Rexinoid signalling during early myogenic differentiation
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ABSTRACT:
PROVIDER: PRJNA371483 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of the transcriptome of zebrafish mononuclear myogenic cells (zMNCs) during myogenic differentiation. The main goal is to identify the similarities of zMNC myogenic differentiation with that of mammalian myoblast differentiation. Critical time points were used to identify a switch from the activity of cell proliferation genes to myogenic structural genes. 15-20 adult zebrafish dorsal skeletal muscles were isolated at each of 6 distinct time points (day 0, day 1, day 4, day 7, day 10, day 14) in replicates.
2010-04-07 | E-GEOD-19754 | biostudies-arrayexpress
Project description:ChIP-seq profiling of transcriptional co-activator p300 during early myogenic differentiation
| PRJNA431571 | ENA
Project description:Analysis of the transcriptome of zebrafish mononuclear myogenic cells (zMNCs) during myogenic differentiation. The main goal is to identify the similarities of zMNC myogenic differentiation with that of mammalian myoblast differentiation. Critical time points were used to identify a switch from the activity of cell proliferation genes to myogenic structural genes.
2010-03-30 | GSE19754 | GEO
Project description:Molecular regulation of stem cell differentiation is exerted through both genetic and epigenetic determinants over distal regulatory or enhancer regions. Understanding the mechanistic action of active or poised enhancers is thus imperative for control of stem cell differentiation. Based on a genome-wide co-occurrence of different epigenetic marks in committed proliferating myoblasts, we have previously generated a 14-state chromatin state model to profile residue-specific histone acetylation in early myoblast differentiation. Here, we use genome-wide chromatin state association to delineate the functional mode of transcription regulators in early myogenic differentiation. We define a role of transcriptional coactivator p300, when recruited by master muscle regulator MyoD, in the establishment and regulation of myogenic loci at the onset of terminal differentiation. In addition, we reveal an enrichment of residue- and loci-specific histone acetylation at p300 associated active or poised enhancers, particularly when enlisted by MyoD. We provide novel molecular insights into the regulation of myogenic enhancers by p300 in concert with MyoD. Our studies present a valuable aptitude for driving stage specific chromatin state or enhancers pharmacologically to treat muscle related diseases and for the identification of additional myogenic targets and molecular interactions for therapeutic development.
2018-07-30 | GSE109636 | GEO
Project description:Myocardial Differentiation is Dependent upon Endocardial Signalling During Early Cardiogenesis in vitro
| PRJNA489433 | ENA
Project description:While skeletal myogenesis is tightly coordinated by myogenic regulatory factors including MyoD and myogenin, chromatin modifications have emerged as vital mechanisms of myogenic regulation. We have previously established that bexarotene, a clinically approved agonist of retinoid X receptor, promotes the specification and differentiation of skeletal muscle lineage. Here, we examine a genome-wide impact of rexinoids on myogenic differentiation through integral RNA-seq and ChIP-seq analyses. We found that bexarotene promotes myoblast differentiation through the coordination of exit from the cell cycle and the activation of muscle-related genes. We uncovered a new mechanism of rexinoid action which is mediated by the nuclear receptor and largely reconciled through a direct regulation of MyoD gene expression. In addition, we determined a rexinoid-responsive residue-specific histone acetylation at a distinct chromatin state associated to MyoD and myogenin. Thus, we provide novel molecular insights into the interplay between retinoid X receptor signaling and chromatin states pertinent to myogenic programs in early myoblast differentiation.
2017-09-13 | GSE94560 | GEO
Project description:While skeletal myogenesis is tightly coordinated by myogenic regulatory factors including MyoD and myogenin, chromatin modifications have emerged as vital mechanisms of myogenic regulation. We have previously established that bexarotene, a clinically approved agonist of retinoid X receptor, promotes the specification and differentiation of skeletal muscle lineage. Here, we examine a genome-wide impact of rexinoids on myogenic differentiation through integral RNA-seq and ChIP-seq analyses. We found that bexarotene promotes myoblast differentiation through the coordination of exit from the cell cycle and the activation of muscle-related genes. We uncovered a new mechanism of rexinoid action which is mediated by the nuclear receptor and largely reconciled through a direct regulation of MyoD gene expression. In addition, we determined a rexinoid-responsive residue-specific histone acetylation at a distinct chromatin state associated to MyoD and myogenin. Thus, we provide novel molecular insights into the interplay between retinoid X receptor signaling and chromatin states pertinent to myogenic programs in early myoblast differentiation.
2017-09-13 | GSE94558 | GEO
Project description:We sought to investigate whether the reduced differentiation and fusion competence in DMD-R3381X cultures was due to aberrant myogenic gene expression. We performed transcriptome sequencing and analysis of DMD-R3381X and CORR-R3381X myogenic cultures during secondary differentiation at 0, 24 and 120 hours timepoints.
2021-09-10 | GSE159273 | GEO
Project description:Rhabdomyosarcoma (RMS) is a frequent non-epithelial tumor of soft tissue that originates from a myogenic differentiation defect. Expression of SNAIL transcription factor is elevated in the alveolar subtype of RMS, characterized by a low myogenic differentiation status and high aggressiveness. SNAIL affects RMS metastasis by reorganization of actin cytoskeleton, regulation of ezrin expression and chemotaxis to HGF and SDF-1. The differentiation of human RMS diminishes SNAIL level. SNAIL silencing completely abolishes the growth of human RMS xenotransplants. SNAIL inhibits myogenic differentiation of RMS by binding to the MYF5 promoter, suppressing its expression, displacing MYOD from canonical to alternative E-box sequences and regulating myomiRs expression. SNAIL silencing allows the re-expression of MYF5 and canonical MYOD binding, promoting RMS cell myogenic differentiation. These novel results open potential avenues for the development of innovative therapeutic strategies based on SNAIL silencing.
2020-07-14 | PXD006711 | Pride
Project description:Skeletal muscle differentiation (myogenesis) is a complex and highly coordinated biological process regulated by a series of myogenic marker genes. Chromatin interactions between gene’s promoters and their enhancers have an important role in transcriptional control. However, the high-resolution chromatin interactions of myogenic genes and their functional enhancers during myogenesis remain largely unclear. Here, we used circularized chromosome conformation capture coupled with next-generation sequencing (4C-seq) to investigate eight myogenic marker genes in C2C12 myoblasts (C2C12-MBs) and C2C12 myotubes (C2C12-MTs). We revealed dynamic chromatin interactions of these marker genes during differentiation, and identified 163 and 314 significant interaction sites (SISs) in C2C12-MBs and C2C12-MTs, respectively. The interacting genes of SISs in C2C12-MTs were mainly involved in muscle development, and histone modifications of the SISs changed during differentiation. Through functional genomic screening, we also identified 25 and 41 putative active enhancers in C2C12-MBs and C2C12-MTs, respectively. Using luciferase reporter assays for putative enhancers of Myog and Myh3, we identified eight activating enhancers. Furthermore, dCas9-KRAB epigenome editing and RNA-seq revealed a role for Myog enhancers in the regulation of Myog expression and myogenic differentiation in the native genomic context. Taken together, this study lays the groundwork for understanding 3D chromatin interaction changes of myogenic genes during myogenesis and provides insights that contribute to our understanding of the role of enhancers in regulating myogenesis.
2022-06-10 | GSE201138 | GEO