Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression analysis of differentiating skeletal muscle myoblast cell line overexpressing MyoD

ABSTRACT: We tested the hypothesis that ectopic expression of the MyoD-dependent gene program in differentiating myoblasts and myotubes compromises the integrity of the plasma membrane/sarcolemma by using a doxycycline-inducible system to overexpress MyoD in C2C12 myoblasts during differentiation. The overarching goals of this analysis pipeline were to (a) determine changes in transcriptional profiles upon sustained overexpression of MyoD during and upon differentiation; and, (b) utilize these profiles to identify potential drivers of sarcolemmal fragility that exacerbate myofiber damage and loss in dystrophic muscle. We used microarrays to generate information about transcriptional profiles in differentiating myoblasts and myotubes overexpressing the myogenic transcription factor myoblast determination protein 1 (MyoD1).

ORGANISM(S): Mus musculus

PROVIDER: GSE168703 | GEO | 2022/05/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE24811: Time Series of Mouse skeletal muscle cell differentiation GSE24852: ChIP-Seq of MyoD, Myf5, Snai1, HDAC1, HDAC2, E47 and empty vector controls in mouse skeletal myoblasts or myotubes GSE38236: RNA-Seq of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated myoblasts Refer to individual Series

2012-07-04 | E-GEOD-24904 | biostudies-arrayexpress

Inducible expression of MyoD directly mediates myogenic conversion of human induced pluripotent stem cells (iPSCs) derived from Duchenne muscular dystrophy (DMD).

2014-01-09 | GSE46633 | GEO

Inducible expression of MyoD directly mediates myogenic conversion of human induced pluripotent stem cells (iPSCs) derived from Duchenne muscular dystrophy (DMD).

Project description:Genome-wide gene expression analysis of MyoD-infected DMD-specific iPSCs (GM05112-M5.1) on days 0 (untreated), day 3 and day 8 post Dox treatment, human primary myoblasts (undifferentiated and as differentiated myotubes), and undifferentiated iPSCs from healthy donors (iPSCs-1 and iPSCs-2). DMD-specific iPSCs were infected with lentivirus expressing MyoD under the control of Tet-inducible promoter and another lentivirus expressing the transactivator. To initiate myogenic differentiation, iPSCs were treated with 1Âµg/ml Dox. RNA was isolated 0, 3 and 8 days later and gene expression analysis was performed.

2014-01-09 | E-GEOD-46633 | biostudies-arrayexpress

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies [Dnase-Seq]

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

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies [RNA-Seq]

2017-01-07 | GSE93263 | GEO

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies [ChIP-Seq]

2017-01-07 | GSE93258 | GEO

The Ankrd2, Cdkn1c and Calcyclin Genes are Under the Control of MyoD During Myogenic Differentiation

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

Comparison of Genome-Wide Binding of MyoD in Normal Human Myogenic Cells and Rhabdomyosarcomas Identifies Regional and Local Suppression of Promyogenic Transcription Factors (MyoD ChIP-Seq profiling).

Project description:Rhabdomyosarcoma is a pediatric tumor of skeletal muscle that expresses the myogenic basic helix-loop-helix protein MyoD but fails to undergo terminal differentiation. Prior work has determined that DNA binding by MyoD occurs in the tumor cells, but myogenic targets fail to activate. Using MyoD chromatin immunoprecipitation coupled to high-throughput sequencing and gene expression analysis in both primary human muscle cells and RD rhabdomyosarcoma cells, we demonstrate that MyoD binds in a similar genome-wide pattern in both tumor and normal cells but binds poorly at a subset of myogenic genes that fail to activate in the tumor cells. Binding differences are found both across genomic regions and locally at specific sites that are associated with binding motifs for RUNX1, MEF2C, JDP2, and NFIC. These factors are expressed at lower levels in RD cells than muscle cells and rescue myogenesis when expressed in RD cells. MEF2C is located in a genomic region that exhibits poor MyoD binding in RD cells, whereas JDP2 exhibits local DNA hypermethylation in its promoter in both RD cells and primary tumor samples. These results demonstrate that regional and local silencing of differentiation factors contributes to the differentiation defect in rhabdomyosarcomas. Total RNA samples were collected from primary human muscle cells (myoblasts and myotubes). Each sample has three biological replicates.

2013-08-29 | E-GEOD-50411 | biostudies-arrayexpress

MyoD-/-, Time Course

Project description:Myogenic Primary Myoblast Time Course in vitro Differentiation into Myotubes for Ontario Genome Project 2004-05. The Differentiation is leaded by removing the Proliferation Medium (Ham's F10 Medium + growth factors) and feeding with Differentiation Medium (DMEM hg + 2.5% Horse serum). The expected data are: % Viability of cells; Total RNA extraction; BioAnalysis and MicroArray of Undifferentiated and Differentiated cells. Time course: 0 hr, 6 hr, 12 hr, 18 hr, 24 hr, 36 hr, 48 hr, 3 days, 4 days, 7 days. Note that the Triplicate1 sample = MyoD-/-1999; Triplicate 2 sample = MyoD-/-p6; Triplicate 3 sample = MyoD-/-p10. Keywords: other

2008-03-01 | GSE10430 | GEO

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

Project description: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)

2019-09-10 | GSE98509 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data