The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.
CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function
Open accessAbstract
MyoD , a master regulator of myogenesis, exhibits a circadian rhythm in its mRNA and protein levels, suggesting a possible role in the daily maintenance of muscle phenotype and function. We report that MyoD is a direct target of the circadian transcriptional activators CLOCK and BMAL1, which bind in a rhythmic manner to the core enhancer of the MyoD promoter. Skeletal muscle of Clock Δ19 and Bmal1 −/− mutant mice exhibited ∼30% reductions in normalized maximal force. A similar reduction in force was observed at the single-fiber level. Electron microscopy (EM) showed that the myofilament architecture was disrupted in skeletal muscle of Clock Δ19 , Bmal1 −/− , and MyoD −/− mice. The alteration in myofilament organization was associated with decreased expression of actin, myosins, titin, and several MyoD target genes. EM analysis also demonstrated that muscle from both Clock Δ19 and Bmal1 −/− mice had a 40% reduction in mitochondrial volume. The remaining mitochondria in these mutant mice displayed aberrant morphology and increased uncoupling of respiration. This mitochondrial pathology was not seen in muscle of MyoD −/− mice. We suggest that altered expression of both Pgc-1α and Pgc-1β in Clock Δ19 and Bmal1 −/− mice may underlie this pathology. Taken together, our results demonstrate that disruption of CLOCK or BMAL1 leads to structural and functional alterations at the cellular level in skeletal muscle. The identification of MyoD as a clock-controlled gene provides a mechanism by which the circadian clock may generate a muscle-specific circadian transcriptome in an adaptive role for the daily maintenance of adult skeletal muscle.
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“The functional significance of disrupting the molecular clock has been shown in genetic mouse models (i.e., Clock mutant mice and the Bmal1 KO mouse), which display reduced glucose tolerance, mitochondrial respiratory function, and skeletal muscle contractile function [20,21].”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [21]
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“Considering the negative metabolic consequences, such as reduction in insulin sensitivity and mitochondrial function, attributed to both circadian misalignment and sleep loss [21,67] and the potential benefits of exercise in this context [17,68], further research is warranted.”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [21]
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Cites
Obesity and Metabolic Syndrome in Circadian Clock Mutant Mice
Turek, F. W., Joshu, C., Kohsaka, A., Lin, E., Ivanova, G., McDearmon, E., Laposky, A., Losee-Olson, S., Easton, A., Jensen, D. R., et al. (2005) · Science · doi:10.1126/science.1108750 · Cited by 2,485
Self-citationTranscriptional paradigms in mammalian mitochondrial biogenesis and function
Scarpulla, R. C. (2008) · Physiological Reviews · doi:10.1152/physrev.00025.2007 · Cited by 1,666
Mutagenesis and Mapping of a Mouse Gene, Clock , Essential for Circadian Behavior
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Mop3 is an essential component of the master circadian pacemaker in mammals.
Bunger, M. K., Wilsbacher, L. D., Moran, S. M., Clendenin, C., Radcliffe, L. A., Hogenesch, J. B., Simon, M. C., Takahashi, J. S., & Bradfield, C. A. (2000) · Cell · doi:10.1016/s0092-8674(00)00205-1 · Cited by 1,621
Self-citationThe genetics of mammalian circadian order and disorder: implications for physiology and disease
Takahashi, J. S., Hong, H.-K., Ko, C. H., & McDearmon, E. L. (2008) · Nature Reviews Genetics · doi:10.1038/nrg2430 · Cited by 1,611
Self-citationCircadian rhythms from multiple oscillators: lessons from diverse organisms
Bell‐Pedersen, D., Cassone, V. M., Earnest, D. J., Golden, S. S., Hardin, P. E., Thomas, T. L., & Zoran, M. J. (2005) · Nature Reviews Genetics · doi:10.1038/nrg1633 · Cited by 1,523
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SIRT1 regulates circadian clock gene expression through PER2 deacetylation
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Circadian Clock Feedback Cycle Through NAMPT-Mediated NAD + Biosynthesis
Ramsey, K. M., Yoshino, J., Brace, C. S., Abrassart, D., Kobayashi, Y., Marcheva, B., Hong, H.-K., Chong, J. L., Buhr, E. D., Lee, C., et al. (2009) · Science · doi:10.1126/science.1171641 · Cited by 1,126
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Woldt, E., Sebti, Y., Solt, L. A., Duhem, C., Lancel, S., Eeckhoute, J., Hesselink, M. K. C., Paquet, C., Delhaye, S., Shin, Y., et al. (2013) · Nature Medicine · doi:10.1038/nm.3213 · Cited by 467
Metadata
- Authors
- Andrews, J. L., Zhang, X., McCarthy, J. J., McDearmon, E. L., Hornberger, T. A., Russell, B., Campbell, K. S., Arbogast, S., Reid, M. B., Walker, J. R., Hogenesch, J. B., Takahashi, J. S., & Esser, K. A.
- Affiliations
- University of Illinois Chicago (US)
- University of Kentucky (US)
- Northwestern University (US)
- Genomics Institute of the Novartis Research Foundation (US)
- University of Pennsylvania (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-10-18
- Volume
- 107
- Issue
- 44
- Pages
- 19090-19095
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2973897
- OpenAlex
- W2053866174
- Cited by
- 389
- References
- 49
- Citations by year
- 2026: 30 · 2025: 29 · 2024: 31 · 2023: 28 · 2022: 36 · 2021: 26 · 2020: 25 · 2019: 19 · 2018: 27 · 2017: 23 · 2016: 32 · 2015: 20 · 2014: 19 · 2013: 17 · 2012: 15
- FWCI
- 6.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (5p50mh074924-05)
- National Heart, Lung, and Blood Institute (HL45721, R01HL045721)
- National Institute of Mental Health (U01MH061915, P50 MH-074924, U01 MH 61915)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R03AR053641, R21AR050717, AR050717, R01AR055246, AR-053641)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- circadian clock, clocks, Bmal1, MyoD, skeletal muscle, myogenesis, clock-controlled genes, mitochondrial dysfunction, uncoupled respiration, PGC-1α, PGC-1β, muscle force, muscle phenotype
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Animals, Gene Expression Regulation, Mice, Inbred BALB C, Mitochondria, Muscle, Transcription Factors, Trans-Activators, MyoD Protein, Mice, Knockout, Muscle, Skeletal, Gene Expression Profiling, Muscle Development, Mice, Electron Microscope Tomography, CLOCK Proteins, ARNTL Transcription Factors, Circadian Clocks
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