Cited by 97Muscle Physiology and DisordersCancer-related gene regulationCongenital heart defects research

PRMT7 Preserves Satellite Cell Regenerative Capacity

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Blanc, Roméo Sébastien, Vogel, Gillian, Chen, Taiping, Crist, Colin, Richard, Stéphane·2016·Cell Reports

Abstract

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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Crossref · 10.1016/j.celrep.2016.01.022

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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
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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