ArticleDevelopment (Cambridge, England)2007
Mef2s are required for thick filament formation in nascent muscle fibres.
Article in Development (Cambridge, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
68 citing papers in PubMed, 135 citations in OpenAlex.
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- Characterization of myogenesis in European sea bass (Dicentrarchus labrax) using primary white muscle cell cultures.Scientific reports · 2025Article
- 3D-environment and muscle contraction regulate the heterogeneity of myonuclei.Skeletal muscle · 2024Article
- Slow myosin heavy chain 1 is required for slow myofibril and muscle fibre growth but not for myofibril initiation.Developmental biology · 2023Article
- Differentiation and Maturation of Muscle and Fat Cells in Cultivated Seafood: Lessons from Developmental Biology.Marine biotechnology (New York, N.Y.) · 2023Review
- Phosphorylation of the Myogenic Factor Myocyte Enhancer Factor-2 Impacts Myogenesis In Vivo.Molecular and cellular biology · 2023Article
- The LIM domain protein nTRIP6 modulates the dynamics of myogenic differentiation.Scientific reports · 2021Article
- Knockout of zebrafish desmin genes does not cause skeletal muscle degeneration but alters calcium flux.Scientific reports · 2021Article
- Mef2c factors are required for early but not late addition of cardiomyocytes to the ventricle.Developmental biology · 2021Article
- The Effect of Mechanical Stretch on Myotube Growth Suppression by Colon-26 Tumor-Derived Factors.Frontiers in cell and developmental biology · 2021Article
- Article
- Exploring the Expression of Cardiac Regulators in a Vertebrate Extremophile: The Cichlid FishJournal of developmental biology · 2020Article
- Scleraxis genes are required for normal musculoskeletal development and for rib growth and mineralization in zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Common CarpGenes · 2019Article
- EGF receptor (EGFR) inhibition promotes a slow-twitch oxidative, over a fast-twitch, muscle phenotype.Scientific reports · 2019Article
- Myogenin promotes myocyte fusion to balance fibre number and size.Nature communications · 2018Article
- Lack of cyclin D3 induces skeletal muscle fiber-type shifting, increased endurance performance and hypermetabolism.Scientific reports · 2018Article
- Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
During skeletal muscle differentiation, the actomyosin motor is assembled into myofibrils, multiprotein machines that generate and transmit force to cell ends. How expression of muscle proteins is coordinated to build the myofibril is unknown. Here we show that zebrafish Mef2d and Mef2c proteins are required redundantly for assembly of myosin-containing thick filaments in nascent muscle fibres, but not for the earlier steps of skeletal muscle fibre differentiation, elongation, fusion or thin filament gene expression. mef2d mRNA and protein is present in myoblasts, whereas mef2c expression commences in muscle fibres. Knockdown of both Mef2s with antisense morpholino oligonucleotides or in mutant fish blocks muscle function and prevents sarcomere assembly. Cell transplantation and heat-shock-driven rescue reveal a cell-autonomous requirement for Mef2 within fibres. In nascent fibres, Mef2 drives expression of genes encoding thick, but not thin, filament proteins. Among genes analysed, myosin heavy and light chains and myosin-binding protein C require Mef2 for normal expression, whereas actin, tropomyosin and troponin do not. Our findings show that Mef2 controls skeletal muscle formation after terminal differentiation and define a new maturation step in vertebrate skeletal muscle development at which thick filament gene expression is controlled.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.