ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Otoferlin couples to clathrin-mediated endocytosis in mature cochlear inner hair cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 93 citations in OpenAlex.
- OTOF Promotes Clear Cell Renal Cell Carcinoma Progression and Angiogenesis Through AKT-Dependent HIF/VEGFA Signaling.Cancers · 2026Article
- Functional, sustained recovery of hearing in Otoferlin-deficient mice using DB-OTO, a hair-cell-specific AAV-based gene therapy.Molecular therapy. Methods & clinical development · 2025Article
- Structure and function of otoferlin, a synaptic protein of sensory hair cells essential for hearing.Science advances · 2025Article
- Expression of nestin, parvalbumin and otoferlin during cochlear development in the mouse: an immunofluorescence study.European journal of histochemistry : EJH · 2025Article
- Proteomic analysis of Buffalo milk somatic cells reveals metabolomic and immunological transitions during early lactation.Scientific reports · 2025Article
- Structural insights into lipid membrane binding by human ferlins.The EMBO journal · 2025Article
- miR-145b/AP2B1 Axis Contributes to Noise-induced Sensorineural Hearing Loss In a Male Mouse Model.Cell biochemistry and biophysics · 2025Article
- DMXL2 Is Required for Endocytosis and Recycling of Synaptic Vesicles in Auditory Hair Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Cochlear transcript diversity and its role in auditory functions implied by an otoferlin short isoform.Nature communications · 2023Article
- Probing the role of the CFrontiers in molecular neuroscience · 2023Article
- Otoferlin as a multirole CaFrontiers in cellular neuroscience · 2023Review
- Truncation of the otoferlin transmembrane domain alters the development of hair cells and reduces membrane docking.Molecular biology of the cell · 2021Article
- Quantitative FluorescentFrontiers in cellular neuroscience · 2021Article
- The Many Faces of DFNB9: RelatingGenes · 2020Review
- Molecular Assembly and Structural Plasticity of Sensory Ribbon Synapses-A Presynaptic Perspective.International journal of molecular sciences · 2020Review
- Functions of Vertebrate Ferlins.Cells · 2020Review
- Synaptojanin2 Mutation Causes Progressive High-frequency Hearing Loss in Mice.Frontiers in cellular neuroscience · 2020Article
- Guanylyl Cyclase A/cGMP Signaling Slows Hidden, Age- and Acoustic Trauma-Induced Hearing Loss.Frontiers in aging neuroscience · 2020Article
- Hair Cell Afferent Synapses: Function and Dysfunction.Cold Spring Harbor perspectives in medicine · 2019Review
- Otoferlin Depletion Results in Abnormal Synaptic Ribbons and Altered Intracellular Calcium Levels in Zebrafish.Scientific reports · 2019Article
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
The encoding of auditory information with indefatigable precision requires efficient resupply of vesicles at inner hair cell (IHC) ribbon synapses. Otoferlin, a transmembrane protein responsible for deafness in DFNB9 families, has been postulated to act as a calcium sensor for exocytosis as well as to be involved in rapid vesicle replenishment of IHCs. However, the molecular basis of vesicle recycling in IHCs is largely unknown. In the present study, we used high-resolution liquid chromatography coupled with mass spectrometry to copurify otoferlin interaction partners in the mammalian cochlea. We identified multiple subunits of the adaptor protein complex AP-2 (CLAP), an essential component of clathrin-mediated endocytosis, as binding partners of otoferlin in rats and mice. The interaction between otoferlin and AP-2 was confirmed by coimmunoprecipitation. We also found that AP-2 interacts with myosin VI, another otoferlin binding partner important for clathrin-mediated endocytosis (CME). The expression of AP-2 in IHCs was verified by reverse transcription PCR. Confocal microscopy experiments revealed that the expression of AP-2 and its colocalization with otoferlin is confined to mature IHCs. When CME was inhibited by blocking dynamin action, real-time changes in membrane capacitance showed impaired synaptic vesicle replenishment in mature but not immature IHCs. We suggest that an otoferlin-AP-2 interaction drives Ca(2+)- and stimulus-dependent compensating CME in mature IHCs.
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