ChIPseq) to assess localization of ETO2, MYB, EP300, H3K27ac and H3K4me3 was performed in control and ETO2-deficient cells. ChIPseq analyses were also performed on cells from human AEL patient-derived xenograft models.

2023-07-02 | E-MTAB-10346 | biostudies-arrayexpress

MyoD-/-, Time Course

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