ArticleCell death & disease2019
SUMOylation of G9a regulates its function as an activator of myoblast proliferation.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Histone methyltransferase G9a crosstalks with H3K36 histone methyltransferases NSD3 and SETD2 to mediate gene activation.Frontiers in cell and developmental biology · 2026Article
- LncRNA Xist acts as a miR-486-5p sponge to modulate myoblast proliferation by recruiting Stk4.Journal of muscle research and cell motility · 2025Article
- Histone Methyltransferase G9a in Primary Sensory Neurons Promotes Inflammatory Pain and Transcription ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Review
- Review
- An interplay between BRD4 and G9a regulates skeletal myogenesis.Frontiers in cell and developmental biology · 2022Article
- Sumoylation-deficient phosphoglycerate mutase 2 impairs myogenic differentiation.Frontiers in cell and developmental biology · 2022Article
- Structure, Activity, and Function of the Protein Lysine Methyltransferase G9a.Life (Basel, Switzerland) · 2021Review
- Review
- SUMO and Transcriptional Regulation: The Lessons of Large-Scale Proteomic, Modifomic and Genomic Studies.Molecules (Basel, Switzerland) · 2021Review
- Insight into the multi-faceted role of the SUV family of H3K9 methyltransferases in carcinogenesis and cancer progression.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- Complex interactomes and post-translational modifications of the regulatory proteins HABP4 and SERBP1 suggest pleiotropic cellular functions.World journal of biological chemistry · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lysine methyltransferase G9a plays a role in many cellular processes. It is a potent repressor of gene expression, a function attributed to its ability to methylate histone and non-histone proteins. Paradoxically, in some instances, G9a can activate gene expression. However, regulators of G9a expression and activity are poorly understood. In this study, we report that endogenous G9a is SUMOylated in proliferating skeletal myoblasts. There are four potential SUMOylation consensus motifs in G9a. Mutation of all four acceptor lysine residues [K79, K152, K256, and K799] inhibits SUMOylation. Interestingly, SUMOylation does not impact G9a-mediated repression of MyoD transcriptional activity or myogenic differentiation. In contrast, SUMO-defective G9a is unable to enhance proliferation of myoblasts. Using complementation experiments, we show that the proliferation defect of primary myoblasts from conditional G9a-deficient mice is rescued by re-expression of wild-type, but not SUMOylation-defective, G9a. Mechanistically, SUMOylation acts as signal for PCAF (P300/CBP-associated factor) recruitment at E2F1-target genes. This results in increased histone H3 lysine 9 acetylation marks at E2F1-target gene promoters that are required for S-phase progression. Our studies provide evidence by which SUMO modification of G9a influences the chromatin environment to impact cell cycle progression.
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