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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

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			Action	DRS
	SRR5151640.fastq.gz	Fastqsanger.gz
	SRR5151760.fastq.gz	Fastqsanger.gz
	SRR5151770.fastq.gz	Fastqsanger.gz
	SRR5151641.fastq.gz	Fastqsanger.gz
	SRR5151761.fastq.gz	Fastqsanger.gz

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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:Our current understanding of cellular transdifferentiation systems is limited. It is oftentimes unknown, at a genome-wide scale, how much transdifferentiated cells differ quantitatively from both the starting cells and the target cells. Focusing on transdifferentiation of primary human skin fibroblasts by forced expression of myogenic transcription factor MyoD, we performed quantitative analyses of gene expression and chromatin accessibility profiles of transdifferentiated cells compared to fibroblasts and myoblasts. In this system, we find that while many of the early muscle marker genes are reprogrammed, global gene expression and accessibility changes are still incomplete when compared to myoblasts. In addition, we find evidence of epigenetic memory in the transdifferentiated cells, with reminiscent features of fibroblasts being visible both in chromatin accessibility and gene expression. Quantitative analyses revealed a continuum of changes in chromatin accessibility induced by MyoD, and a strong correlation between chromatin-remodeling deficiencies and incomplete gene expression reprogramming. Classification analyses identified genetic and epigenetic features that distinguish reprogrammed from non-reprogrammed sites, and suggested ways to potentially improve transdifferentiation efficiency. Our approach for combining gene expression, DNA accessibility, and protein-DNA binding data to quantify and characterize the efficiency of cellular transdifferentiation on a genome-wide scale can be applied to any transdifferentiation system.

| 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 [Dnase-Seq]

| PRJNA360446 | 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

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

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