ArticleScientific reports2018
The imprinted gene Pw1/Peg3 regulates skeletal muscle growth, satellite cell metabolic state, and self-renewal.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
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- Effects of paternal exposure to cigarette smoke on sperm DNA methylation and long-term metabolic syndrome in offspring.Epigenetics & chromatin · 2022Article
- Paternally expressed gene 3 (Pw1/Peg3) promotes sexual dimorphism in metabolism and behavior.PLoS genetics · 2022Article
- Myonuclear transcriptional dynamics in response to exercise following satellite cell depletion.iScience · 2021Article
- Review
- Timing of exposure to gonadotropins has differential effects on the conceptus: evidence from a mouse model†.Biology of reproduction · 2020Article
- Mouse CD146+ muscle interstitial progenitor cells differ from satellite cells and present myogenic potential.Stem cell research & therapy · 2020Article
- Differential gene responses 3 days following infarction in the fetal and adolescent sheep heart.Physiological genomics · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Pw1/Peg3 is an imprinted gene expressed from the paternally inherited allele. Several imprinted genes, including Pw1/Peg3, have been shown to regulate overall body size and play a role in adult stem cells. Pw1/Peg3 is expressed in muscle stem cells (satellite cells) as well as a progenitor subset of muscle interstitial cells (PICs) in adult skeletal muscle. We therefore examined the impact of loss-of-function of Pw1/Peg3 during skeletal muscle growth and in muscle stem cell behavior. We found that constitutive loss of Pw1/Peg3 function leads to a reduced muscle mass and myofiber number. In newborn mice, the reduction in fiber number is increased in homozygous mutants as compared to the deletion of only the paternal Pw1/Peg3 allele, indicating that the maternal allele is developmentally functional. Constitutive and a satellite cell-specific deletion of Pw1/Peg3, revealed impaired muscle regeneration and a reduced capacity of satellite cells for self-renewal. RNA sequencing analyses revealed a deregulation of genes that control mitochondrial function. Consistent with these observations, Pw1/Peg3 mutant satellite cells displayed increased mitochondrial activity coupled with accelerated proliferation and differentiation. Our data show that Pw1/Peg3 regulates muscle fiber number determination during fetal development in a gene-dosage manner and regulates satellite cell metabolism in the adult.
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