ArticleNucleic acids research2017
Incomplete MyoD-induced transdifferentiation is associated with chromatin remodeling deficiencies.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Chromatin remodelling: a driving force in reverse mechanotransduction.RNA biology · 2026Review
- Elevated MyoD1 levels expand genome-wide binding and the repertoire of regulated genes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Developmental dynamics of skeletal muscle can be recapitulated in vitro from pig embryonic stem cells.Stem cell reports · 2026Article
- Designed Minibinders Rewire Receptor Signaling to Enable Functional Human Myogenic Reprogramming.bioRxiv : the preprint server for biology · 2026Article
- Delineating transcriptomic signatures of in vitro human skeletal muscle models in comparison to in vivo references.Stem cell reports · 2025Article
- Transgene-free direct conversion of murine fibroblasts into functional muscle stem cells.NPJ Regenerative medicine · 2023Article
- Cellular and Genomic Features of Muscle Differentiation from Isogenic Fibroblasts and Myoblasts.Cells · 2023Article
- Review
- Novel integrated workflow allows production and in-depth quality assessment of multifactorial reprogrammed skeletal muscle cells from human stem cells.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- Dissecting dual roles of MyoD during lineage conversion to mature myocytes and myogenic stem cells.Genes & development · 2021Article
- Article
- Muscle regeneration controlled by a designated DNA dioxygenase.Cell death & disease · 2021Article
- Molecular Mechanisms Underlying Ascl1-Mediated Astrocyte-to-Neuron Conversion.Stem cell reports · 2021Article
- Interaction between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion Negative Rhabdomyosarcoma.Nature communications · 2021Article
- Chromatin-modifying drugs and metabolites in cell fate control.Cell proliferation · 2020Review
- Poly(ADP-ribose) Polymerase 1 (PARP1) restrains MyoD-dependent gene expression during muscle differentiation.Scientific reports · 2020Article
- Engineered skeletal muscles for disease modeling and drug discovery.Biomaterials · 2019Review
- The Hox transcription factor Ubx stabilizes lineage commitment by suppressing cellular plasticity ineLife · 2019Article
- Development and application of human skeletal muscle microphysiological systems.Lab on a chip · 2018Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
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.
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