ArticleSkeletal muscle2016
The lysine methyltransferase Ehmt2/G9a is dispensable for skeletal muscle development and regeneration.
Article in Skeletal muscle, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Skeletal muscle reprogramming of metabolic, ribosomal and developmental pathways contributes to Roux-en-Y gastric bypass-induced adaptation in women.EBioMedicine · 2026Article
- Deficiency of G9a boosts muscle regeneration through IL13/Musclin-mediated crosstalk between macrophage and myofiber.Cell death & disease · 2026Article
- EHMT2 Controls Neural Crest-Derived Craniofacial Development but is Dispensable in Limb Development.bioRxiv : the preprint server for biology · 2025Article
- The SUV39 Family of H3K9 Methyltransferases in Skeletal Muscle Stem Cells.FASEB bioAdvances · 2025Review
- The Functions and Regulatory Mechanisms of Histone Modifications in Skeletal Muscle Development and Disease.International journal of molecular sciences · 2025Review
- RNAi Knockdown ofGenes · 2024Article
- Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024Review
- Lysine methylation signaling in skeletal muscle biology: from myogenesis to clinical insights.The Biochemical journal · 2023Review
- Targeting the LSD1/KDM1 Family of Lysine Demethylases in Cancer and Other Human Diseases.Advances in experimental medicine and biology · 2023Review
- Establishment of H3K9-methylated heterochromatin and its functions in tissue differentiation and maintenance.Nature reviews. Molecular cell biology · 2022Review
- Structure, Activity, and Function of the Protein Lysine Methyltransferase G9a.Life (Basel, Switzerland) · 2021Review
- Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Prdm16-mediated H3K9 methylation controls fibro-adipogenic progenitors identity during skeletal muscle repair.Science advances · 2021Article
- Histone Lysine Methylation and Long Non-Coding RNA: The New Target Players in Skeletal Muscle Cell Regeneration.Frontiers in cell and developmental biology · 2021Review
- Inactivation of the Euchromatic Histone-LysineFrontiers in cell and developmental biology · 2021Article
- EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma.eLife · 2020Article
- (Epi)genetic Modifications in Myogenic Stem Cells: From Novel Insights to Therapeutic Perspectives.Cells · 2019Review
- SUMOylation of G9a regulates its function as an activator of myoblast proliferation.Cell death & disease · 2019Article
- Inhibition of Methyltransferase Setd7 Allows the In Vitro Expansion of Myogenic Stem Cells with Improved Therapeutic Potential.Cell stem cell · 2018Article
- Temporal regulation of chromatin during myoblast differentiation.Seminars in cell & developmental biology · 2017Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEuchromatic histone-lysine N-methyltransferase 2 (G9a/Ehmt2) is the main enzyme responsible for the apposition of H3K9 di-methylation on histones. Due to its dual role as an epigenetic regulator and in the regulation of non-histone proteins through direct methylation, G9a has been implicated in a number of biological processes relevant to cell fate control. Recent reports employing in vitro cell lines indicate that Ehmt2 methylates MyoD to repress its transcriptional activity and therefore its ability to induce differentiation of activated myogenic cells.
methodsTo further investigate the importance of G9a in modulating myogenic regeneration in vivo, we crossed Ehmt2 (floxed) mice to animals expressing Cre recombinase from the Myod locus, resulting in efficient knockout in the entire skeletal muscle lineage (Ehmt2 (ΔmyoD) ).
resultsSurprisingly, despite a dramatic drop in the global levels of H3K9me2, knockout animals did not show any developmental phenotype in muscle size and appearance. Consistent with this finding, purified Ehmt2 (ΔmyoD) satellite cells had rates of activation and proliferation similar to wild-type controls. When induced to differentiate in vitro, Ehmt2 knockout cells differentiated with kinetics similar to those of control cells and demonstrated normal capacity to form myotubes. After acute muscle injury, knockout mice regenerated as efficiently as wildtype. To exclude possible compensatory mechanisms elicited by the loss of G9a during development, we restricted the knockout within adult satellite cells by crossing Ehmt2 (floxed) mice to Pax7 (CreERT2) and also found normal muscle regeneration capacity.
conclusionsThus, Ehmt2 and H3K9me2 do not play significant roles in skeletal muscle development and regeneration in vivo.
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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.