ArticleNeural plasticity2018
Knock-In Mice with Myo3a Y137C Mutation Displayed Progressive Hearing Loss and Hair Cell Degeneration in the Inner Ear.
Article in Neural plasticity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Limited Potential to Reverse Deafness Caused by Mutation of Myo7a.Journal of the Association for Research in Otolaryngology : JARO · 2026Article
- The dynamics of actin protrusions can be controlled by tip-localized myosin motors.The Journal of biological chemistry · 2024Article
- The actin cytoskeleton in hair bundle development and hearing loss.Hearing research · 2023Review
- The applications of CRISPR/Cas-mediated genome editing in genetic hearing loss.Cell & bioscience · 2023Review
- Gene therapy: an emerging therapy for hair cells regeneration in the cochlea.Frontiers in neuroscience · 2023Review
- Identification of novel differentially expressed genes in type 1 diabetes mellitus complications using transcriptomic profiling of UAE patients: a multicenter study.Scientific reports · 2022Article
- Selective binding and transport of protocadherin 15 isoforms by stereocilia unconventional myosins in a heterologous expression system.Scientific reports · 2022Article
- Piccolo is essential for the maintenance of mouse retina but not cochlear hair cell function.Aging · 2021Article
- CRISPR-Cas systems: Overview, innovations and applications in human disease research and gene therapy.Computational and structural biotechnology journal · 2020Review
Corrections and comments
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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
Myo3a is expressed in cochlear hair cells and retinal cells and is responsible for human recessive hereditary nonsyndromic deafness (DFNB30). To investigate the mechanism of DFNB30-type deafness, we established a mouse model of Myo3a kinase domain Y137C mutation by using CRISPR/Cas9 system. No difference in hearing between 2-month-old Myo3a mutant mice and wild-type mice was observed. The hearing threshold of the ≥6-month-old mutant mice was significantly elevated compared with that of the wild-type mice. We observed degeneration in the inner ear hair cells of 6-month-old Myo3a mutant mice, and the degeneration became more severe at the age of 12 months. We also found structural abnormality in the cochlear hair cell stereocilia. Our results showed that Myo3a is essential for normal hearing by maintaining the intact structure of hair cell stereocilia, and the kinase domain plays a critical role in the normal functions of Myo3a. This mouse line is an excellent model for studying DFNB30-type deafness in humans.
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