ArticlePloS one2013
MicroRNA-3906 regulates fast muscle differentiation through modulating the target gene homer-1b in zebrafish embryos.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Transcriptome integration analysis revealed that miR-103-3p regulates goat myoblast proliferation by targeting FGF18.BMC genomics · 2025Article
- Genome-wide association study for growth traits with 1066 individuals in largemouth bass (Frontiers in molecular biosciences · 2024Article
- Skeletal muscle feature of different populations in large yellow croaker (Frontiers in molecular biosciences · 2024Article
- Congenital Splay Leg Syndrome in Piglets-Current Knowledge and a New Approach to Etiology.Frontiers in veterinary science · 2021Review
- Functional Non-coding RNA During Embryonic Myogenesis and Postnatal Muscle Development and Disease.Frontiers in cell and developmental biology · 2021Review
- Molecular Mechanisms Regulating Muscle Plasticity in Fish.Animals : an open access journal from MDPI · 2020Review
- Article
- Genome-wide association study identifies candidate genes for piglet splay leg syndrome in different populations.BMC genetics · 2017Article
- Article
- "Muscling" Throughout Life: Integrating Studies of Muscle Development, Homeostasis, and Disease in Zebrafish.Current topics in developmental biology · 2017Review
- Zebrafish and Medaka: new model organisms for modern biomedical research.Journal of biomedical science · 2016Review
- miR-487b, miR-3963 and miR-6412 delay myogenic differentiation in mouse myoblast-derived C2C12 cells.BMC cell biology · 2015Article
- Noncoding RNAs, Emerging Regulators of Skeletal Muscle Development and Diseases.BioMed research international · 2015Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A microRNA, termed miR-In300 or miR-3906, suppresses the transcription of myf5 through silencing dickkopf-related protein 3 (dkk3r/dkk3a) during early development when myf5 is highly transcribed, but not at late stages when myf5 transcription is reduced. Moreover, after 24 hpf, when muscle cells are starting to differentiate, Dkk3a could not be detected in muscle tissue at 20 hpf. To explain these reversals, we collected embryos at 32 hpf, performed assays, and identified homer-1b, which regulates calcium release from sarcoplasmic reticulum, as the target gene of miR-3906. We further found that either miR-3906 knockdown or homer-1b overexpression increased expressions of fmhc4 and atp2a1 of calcium-dependent fast muscle fibrils, but not slow muscle fibrils, and caused a severe disruption of sarcomeric actin and Z-disc structure. Additionally, compared to control embryos, the intracellular calcium concentration ([Ca(2+)]i) of these treated embryos was increased as high as 83.9-97.3% in fast muscle. In contrast, either miR-3906 overexpression or homer-1b knockdown caused decreases of [Ca(2+)]i and, correspondingly, defective phenotypes in fast muscle. These defects could be rescued by inducing homer-1b expression at later stage. These results indicate that miR-3906 controls [Ca(2+)]i homeostasis in fast muscle through fine tuning homer-1b expression during differentiation to maintain normal muscle development.
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