ArticleMolecular metabolism2017
Muscle-specific knockout of general control of amino acid synthesis 5 (GCN5) does not enhance basal or endurance exercise-induced mitochondrial adaptation.
Article in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Post-translational Modifications: The Signals at the Intersection of Exercise, Glucose Uptake, and Insulin Sensitivity.Endocrine reviews · 2022Review
- GCN5 maintains muscle integrity by acetylating YY1 to promote dystrophin expression.The Journal of cell biology · 2022Article
- Epigenetic regulation of energy metabolism in obesity.Journal of molecular cell biology · 2021Review
- Complex functions of Gcn5 and Pcaf in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- GCN5 acetyltransferase in cellular energetic and metabolic processes.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- Exercise adaptations: molecular mechanisms and potential targets for therapeutic benefit.Nature reviews. Endocrinology · 2020Review
- Combined overexpression of SIRT1 and knockout of GCN5 in adult skeletal muscle does not affect glucose homeostasis or exercise performance in mice.American journal of physiology. Endocrinology and metabolism · 2020Article
- Skeletal muscle mitochondrial function and exercise capacity are not impaired in mice with knockout of STAT3.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Sex differences in mitochondrial respiratory function in human skeletal muscle.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Calorie Restriction-Induced Increase in Skeletal Muscle Insulin Sensitivity Is Not Prevented by Overexpression of the p55α Subunit of Phosphoinositide 3-Kinase.Frontiers in physiology · 2018Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveLysine acetylation is an important post-translational modification that regulates metabolic function in skeletal muscle. The acetyltransferase, general control of amino acid synthesis 5 (GCN5), has been proposed as a regulator of mitochondrial biogenesis via its inhibitory action on peroxisome proliferator activated receptor-γ coactivator-1α (PGC-1α). However, the specific contribution of GCN5 to skeletal muscle metabolism and mitochondrial adaptations to endurance exercise in vivo remain to be defined. We aimed to determine whether loss of GCN5 in skeletal muscle enhances mitochondrial density and function, and the adaptive response to endurance exercise training.
methodsWe used Cre-LoxP methodology to generate mice with muscle-specific knockout of GCN5 (mKO) and floxed, wildtype (WT) littermates. We measured whole-body energy expenditure, as well as markers of mitochondrial density, biogenesis, and function in skeletal muscle from sedentary mice, and mice that performed 20 days of voluntary endurance exercise training.
resultsDespite successful knockdown of GCN5 activity in skeletal muscle of mKO mice, whole-body energy expenditure as well as skeletal muscle mitochondrial abundance and maximal respiratory capacity were comparable between mKO and WT mice. Further, there were no genotype differences in endurance exercise-mediated mitochondrial biogenesis or increases in PGC-1α protein content.
conclusionThese results demonstrate that loss of GCN5 in vivo does not promote metabolic remodeling in mouse skeletal muscle.
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