Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA93195 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Skeletal muscle development requires the coordinated expression of numerous transcription factors to control the specification of the muscle fate in mesodermal cells and the differentiation of the committed myoblasts into functional contractile fibers. The bHLH transcription factor MyoD plays a key role in these processes, since its forced expression is sufficient to induce the myogenesis in a variety of non-muscle cells in culture. Consistent with this observation, the majority of skeletal muscle genes requires MyoD to activate their own transcription. In order to identify novel MyoD-target genes we generated C2C12 MyoD-silenced clones, and used a muscle-specific cDNA microarray to study the induced modifications of the transcriptional profile. Gene expression was analyzed at three different stages in differentiating MyoD(-)C2C12 myoblasts. These microarray data sets identified many additional uncharacterized downstream MyoD transcripts that may play important functions in muscle cell differentiation. Among these genes, we concentrated our study on the cell cycle regulators Cdkn1c and calcyclin and on the muscle-specific putative myogenic regulator Ankrd2. Bioinformatic and functional studies on the promoters of these genes clarified their dependence on MyoD activity. Clues of other regulatory mechanisms that might interact with the principal bHLH transcription factor have been revealed by the unexpected up regulation in MyoD(-) cells of these novel (and other) target transcripts, at the differentiation stage in which MyoD became normally down regulated. Keywords: MyoD, cell cycle regulation, cDNA microarray, myogenic differentiation, gene regulation
2005-07-28 | GSE3014 | GEO
Project description:MyoD and FoxO3 mediated hotspot interaction orchestrates super-enhancer activity during myogenic differentiation
| PRJNA362824 | ENA
Project description:Integrated analysis of genome-wide ChIP-Seq and RNA-Seq data revealed the first dynamic chromatin and transcriptional landscape of Twist2 binding during myogenic differentiation. During differentiation, Twist2 competes with MyoD at shared DNA motifs to direct global gene transcription and repression of the myogenic program. Additionally, TWIST2 shapes the epigenetic landscape to drive chromatin opening at oncogenic loci and chromatin closing at myogenic loci. These epigenetic changes redirect MyoD binding from myogenic genes towards oncogenic, metabolic, and growth genes.
2019-03-08 | GSE127998 | 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:We identify a subset of highly expressed genes related to muscle development, which show static H3K4me2 enrichment over the gene body and H3K4me3 enrichment towards the gene body during myogenic differentiation. This study reveals that MyoD significantly binds to this particular subset of genes and further systematic analysis shows the repressive role of MyoD. Interestingly, MyoD binds and down-regulates Patz1 which is important for maintaining pluripotency. These findings might provide a key regulatory mechanism to promote myogenic differentiation.
2017-06-14 | GSE63716 | GEO
Project description:MyoD and FoxO3 mediated hotspot interaction orchestrates super-enhancer activity during myogenic differentiation (Foxo3 ChIP-seq)
| PRJNA387570 | ENA
Project description:In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snail does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells. Genome wide binding sites of various transcription factors and chromatin modifiers in muscle cells
2012-07-04 | E-GEOD-24852 | biostudies-arrayexpress
Project description:In skeletal myogenesis, the transcription factor MyoD, activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snai1/2-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snai1/2 does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1/2-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail1/2- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells. In vivo depletion of transcription factor with siRNA followed by whole transcriptome analysis (RNA-seq) to identify target genes.
2012-07-04 | E-GEOD-38236 | biostudies-arrayexpress
Project description:In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snail does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells. This data set contains 3 replicates of a myotube growth time series (0h, 2d, 5d). The data was RMA normalized per replicate set.
2012-07-04 | E-GEOD-24811 | biostudies-arrayexpress
Project description:Skeletal muscle growth and regeneration rely on myogenic progenitor and satellite cells, the stem cells of postnatal muscle. Elimination of Notch signals during mouse development results in premature differentiation of myogenic progenitors and formation of very small muscle groups. Here we show that this drastic effect is rescued by mutation of the muscle differentiation factor MyoD. However, rescued myogenic progenitors do not assume a satellite cell position and contribute poorly to myofiber growth. The disrupted homing is due to a deficit in basal lamina assembly around emerging satellite cells and to their impaired adhesion to myofibers. On a molecular level, emerging satellite deregulate the expression of basal lamina components and adhesion molecules like integrin a7, collagen XVIIIa1, Megf10 and Mcam. We conclude that Notch signals control homing of satellite cells, stimulating them to contribute to their own microenvironment and to adhere to myofibers. Gene expression analysis using total RNA from FACS-isolated Vcam-1+/CD31-/CD45-/Sca1- embryonic muscle progenitor cells from E17.5 back muscle tissue of MyoD-/-, Pax3cre/+;Rbpjflox/flox;MyoD-/- and Pax3cre/+;DnMamlflox/flox;MyoD-/- mice.
2012-12-31 | E-GEOD-39379 | biostudies-arrayexpress