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MRNAseq of undifferentiated iPSCs, iPSC-derived skeletal muscles induced by dox-inducible MYOD1 expression, and those derived from human myoblast cell line (Hu5/KD3)

ABSTRACT: We sequenced mRNA from skeletal muscles derived from MYOD1-hiPSCs generated by different selection methods, and compared the results with those derived from human myoblast cell line (Hu5/KD3). This analysis enables us to understand the effects of different selection methods on the generation of MYOD1-hiPSCs and skeletal muscle differentiation from them. mRNAs from undifferentiated MYOD1-hiPSCs were also sequenced.(*RAW data not provided due to patient privacy concerns)

ORGANISM(S): Homo sapiens

PROVIDER: GSE212366 | GEO | 2023/04/18

REPOSITORIES: GEO

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MYOD1 functions as a clock amplifier as well as a critical co-factor for downstream circadian gene expression in muscle

Project description:In the present study we show that the master myogenic regulatory factor, MYOD1, is a positive modulator of molecular clock amplitude and functions with the core clock factors for expression of clock-controlled genes in skeletal muscle. We demonstrate that MYOD1 directly regulates the expression and circadian amplitude of the positive core clock factor Bmal1. We identify a non-canonical E-box element in Bmal1 and demonstrate that is required for full MYOD1-responsiveness. Bimolecular fluorescence complementation assays demonstrate that MYOD1 colocalizes with both BMAL1 and CLOCK throughout myonuclei. We demonstrate that MYOD1 and BMAL1:CLOCK work in a synergistic fashion through a tandem Ebox to regulate the expression and amplitude of the muscle specific clock-controlled gene, Titin-cap (Tcap). In conclusion, these findings reveal mechanistic roles for the muscle specific transcription factor MYOD1 in the regulation of amplitude of the molecular clock as well as synergistic regulation of clock-controlled genes in skeletal muscle.

2018-11-02 | GSE122082 | GEO

mRNAseq of undifferentiated iPSCs, iPSC-derived skeletal muscles induced by dox-inducible MYOD1 expression, and those derived from human myoblast cell line (Hu5/KD3)

Project description:mRNAseq of undifferentiated iPSCs, iPSC-derived skeletal muscles induced by dox-inducible MYOD1 expression, and those derived from human myoblast cell line (Hu5/KD3)

| PRJNA875120 | ENA

RNA-seq analyses of JMJD3c-MYOD1-induced myogenic cells and human skeletal myotubes

Project description:We generated the human ES lines, in which the genome-wide reduction of H3K27me3 can be induced by the ectopic expression of catalytic domain of histone demethylase JMJD3 with doxycycline treatment (JMJD3c-hESCs). The overexpression of JMJD3c enhances MYOD1-mediated myogenic differentiation of hESCs. We compared the gene expression patterns of the generated myogenic cells with those of human skeletal myotubes.

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Pro-neuronal activity of Myod1 due to promiscuous binding [ATAC-seq]

Project description:Basic helix-loop-helix (bHLH) pioneer transcription factors Myod1 and Ascl1 are biochemically related but produce fundamentally different outcomes when expressed in fibroblasts: Myod1 produces muscle cells and Ascl1 induces neurons. Here, we sought to investigate the molecular mechanisms explaining the differential activity. Surprisingly, we found a large overlap in the overall binding patterns of Ascl1 and Myod1 in fibroblasts, with both transcription factors accessing both neuronal and myogenic targets. We also observed similar changes in chromatin accessibility and transcriptional activation. Yet, Myod1 predominantly induced a muscle program and Ascl1 a neuronal program. We found that differences in binding affinity at key targets resulted in largely distinct reprogramming outcomes. Accordingly, exchanging Myod1’s C-terminal protein-protein interacting domain and DNA-binding basic domain with those of Ascl1 induces an Ascl1-like binding and converts Myod1 into a pro-neuronal factor. Finally, we found that co-expression of Myod1 with the transcriptional repressor Myt1l inhibits induction of the muscle program and yields functional neuronal cells. Our findings are compatible with the notion that pioneer factor activity is associated with high-affinity protein-DNA and suggest that promiscuous binding of pioneer factors can induce unspecific lineage features which need to be kept in check by co-factor interactions.

2020-02-03 | GSE126413 | GEO

Pro-neuronal activity of Myod1 due to promiscuous binding [RNA-seq]

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Pro-neuronal activity of Myod1 due to promiscuous binding [FLAG ChIP-seq]

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Pro-neuronal activity of Myod1 due to promiscuous binding [H3K27ac ChIP-seq]

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Pro-neuronal activity of Myod1 due to promiscuous binding [FLAG ChIP-seq mESC]

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Chromatin looping evidence between PAX3-FOXO1 bound super enhancer and MYOD1 promoter [4C-seq]

Project description:Circular chromatin confirmation capture in rhabdomyosarcoma cells was performed with viewpoints at the PAX3-FOXO1 bound super enhancer upstream of MYOD1, and also at the MYOD1 promoter, to find support for looping between these two genetic elements almost 80 thousand base pairs apart.

2017-04-27 | GSE83727 | GEO

ChIP-Seq data for histone marks in estrogen-inducible MyoD1 fibroblasts

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