ArticleScience advances2021
Prdm16-mediated H3K9 methylation controls fibro-adipogenic progenitors identity during skeletal muscle repair.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 71 citations in OpenAlex.
- PRDM16 modulates aspects of cell cycle dynamics and maturation in human iPSC-derived cardiomyocytes.Stem cell reports · 2026Article
- Deficiency of G9a boosts muscle regeneration through IL13/Musclin-mediated crosstalk between macrophage and myofiber.Cell death & disease · 2026Article
- The Role of Fibro/adipogenic Progenitors (FAPs) in Sarcopenia: Mechanisms and Potential Therapeutic Strategies.Stem cell reviews and reports · 2026Review
- Cellular and molecular mechanisms of fatty infiltration in paraspinal muscles in spine-specific sarcopenia.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- PRDM16 Regulates Prostate Cancer Cell Dormancy and Prevents Bone Metastatic Outgrowth.Cancer research · 2026Article
- Underexplored terrain: effects of high priority environmental toxicants on skeletal muscle.Journal of toxicology and environmental health. Part B, Critical reviews · 2026Review
- PRDM16 Drives Thyroid Cancer Differentiation via a TRIM58-MVP Axis to Suppress MAPK and PI3K/AKT Signaling.International journal of biological sciences · 2026Article
- PRDM16 regulates smooth muscle cell identity and atherosclerotic plaque composition.Nature cardiovascular research · 2025Article
- The Functional Interaction Between PRDM16 and the SREBP Pathway Controls Lipid Metabolism.International journal of molecular sciences · 2025Article
- Mechanistic and Epigenetic Partitioning of Lamina-Associated Chromatin Revealed by a Genome-Wide Imaging Screen.bioRxiv : the preprint server for biology · 2025Article
- PRDM16, a new kid on the block in cardiovascular health and disease.Cardiovascular research · 2025Review
- SMCHD1 maintains heterochromatin, genome compartments and epigenome landscape in human myoblasts.Nature communications · 2025Article
- The SUV39 Family of H3K9 Methyltransferases in Skeletal Muscle Stem Cells.FASEB bioAdvances · 2025Review
- MyoD1 localization at the nuclear periphery is mediated by association of WFS1 with active enhancers.Nature communications · 2025Article
- Article
- PDZRN3 regulates adipogenesis of mesenchymal progenitors in muscle.Regenerative therapy · 2025Article
- PdgfrαGenes & diseases · 2025Review
- Integrating spatial transcriptomics and single-nucleus RNA-seq revealed the specific inhibitory effects of TGF-β on intramuscular fat deposition.Science China. Life sciences · 2025Article
- Role of the cytoskeleton in cellular reprogramming: effects of biophysical and biochemical factors.Frontiers in molecular biosciences · 2025Review
- Report and Abstracts of the 20th Meeting of IIM, the Interuniversity Institute of Myology: Assisi, October 12-15, 2023.European journal of translational myology · 2024Article
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
H3K9 methylation maintains cell identity orchestrating stable silencing and anchoring of alternate fate genes within the heterochromatic compartment underneath the nuclear lamina (NL). However, how cell type-specific genomic regions are specifically targeted to the NL is still elusive. Using fibro-adipogenic progenitors (FAPs) as a model, we identified Prdm16 as a nuclear envelope protein that anchors H3K9-methylated chromatin in a cell-specific manner. We show that Prdm16 mediates FAP developmental capacities by orchestrating lamina-associated domain organization and heterochromatin sequestration at the nuclear periphery. We found that Prdm16 localizes at the NL where it cooperates with the H3K9 methyltransferases G9a/GLP to mediate tethering and silencing of myogenic genes, thus repressing an alternative myogenic fate in FAPs. Genetic and pharmacological disruption of this repressive pathway confers to FAP myogenic competence, preventing fibro-adipogenic degeneration of dystrophic muscles. In summary, we reveal a druggable mechanism of heterochromatin perinuclear sequestration exploitable to reprogram FAPs in vivo.
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Registered trials
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.