Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

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

PROVIDER: PRJNA360446 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5151640.fastq.gz	Fastqsanger.gz
	SRR5151641.fastq.gz	Fastqsanger.gz
	SRR5151642.fastq.gz	Fastqsanger.gz
	SRR5151643.fastq.gz	Fastqsanger.gz
	SRR5151644.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 13

Similar Datasets

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies

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

| PRJNA360439 | 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 [ChIP-Seq]

| PRJNA360445 | ENA

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

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

Genetic and epigenetic determinants of neurogenesis and myogenesis [ChIP-seq]

Project description:The regulatory networks of differentiation programs have been partly characterized; however, the molecular mechanisms of lineage-specific gene regulation by highly similar transcription factors remain largely unknown. Here we compare the genome-wide binding and transcription profiles of NEUROD2-mediated neurogenesis with MYOD-mediated myogenesis. We demonstrate that NEUROD2 and MYOD bind a shared CAGCTG E-box motif and E-box motifs specific for each factor: CAGGTG for MYOD and CAGATG for NEUROD2. Binding at factor-specific motifs is associated with gene transcription, whereas binding at shared sites is associated with regional epigenetic modifications but not as strongly associated with gene transcription. Binding is largely constrained to E-boxes pre-set in an accessible chromatin context that determines the set of target genes activated in each cell type. These findings demonstrate that the differentiation program is genetically determined by E-box sequence whereas cell lineage epigenetically determines the availability of E-boxes for each differentiation program. Comparing NeuroD2 induced neurogenesis and MyoD induced myogenesis by examining NeuroD2/MyoD binding sites in fibroblasts and P19 cells and corresponding changes in AcH4 using Chip-Seq. Assess chromatin accessibility using PvuII assay followed by high throughput sequencing.

2012-03-26 | E-GEOD-34906 | biostudies-arrayexpress

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

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

| PRJNA667738 | ENA

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 ›

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