The Corepressor NCoR1 Antagonizes PGC-1 α and Estrogen-Related Receptor α in the Regulation of Skeletal Muscle Function and Oxidative Metabolism
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Skeletal muscle exhibits a high plasticity and accordingly can quickly adapt to different physiological and pathological stimuli by changing its phenotype largely through diverse epigenetic mechanisms. The nuclear receptor corepressor 1 (NCoR1) has the ability to mediate gene repression; however, its role in regulating biological programs in skeletal muscle is still poorly understood. We therefore studied the mechanistic and functional aspects of NCoR1 function in this tissue. NCoR1 muscle-specific knockout mice exhibited a 7.2% higher peak oxygen consumption (VO(2peak)), a 11% reduction in maximal isometric force, and increased ex vivo fatigue resistance during maximal stimulation. Interestingly, global gene expression analysis revealed a high overlap between the effects of NCoR1 deletion and peroxisome proliferator-activated receptor gamma (PPARγ) coactivator 1α (PGC-1α) overexpression on oxidative metabolism in muscle. Importantly, PPARβ/δ and estrogen-related receptor α (ERRα) were identified as common targets of NCoR1 and PGC-1α with opposing effects on the transcriptional activity of these nuclear receptors. In fact, the repressive effect of NCoR1 on oxidative phosphorylation gene expression specifically antagonizes PGC-1α-mediated coactivation of ERRα. We therefore delineated the molecular mechanism by which a transcriptional network controlled by corepressor and coactivator proteins determines the metabolic properties of skeletal muscle, thus representing a potential therapeutic target for metabolic diseases.
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If a high-volume mechanical stimulus induces severe microtrauma, the subsequent inflammatory response can drastically increase the non-muscle cell population within the biopsy sample, falsely elevating bulk total RNA concentration.
“If a high-volume mechanical stimulus induces severe microtrauma, the subsequent inflammatory response can drastically increase the non-muscle cell population within the biopsy sample, falsely elevating the bulk total RNA concentration [48,73].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [48]
Bulk tissue homogenization blends transcriptomic profiles of multinucleated myofibers with RNA from resident non-muscle cells, including fibroblasts, endothelial cells, infiltrating immune cells, and uncommitted satellite cells.
“First, bulk tissue homogenization inherently blends the transcriptomic profiles of multinucleated myofibers with the RNA derived from resident non-muscle cells, including fibroblasts, endothelial cells, infiltrating immune cells (macrophages and neutrophils), and uncommitted satellite cells [48,72].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [48]
Whole-muscle RNA-seq remains hindered by profound cellular infiltration confounders.
“While the integration of whole-muscle RNA sequencing (RNA-seq) has successfully mapped the global transcriptomic landscape of exercise adaptation—revealing that snoRNAs and Pol II-derived ribosomal proteins are dynamically synchronized with Pol I activity—this approach remains hindered by profound cellular infiltration confounders [33,48,55].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [48]
Whole-muscle RNA-seq has mapped the global transcriptomic landscape of exercise adaptation, revealing that snoRNAs and Pol II-derived ribosomal proteins are dynamically synchronized with Pol I activity.
“While the integration of whole-muscle RNA sequencing (RNA-seq) has successfully mapped the global transcriptomic landscape of exercise adaptation—revealing that snoRNAs and Pol II-derived ribosomal proteins are dynamically synchronized with Pol I activity—this approach remains hindered by profound cellular infiltration confounders [33,48,55].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [48]
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- Authors
- Pérez-Schindler, J., Summermatter, S., Salatino, S., Zorzato, F., Beer, M., Balwierz, P. J., van Nimwegen, E., Feige, J. N., Auwerx, J., & Handschin, C.
- Affiliations
- Biozentrum, University of Basel, Basel, Switzerland
- University of Basel (CH)
- University of Ferrara (IT)
- SIB Swiss Institute of Bioinformatics (CH)
- Novartis (Switzerland) (CH)
- École Polytechnique Fédérale de Lausanne (CH)
- ORCID
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2012-12-01
- Volume
- 32
- Issue
- 24
- Pages
- 4913-4924
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC3510532
- OpenAlex
- W2159030474
- Cited by
- 82
- References
- 53
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 7 · 2019: 7 · 2018: 10 · 2017: 8 · 2016: 3 · 2015: 10 · 2014: 9 · 2013: 6
- FWCI
- 5.36
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Molecular and Cellular Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- edoc (University of Basel) (acceptedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion)
- edoc (University of Basel)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (132900, 310030)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- NCOR1, PGC-1α, estrogen-related receptor alpha, skeletal muscle, oxidative metabolism, oxidative phosphorylation, muscle fatigue resistance, muscle-specific knockout mice, PPARδ, gene repression, muscle plasticity, peak oxygen uptake, isometric force
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, ERRalpha Estrogen-Related Receptor, Animals, Male, Mice, Transgenic, Models, Biological, Muscle Contraction, Oxidative Phosphorylation, Oxygen Consumption, Receptors, Estrogen, RNA, Messenger, Transcription Factors, Trans-Activators, Mice, Knockout, Muscle, Skeletal, PPAR delta, PPAR-beta, Mice, Nuclear Receptor Co-Repressor 1
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