PRMT7 Preserves Satellite Cell Regenerative Capacity
Open accessAbstract
Regeneration of skeletal muscle requires the continued presence of quiescent muscle stem cells (satellite cells), which become activated in response to injury. Here, we report that whole-body protein arginine methyltransferase PRMT7(-/-) adult mice and mice conditionally lacking PRMT7 in satellite cells using Pax7-CreERT2 both display a significant reduction in satellite cell function, leading to defects in regenerative capacity upon muscle injury. We show that PRMT7 is preferentially expressed in activated satellite cells and, interestingly, PRMT7-deficient satellite cells undergo cell-cycle arrest and premature cellular senescence. These defects underlie poor satellite cell stem cell capacity to regenerate muscle and self-renew after injury. PRMT7-deficient satellite cells express elevated levels of the CDK inhibitor p21CIP1 and low levels of its repressor, DNMT3b. Restoration of DNMT3b in PRMT7-deficient cells rescues PRMT7-mediated senescence. Our findings define PRMT7 as a regulator of the DNMT3b/p21 axis required to maintain muscle stem cell regenerative capacity.
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Prmt7 is required for the maintenance of muscle stem cell regenerative capacity.
“Prmt7 is also required for the maintenance of muscle stem cell regenerative capacity [13].”
From Apigenin Enhances Skeletal Muscle Hypertrophy and Myoblast Differentiation by Regulating Prmt7 (2017) · cites this paper as [13]
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BindingDB (2026) · UC San Diego · doi:10.7270/q22r3xkr
- Authors
- Blanc, R. S., Vogel, G., Chen, T., Crist, C., & Richard, S.
- Affiliations
- Jewish General Hospital (CA)
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- Crist, Colin
- Richard, Stéphane
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2016-02
- Volume
- 14
- Issue
- 6
- Pages
- 1528-1539
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W2256875843
- Cited by
- 97
- References
- 39
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 9 · 2023: 12 · 2022: 8 · 2021: 11 · 2020: 7 · 2019: 15 · 2018: 5 · 2017: 11 · 2016: 4
- FWCI
- 6.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- McGill University
- Canadian Institutes of Health Research (MOP93811)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer-related gene regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Keywords
- PRMT7, protein arginine methyltransferase, satellite cells, skeletal muscle regeneration, muscle stem cells, cellular senescence, cell cycle arrest, p21, DNMT3B, Pax7, muscle damage, self-renewal
- MeSH terms
- DNA Methyltransferase 3B, Animals, Cell Differentiation, DNA (Cytosine-5-)-Methyltransferases, Female, Gene Expression Regulation, Male, Protein-Arginine N-Methyltransferases, Regeneration, Stem Cells, Signal Transduction, Cellular Senescence, Mice, Knockout, Muscle, Skeletal, Integrases, Satellite Cells, Skeletal Muscle, Cyclin-Dependent Kinase Inhibitor p21, Mice, PAX7 Transcription Factor, Cell Cycle Checkpoints
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