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Myogenesis MyoD

ABSTRACT: The transcription factor MyoD can coax na?e fibroblasts or otherwise committed cells to adopt the skeletal muscle phenotype by activating the muscle gene expression program. Activation of muscle gene expression occurs in quantal steps with not all the target genes of MyoD being activated at the same time. Some genes are induced in the initial phases, others at later stages despite the fact that MyoD is present throughout the differentiation process. MyoD is post-translationally modified by phosphorylation, ubiquitination, and acetylation. Here, we have employed a model system in which MyoD and its non-acetylatable version were inducibly expressed in mouse embryonic fibroblasts derived from mice to investigate how MyoD acetylation may contribute to differential gene activation. Keywords: Time-Series

ORGANISM(S): Mus musculus

PROVIDER: GSE6487 | GEO | 2006/12/13

SECONDARY ACCESSION(S): PRJNA98659

REPOSITORIES: GEO

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Transcription profiling of mouse embryoic fibroblasts expressing wild type MyoD or its non-acetylatable version MyoD RRR to investigate how MyoD acetylation may contribute to differential gene activation.

Project description:The transcription factor MyoD can coax na?e fibroblasts or otherwise committed cells to adopt the skeletal muscle phenotype by activating the muscle gene expression program. Activation of muscle gene expression occurs in quantal steps with not all the target genes of MyoD being activated at the same time. Some genes are induced in the initial phases, others at later stages despite the fact that MyoD is present throughout the differentiation process. MyoD is post-translationally modified by phosphorylation, ubiquitination, and acetylation. Here, we have employed a model system in which MyoD and its non-acetylatable version were inducibly expressed in mouse embryonic fibroblasts derived from mice to investigate how MyoD acetylation may contribute to differential gene activation. Experiment Overall Design: Mouse embryos fibroblasts (MEFs) obtained from MyoD-/-/Myf5-/- animals will be transduced with retroviruses expressing an estrogen receptor hormone binding domain fused to either mouse MyoD wild type (ER-MyoD wt) or MyoD bearing three point mutations at lysine residues 99, 102, and 104 that render it no longer acetylatable ( ER-MyoD RRR). A retrovirus without the ER-MyoD insert was also employed as negative control.</p> Aim 2. We will compare genome-wide expression profiling of MEFs transduced with either ER-MyoD wt or ER-MyoD RRR cultured in the presence of a medium that promotes skeletal muscle differentiation (DM) supplemented with beta-estradiol for 0, 6, 12, and 24 hours, respectively.

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Distinct activities of Myf5 and MyoD indicate sequential roles in skeletal muscle lineage specification and differentiation (RNA-Seq)

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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.

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

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

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Project description:The generation of myotubes from fibroblasts upon forced MyoD expression is a classic example of factor-induced reprogramming in mammals. We recently discovered that additional modulation of signaling pathways with small molecules facilitates reprogramming to more primitive induced muscle progenitor cells (iMPCs). However, the mechanisms by which a single transcription factor drives differentiated cells into distinct developmental states remain unknown. We therefore dissected the transcriptional and epigenetic dynamics of fibroblasts undergoing MyoD-dependent reprogramming to either myotubes or iMPCs using a novel MyoD transgenic model. To this end, we performed single cell RNA sequencing for Pax7-nGFP positive iMPCs/satellite cells and cells undergoing dedifferentiation (i.e. Dox+FRG) or transdifferentiation (i.e. Dox) Our analyses elucidate the role of MyoD in myogenic reprogramming and derive general principles by which transcription factors and signaling pathways cooperate to rewire cell identity. Our results may also inform on potential therapeutic applications of direct reprogramming.

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