ArticlePloS one2014
Expression and functional characterization of Smyd1a in myofibril organization of skeletal muscles.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024Review
- Lysine methylation signaling in skeletal muscle biology: from myogenesis to clinical insights.The Biochemical journal · 2023Review
- Article
- Smyd1 is essential for myosin expression and sarcomere organization in craniofacial, extraocular, and cardiac muscles.Journal of genetics and genomics = Yi chuan xue bao · 2021Article
- Function of the MYND Domain and C-Terminal Region in Regulating the Subcellular Localization and Catalytic Activity of the SMYD Family Lysine Methyltransferase Set5.Molecular and cellular biology · 2020Article
- Defective sarcomere assembly inFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Zebrafish Embryonic Slow Muscle Is a Rapid System for Genetic Analysis of Sarcomere Organization by CRISPR/Cas9, but Not NgAgo.Marine biotechnology (New York, N.Y.) · 2018Article
- The Smyd Family of Methyltransferases: Role in Cardiac and Skeletal Muscle Physiology and Pathology.Current opinion in physiology · 2018Article
- Overexpression of the double homeodomain protein DUX4c interferes with myofibrillogenesis and induces clustering of myonuclei.Skeletal muscle · 2018Article
- Mouse myofibers lacking the SMYD1 methyltransferase are susceptible to atrophy, internalization of nuclei and myofibrillar disarray.Disease models & mechanisms · 2016Article
- Article
- Homologous Transcription Factors DUX4 and DUX4c Associate with Cytoplasmic Proteins during Muscle Differentiation.PloS one · 2016Article
- Master redox regulator Trx1 upregulates SMYD1 & modulates lysine methylation.Biochimica et biophysica acta · 2015Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSmyd1, the founding member of the Smyd family including Smyd-1, 2, 3, 4 and 5, is a SET and MYND domain containing protein that plays a key role in myofibril assembly in skeletal and cardiac muscles. Bioinformatic analysis revealed that zebrafish genome contains two highly related smyd1 genes, smyd1a and smyd1b. Although Smyd1b function is well characterized in skeletal and cardiac muscles, the function of Smyd1a is, however, unknown. METHODOLOGY/PRINCIPAL
findingsTo investigate the function of Smyd1a in muscle development, we isolated smyd1a from zebrafish, and characterized its expression and function during muscle development via gene knockdown and transgenic expression approaches. The results showed that smyd1a was strongly expressed in skeletal muscles of zebrafish embryos. Functional analysis revealed that knockdown of smyd1a alone had no significant effect on myofibril assembly in zebrafish skeletal muscles. However, knockdown of smyd1a and smyd1b together resulted in a complete disruption of myofibril organization in skeletal muscles, a phenotype stronger than knockdown of smyd1a or smyd1b alone. Moreover, ectopic expression of zebrafish smyd1a or mouse Smyd1 transgene could rescue the myofibril defects from the smyd1b knockdown in zebrafish embryos. CONCLUSION/SIGNIFICANCE: Collectively, these data indicate that Smyd1a and Smyd1b share similar biological activity in myofibril assembly in zebrafish embryos. However, Smyd1b appears to play a major role in this process.
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