ArticleThe Journal of biological chemistry2015
Expression of Non-acetylatable H2A.Z in Myoblast Cells Blocks Myoblast Differentiation through Disruption of MyoD Expression.
Article in The Journal of biological chemistry, 2015. 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, 30 citations in OpenAlex.
- Aberrant skeletal muscle morphogenesis and myofiber differentiation characterize equine myotonic dystrophy.PloS one · 2026Article
- The Tip60 acetylome is a hallmark of the proliferative state in Drosophila.Nucleic acids research · 2025Article
- Article
- Histone H2A.Z Deacetylation and Dedifferentiation in Infarcted/Tip60-depleted Cardiomyocytes.bioRxiv : the preprint server for biology · 2025Article
- The Function of H2A Histone Variants and Their Roles in Diseases.Biomolecules · 2024Review
- Roles of Histone H2A Variants in Cancer Development, Prognosis, and Treatment.International journal of molecular sciences · 2024Review
- Article
- Histone variant H2B.Z acetylation is necessary for maintenance of Toxoplasma gondii biological fitness.Biochimica et biophysica acta. Gene regulatory mechanisms · 2023Article
- Histone variant H2B.Z acetylation is necessary for maintenance ofbioRxiv : the preprint server for biology · 2023Article
- The Role of the Histone Variant H2A.Z in Metazoan Development.Journal of developmental biology · 2022Review
- Epigenetic Regulation of Myogenesis: Focus on the Histone Variants.International journal of molecular sciences · 2021Review
- Histone variants in skeletal myogenesis.Epigenetics · 2021Review
- H2A.Z is dispensable for both basal and activated transcription in post-mitotic mouse muscles.Nucleic acids research · 2020Article
- The SNPs in myoD gene from normal muscle developing individuals have no effect on muscle mass.BMC genetics · 2019Article
- The histone variant H2A.Z in gene regulation.Epigenetics & chromatin · 2019Review
- Histone variant H2A.Z deposition and acetylation directs the canonical Notch signaling response.Nucleic acids research · 2018Article
- Review
- Temporal regulation of chromatin during myoblast differentiation.Seminars in cell & developmental biology · 2017Review
- BRG1 interacts with SOX10 to establish the melanocyte lineage and to promote differentiation.Nucleic acids research · 2017Article
- Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
H2A.Z is a histone H2A variant that is essential for viability in Tetrahymena and Drosophila and also during embryonic development of mice. Although implicated in diverse cellular processes, including transcriptional regulation, chromosome segregation, and heterochromatin formation, its essential function in cells remains unknown. Cellular differentiation is part of the developmental process of multicellular organisms. To elucidate the roles of H2A.Z and H2A.Z acetylation in cellular differentiation, we examined the effects of expressing wild type (WT) or a non-acetylatable form of H2A.Z in the growth and differentiation of the myoblast C2C12 cell line. Ectopic expression of wild type or mutant H2A.Z resulted in distinct phenotypes in the differentiation of the C2C12 cells and the formation of myotubes. Most strikingly, expression of the H2A.Z non-acetylatable mutant (H2A.Z-Ac-mut) resulted in a complete block of myoblast differentiation. We determined that this phenotype is caused by a loss of MyoD expression in the Ac-mut-expressing cells prior to and after induction of differentiation. Moreover, chromatin accessibility assays showed that the promoter region of MyoD is less accessible in the differentiation-defective cells. Altogether, these new findings show that expression of the Ac-mut form of H2A.Z resulted in a dominant phenotype that blocked differentiation due to chromatin changes at the MyoD promoter.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.