ArticleNature communications2018
The Trithorax protein Ash1L promotes myoblast fusion by activating Cdon expression.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Exploring lncRNA-Mediated Mechanisms in Muscle Regulation and Their Implications for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2025Review
- Structure-function relationship of ASH1L and histone H3K36 and H3K4 methylation.Nature communications · 2025Article
- Cystine/glutamate antiporter xCT controls skeletal muscle glutathione redox, bioenergetics and differentiation.Redox biology · 2024Article
- Cdon is essential for organ left-right patterning by regulating dorsal forerunner cells clustering and Kupffer's vesicle morphogenesis.Frontiers in cell and developmental biology · 2024Article
- Integrated Comparative Transcriptome and circRNA-lncRNA-miRNA-mRNA ceRNA Regulatory Network Analyses Identify Molecular Mechanisms Associated with Intramuscular Fat Content in Beef Cattle.Animals : an open access journal from MDPI · 2023Article
- Prolonged FOS activity disrupts a global myogenic transcriptional program by altering 3D chromatin architecture in primary muscle progenitor cells.Skeletal muscle · 2022Article
- Identification of Robust and Key Differentially Expressed Genes during C2C12 Cell Myogenesis Based on Multiomics Data.International journal of molecular sciences · 2022Article
- Review
- Structural insight into ASH1L PHD finger recognizing methylated histone H3K4 and promoting cell growth in prostate cancer.Frontiers in oncology · 2022Article
- Single-cell transcriptomic analyses provide insights into the developmental origins of neuroblastoma.Nature genetics · 2021Article
- Epigenetic regulation of satellite cell fate during skeletal muscle regeneration.Skeletal muscle · 2021Review
- BETs inhibition attenuates oxidative stress and preserves muscle integrity in Duchenne muscular dystrophy.Nature communications · 2020Article
- HRP2-DPF3a-BAF complex coordinates histone modification and chromatin remodeling to regulate myogenic gene transcription.Nucleic acids research · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myoblast fusion (MF) is required for muscle growth and repair, and its alteration contributes to muscle diseases. The mechanisms governing this process are incompletely understood, and no epigenetic regulator has been previously described. Ash1L is an epigenetic activator belonging to the Trithorax group of proteins and is involved in FSHD muscular dystrophy, autism and cancer. Its physiological role in skeletal muscle is unknown. Here we report that Ash1L expression is positively correlated with MF and reduced in Duchenne muscular dystrophy. In vivo, ex vivo and in vitro experiments support a selective and evolutionary conserved requirement for Ash1L in MF. RNA- and ChIP-sequencing indicate that Ash1L is required to counteract Polycomb repressive activity to allow activation of selected myogenesis genes, in particular the key MF gene Cdon. Our results promote Ash1L as an important epigenetic regulator of MF and suggest that its activity could be targeted to improve cell therapy for muscle diseases.
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