ArticleProceedings of the National Academy of Sciences of the United States of America2011
Myosin VIIa and sans localization at stereocilia upper tip-link density implicates these Usher syndrome proteins in mechanotransduction.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 2 of them syntheses that pooled it.
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Who cites it
134 citing papers in PubMed, 2 syntheses or guidelines pooled it, 200 citations in OpenAlex.
- Discovering Age- and Sex-Specific Genetic Risk Factors in Sensorineural Hearing Loss: Genome-Wide Evidence from Large-Scale Biobanks.Journal of the Association for Research in Otolaryngology : JARO · 2026Pooled it
- Genome-wide association analysis on normal hearing function identifies PCDH20 and SLC28A3 as candidates for hearing function and loss.Human molecular genetics · 2015Pooled it
- Limited Potential to Reverse Deafness Caused by Mutation of Myo7a.Journal of the Association for Research in Otolaryngology : JARO · 2026Article
- PIPbioRxiv : the preprint server for biology · 2026Article
- Molecular identity of the mechanotransduction machinery in inner ear hair cells and mechanotransduction-linked hearing loss.Fundamental research · 2026Review
- Tonotopic specialization of MYO7A isoforms in auditory hair cells.Nature communications · 2026Article
- A regulatory axis for tonotopic MYO7A expression in cochlear hair cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Myosin 7a is required for maintaining the transducing stereocilia and for force transmission to the MET channel during cochlear hair cell development.The Journal of physiology · 2026Article
- HomozygousTranslational andrology and urology · 2026Article
- A novel duplication mutation in the MYO7A gene associated with autosomal recessive hearing loss in a Chinese family.Genes & genomics · 2026Article
- Compound heterozygous splicing and missense variants inFrontiers in medicine · 2026Article
- Liquid-Liquid Phase Separation in Hereditary Hearing Loss.Neuroscience bulletin · 2025Review
- Spontaneous calcium transients in hair cell stereocilia.Scientific reports · 2025Article
- Single-molecule fluorescence microscopy reveals regulatory mechanisms of MYO7A-driven cargo transport in stereocilia of live inner ear hair cells.Nature communications · 2025Article
- 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
- Influence of Myosin Regulatory Light Chain and Myosin Light Chain Kinase on the Physiological Function of Inner Ear Hair Cells.Journal of the Association for Research in Otolaryngology : JARO · 2025Article
- Select autosomal dominant DFNA11 deafness variants activate Myo7A targeting in epithelial cells.Journal of cell science · 2025Article
- MYO7A is required for the functional integrity of the mechanoelectrical transduction complex in hair cells of the adult cochlea.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Current approaches for Usher syndrome disease models and developing therapies.Frontiers in cell and developmental biology · 2025Review
74 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
In the most accepted model for hair cell mechanotransduction, a cluster of myosin motors located at the stereocilia upper tip-link density (UTLD) keeps the tip-link under tension at rest. Both myosin VIIa (MYO7A) and myosin 1c have been implicated in mechanotransduction based on functional studies. However, localization studies are conflicting, leaving open the question of which myosin localizes at the UTLD and generates the tip-link resting tension. Using immunofluorescence, we now show that MYO7A and sans, a MYO7A-interacting protein, cluster at the UTLD. Analysis of the immunofluorescence intensity indicates that eight or more MYO7A molecules are present at each UTLD, consistent with a direct role for MYO7A in maintaining tip-link tension. MYO7A and sans localization at the UTLD is confirmed by transfection of hair cells with GFP-tagged constructs for these proteins. Cotransfection studies in a heterologous system show that MYO7A, sans, and the UTLD protein harmonin-b form a tripartite complex and that each protein is capable of interacting with one another independently. We propose that MYO7A, sans, and harmonin-b form the core components of the UTLD molecular complex. In this complex, MYO7A is likely the motor element that pulls on CDH23 to exert tension on the tip-link.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.