ArticlePloS one2012
Inner ear morphology is perturbed in two novel mouse models of recessive deafness.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Limited Potential to Reverse Deafness Caused by Mutation of Myo7a.Journal of the Association for Research in Otolaryngology : JARO · 2026Article
- NGS-based identification of a MYO7A mutation in a Korean family with DFNB2, a subtype of autosomal recessive non-syndromic hearing loss.Genes & genomics · 2025Article
- Current approaches for Usher syndrome disease models and developing therapies.Frontiers in cell and developmental biology · 2025Review
- Clinical Heterogeneity Associated withBiomedicines · 2022Article
- Article
- Usher Syndrome: Genetics of a Human Ciliopathy.International journal of molecular sciences · 2021Review
- Usher Syndrome: Genetics and Molecular Links of Hearing Loss and Directions for Therapy.Frontiers in genetics · 2020Review
- A Novel Mouse Model ofFrontiers in neuroscience · 2019Article
- Comparative analysis of the domestic cat genome reveals genetic signatures underlying feline biology and domestication.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Eeyore: a novel mouse model of hereditary deafness.PloS one · 2013Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human MYO7A mutations can cause a variety of conditions involving the inner ear. These include dominant and recessive non-syndromic hearing loss and syndromic conditions such as Usher syndrome. Mouse models of deafness allow us to investigate functional pathways involved in normal and abnormal hearing processes. We present two novel mouse models with mutations in the Myo7a gene with distinct phenotypes. The mutation in Myo7a(I487N/I487N) ewaso is located within the head motor domain of Myo7a. Mice exhibit a profound hearing loss and manifest behaviour associated with a vestibular defect. A mutation located in the linker region between the coiled-coil and the first MyTH4 domains of the protein is responsible in Myo7a(F947I/F947I) dumbo. These mice show a less severe hearing loss than in Myo7a(I487N/I487N) ewaso; their hearing loss threshold is elevated at 4 weeks old, and progressively worsens with age. These mice show no obvious signs of vestibular dysfunction, although scanning electron microscopy reveals a mild phenotype in vestibular stereocilia bundles. The Myo7a(F947I/F947I) dumbo strain is therefore the first reported Myo7a mouse model without an overt vestibular phenotype; a possible model for human DFNB2 deafness. Understanding the molecular basis of these newly identified mutations will provide knowledge into the complex genetic pathways involved in the maintenance of hearing, and will provide insight into recessively inherited sensorineural hearing loss in humans.
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