ArticlePloS one2016
Transgenic Expression of the Formin Protein Fhod3 Selectively in the Embryonic Heart: Role of Actin-Binding Activity of Fhod3 and Its Sarcomeric Localization during Myofibrillogenesis.
Article in PloS one, 2016. 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, 27 citations in OpenAlex.
- Empowering genetic discoveries and cardiovascular risk assessment by predicting electrocardiograms from genotype.NPJ digital medicine · 2026Article
- Human formin FHOD3-mediated actin elongation is required for sarcomere integrity in cardiomyocytes.eLife · 2025Article
- FHOD-1 and profilin protect sarcomeres against contraction-induced deformation> inMolecular biology of the cell · 2024Article
- FHOD-1/profilin-mediated actin assembly protects sarcomeres against contraction-induced deformation inbioRxiv : the preprint server for biology · 2024Article
- Altered Fhod3 expression involved in progressive high-frequency hearing loss via dysregulation of actin polymerization stoichiometry in the cuticular plate.PLoS genetics · 2024Article
- FHODs: Nuclear tethered formins for nuclear mechanotransduction.Frontiers in cell and developmental biology · 2023Review
- The Mechanisms of Thin Filament Assembly and Length Regulation in Muscles.International journal of molecular sciences · 2022Review
- Predicting Heart Cell Types by Using Transcriptome Profiles and a Machine Learning Method.Life (Basel, Switzerland) · 2022Article
- Under construction: The dynamic assembly, maintenance, and degradation of the cardiac sarcomere.Journal of molecular and cellular cardiology · 2020Review
- FHOD-1 is the only formin in Caenorhabditis elegans that promotes striated muscle growth and Z-line organization in a cell autonomous manner.Cytoskeleton (Hoboken, N.J.) · 2020Article
- Assembly and Maintenance of Sarcomere Thin Filaments and Associated Diseases.International journal of molecular sciences · 2020Review
- Interaction between cardiac myosin-binding protein C and formin Fhod3.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- The actin-organizing formin protein Fhod3 is required for postnatal development and functional maintenance of the adult heart in mice.The Journal of biological chemistry · 2018Article
- Segregated localization of two calponin-related proteins within sarcomeric thin filaments in Caenorhabditis elegans striated muscle.Cytoskeleton (Hoboken, N.J.)Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fhod3 is a cardiac member of the formin family proteins that play pivotal roles in actin filament assembly in various cellular contexts. The targeted deletion of mouse Fhod3 gene leads to defects in cardiogenesis, particularly during myofibrillogenesis, followed by lethality at embryonic day (E) 11.5. However, it remains largely unknown how Fhod3 functions during myofibrillogenesis. In this study, to assess the mechanism whereby Fhod3 regulates myofibrillogenesis during embryonic cardiogenesis, we generated transgenic mice expressing Fhod3 selectively in embryonic cardiomyocytes under the control of the β-myosin heavy chain (MHC) promoter. Mice expressing wild-type Fhod3 in embryonic cardiomyocytes survive to adulthood and are fertile, whereas those expressing Fhod3 (I1127A) defective in binding to actin die by E11.5 with cardiac defects. This cardiac phenotype of the Fhod3 mutant embryos is almost identical to that observed in Fhod3 null embryos, suggesting that the actin-binding activity of Fhod3 is crucial for embryonic cardiogenesis. On the other hand, the β-MHC promoter-driven expression of wild-type Fhod3 sufficiently rescues cardiac defects of Fhod3-null embryos, indicating that the Fhod3 protein expressed in a transgenic manner can function properly to achieve myofibril maturation in embryonic cardiomyocytes. Using the transgenic mice, we further examined detailed localization of Fhod3 during myofibrillogenesis in situ and found that Fhod3 localizes to the specific central region of nascent sarcomeres prior to massive rearrangement of actin filaments and remains there throughout myofibrillogenesis. Taken together, the present findings suggest that, during embryonic cardiogenesis, Fhod3 functions as the essential reorganizer of actin filaments at the central region of maturating sarcomeres via the actin-binding activity of the FH2 domain.
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