Genome-wide analysis of chromatin structure changes upon MyoD binding in proliferative myoblasts during the cell cycle
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE161307 | GEO | 2022/05/09
REPOSITORIES: GEO
Similar Datasets
Project description:Genome-wide analysis of chromatin structure changes upon MyoD binding in proliferative myoblasts during the cell cycle
| PRJNA676168 | 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:Muscle satellite cells are a self-renewing pool of stem cells that give rise to daughter myogenic precursor cells in adult skeletal muscle. Published and preliminary data indicated that MyoD and p53 genes are involved in satellite cell differentiation. We would like to know what downstream genes of both transcription factors are affected in satellite cell-derived myoblasts (MyoD-/-, p53 -/-). Experiment Overall Design: this experiment include 3 samples and 25 replicates
2008-06-12 | E-GEOD-3244 | biostudies-arrayexpress
Project description:Myogenic progenitor/stem cells retain their skeletal muscle differentiation potential by maintaining myogenic transcription factors such as MyoD. However, the mechanism of how MyoD expression is maintained in proliferative progenitor cells has not been elucidated. Here, we found that MyoD expression was reduced at the mRNA level by cell cycle arrest in S and G2 phases, which in turn led to the absence of skeletal muscle differentiation. The reduction of MyoD mRNA was correlated with the reduced expression of factors regulating RNA metabolism, including methyltransferase like 3 (Mettl3), which induces N6-methyladenosine (m6A) modifications of RNA. Knockdown of Mettl3 revealed that MyoD RNA was specifically downregulated and that this was caused by a decrease in processed, but not unprocessed, mRNA. Potential m6A modification sites were profiled by m6A sequencing and identified within the 5' untranslated region (UTR) of MyoD mRNA. Deletion of the 5' UTR revealed that it has a role in MyoD mRNA processing. These data showed that Mettl3 is required for MyoD mRNA expression in proliferative myoblasts.
| S-EPMC5627051 | biostudies-literature
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
Project description:The transcription factor MyoD can coax na?e fibroblasts or otherwise committed cells to adopt the skeletal muscle phenotype by activating the muscle gene expression program. Activation of muscle gene expression occurs in quantal steps with not all the target genes of MyoD being activated at the same time. Some genes are induced in the initial phases, others at later stages despite the fact that MyoD is present throughout the differentiation process. MyoD is post-translationally modified by phosphorylation, ubiquitination, and acetylation. Here, we have employed a model system in which MyoD and its non-acetylatable version were inducibly expressed in mouse embryonic fibroblasts derived from mice to investigate how MyoD acetylation may contribute to differential gene activation. Keywords: Time-Series
2006-12-13 | GSE6487 | GEO
Project description:Tissue-specific transcription factors initiate differentiation toward a specialized cell type by inducing transcription-permissive chromatin modifications at target gene promoters, through the recruitment of the SWI/SNF chromatin-remodeling complex (1, 2). The molecular mechanism that regulates the chromatin re-distribution of SWI/SNF in response to differentiation signals is currently unknown. Here we show that the muscle determination factor MyoD and the SWI/SNF structural sub-unit, BAF60c (SMARCD3), form a complex on the regulatory elements of MyoD-target genes in undifferentiated myoblasts, prior to the activation of gene expression. MyoD-BAF60c complex is devoid of the ATP-dependent enzymatic sub-units Brg1 and Brm, is required for stable MyoD binding to Ebox sequences, and marks the chromatin for signal-dependent recruitment of the SWI/SNF core complex to muscle loci. BAF60c phosphorylation on a conserved threonine by differentiation-activated p38 signalling promotes the incorporation of MyoD-BAF60c into a Brg1-based SWI/SNF complex, which is competent to remodel the chromatin and activates transcription of MyoD-target genes. Our data support an unprecedented two-step model, by which pre-assembled BAF60c-MyoD complex directs the SWI/SNF complex chromatin re-distribution to muscle loci in response to differentiation cues. Differentiation of C2C12 cells individually interfered for BRG1, BAF60B, BAF60C
2011-03-07 | E-GEOD-24573 | 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.
2012-07-05 | GSE24852 | GEO
Project description:MyoD is known to transdifferentiate fibroblasts into muscle-like cells. Despite phenotypic resemblance and expression of myogenic marker genes in transdifferentiated cells, our global gene expression data suggests that ~100 genes, many involved in muscle development and function, remain non-reprogrammed. To understand this incomplete reprogramming, we characterized genome-wide chromatin accessibility and MyoD binding in human primary myoblasts and in MyoD-induced skin fibroblast cells. Our analyses revealed thousands of sites with incomplete chromatin reprogramming.Combined analyses of gene expression and epigenetic profiles revealed that many myogenic genes not upregulated during the transdifferentiation process have undergone MyoD-dependent chromatin remodeling, but to a significantly lower extent than reprogrammed genes. Our findings suggest that incomplete MyoD-induced transdifferentiation is due to chromatin-remodeling deficiencies, and that additional factors are required to transdifferentiate cells into a state more similar to myoblasts.
2017-01-07 | GSE93257 | GEO
Project description:MyoD is known to transdifferentiate fibroblasts into muscle-like cells. Despite phenotypic resemblance and expression of myogenic marker genes in transdifferentiated cells, our global gene expression data suggests that ~100 genes, many involved in muscle development and function, remain non-reprogrammed. To understand this incomplete reprogramming, we characterized genome-wide chromatin accessibility and MyoD binding in human primary myoblasts and in MyoD-induced skin fibroblast cells. Our analyses revealed thousands of sites with incomplete chromatin reprogramming.Combined analyses of gene expression and epigenetic profiles revealed that many myogenic genes not upregulated during the transdifferentiation process have undergone MyoD-dependent chromatin remodeling, but to a significantly lower extent than reprogrammed genes. Our findings suggest that incomplete MyoD-induced transdifferentiation is due to chromatin-remodeling deficiencies, and that additional factors are required to transdifferentiate cells into a state more similar to myoblasts.
2017-01-07 | GSE93263 | GEO