Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies

ABSTRACT: Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies

PROVIDER: PRJNA360439 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies [RNA-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 | GSE93263 | GEO

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

2017-01-07 | GSE93258 | GEO

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

2017-01-07 | GSE93257 | GEO

Incomplete MyoD-induced transdifferentiation is associated with chromatin remodeling deficiencies.

Project description: Not available

| S-EPMC5714206 | biostudies-literature

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-01-07 | GSE93268 | GEO

Homo sapiens

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

| PRJNA360445 | ENA

Homo sapiens

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

| PRJNA360449 | ENA

Homo sapiens

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

| PRJNA360446 | ENA

Transcriptome sequencing analysis of MyoD-induced transdifferentiation in 10T1/2 fibroblasts using RNA-seq

Project description:To understand the effect of LncMyod on MyoD-induced transdifferentiation of 10T1/2 fibroblast cells, we performed RNA-seq on LncMyoD-KO 10T1/2 fibroblasts with MyoD-induced transdifferentiation.

2020-12-08 | GSE159133 | GEO

Signal-dependent incorporation of MyoD-BAF60c into Brg1-based SWI/SNF chromatin-remodeling complex

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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