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Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE93268 | GEO | 2017/01/07

SECONDARY ACCESSION(S): PRJNA360439

REPOSITORIES: GEO

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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 [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 mediated by chromatin remodeling deficiencies

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

| PRJNA360439 | ENA

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-01-01 | E-GEOD-26685 | biostudies-arrayexpress

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

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

2013-01-01 | GSE26685 | GEO

Dynamic epigenetic remodeling underlies microRNA-mediated transdifferentiation of human adult fibroblasts into neuronal subtypes

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

2017-08-04 | GSE102035 | GEO

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma.

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

2023-03-20 | GSE207170 | GEO

Enhanced MyoD-induced transdifferentiation to a myogenic lineage by fusion to a potent transactivation domain.

Project description:Genetic reprogramming holds great potential for disease modeling, drug screening, and regenerative medicine. Genetic reprogramming of mammalian cells is typically achieved by forced expression of natural transcription factors that control master gene networks and cell lineage specification. However, in many instances, the natural transcription factors do not induce a sufficiently robust response to completely reprogram cell phenotype. In this study, we demonstrate that protein engineering of the master transcription factor MyoD can enhance the conversion of human dermal fibroblasts and adult stem cells to a skeletal myocyte phenotype. Fusion of potent transcriptional activation domains to MyoD led to increased myogenic gene expression, myofiber formation, cell fusion, and global reprogramming of the myogenic gene network. This work supports a general strategy for synthetically enhancing the direct conversion between cell types that can be applied in both synthetic biology and regenerative medicine.

| S-EPMC4475448 | biostudies-literature

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