A family of microRNAs encoded by myosin genes governs myosin expression and muscle performance
Open accessAbstract
Myosin is the primary regulator of muscle strength and contractility. Here we show that three myosin genes, Myh6, Myh7, and Myh7b, encode related intronic microRNAs (miRNAs), which, in turn, control muscle myosin content, myofiber identity, and muscle performance. Within the adult heart, the Myh6 gene, encoding a fast myosin, coexpresses miR-208a, which regulates the expression of two slow myosins and their intronic miRNAs, Myh7/miR-208b and Myh7b/miR-499, respectively. miR-208b and miR-499 play redundant roles in the specification of muscle fiber identity by activating slow and repressing fast myofiber gene programs. The actions of these miRNAs are mediated in part by a collection of transcriptional repressors of slow myofiber genes. These findings reveal that myosin genes not only encode the major contractile proteins of muscle, but act more broadly to influence muscle function by encoding a network of intronic miRNAs that control muscle gene expression and performance.
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“the antifibrotic effect of TH is also linked to the T 3 -induced inhibition of profibrotic pathways, (29)”
From Thyroid Hormones and Cardiovascular Function and Diseases (2018) · cites this paper as [29]
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- Authors
- van Rooij, E., Quiat, D., Johnson, B. A., Sutherland, L. B., Qi, X., Richardson, J. A., Kelm, R. J., & Olson, E. N.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- University of Vermont (US)
- Corresponding author
- Olson, Eric N.
- ORCID
- Venue
- Developmental Cell
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 17
- Issue
- 5
- Pages
- 662-673
- ISSN
- 1534-5807 (ISSN-L)
- PMC
- PMC2796371
- OpenAlex
- W2134193049
- Cited by
- 960
- References
- 49
- Citations by year
- 2026: 17 · 2025: 30 · 2024: 24 · 2023: 36 · 2022: 51 · 2021: 66 · 2020: 58 · 2019: 53 · 2018: 63 · 2017: 68 · 2016: 82 · 2015: 85 · 2014: 88 · 2013: 69 · 2012: 79
- FWCI
- 22.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1390 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Developmental Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Donald W. Reynolds Foundation
- American Heart Association
- National Institutes of Health
- Fondation Leducq
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Keywords
- intronic microRNA, miR-208a, miR-208b, miR-499, MYH6, MYH7, MYH7B, myocardium, muscle performance, transcriptional repressor, muscle gene expression
- MeSH terms
- Animals, Base Sequence, Cell Line, Chlorocebus aethiops, Muscle, Skeletal, Gene Expression Regulation, Developmental, Myosin Heavy Chains, Myosin Type II, Cardiac Myosins, MicroRNAs, Mice
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