ArticleDisease models & mechanisms
Deficient forward transduction and enhanced reverse transduction in the alpha tectorin C1509G human hearing loss mutation.
Article in Disease models & mechanisms. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A genome-wide meta-analysis uncovers six sequence variants conferring risk of vertigo.Communications biology · 2021Pooled it
- TECTB Variants Reveal Tectorial Membrane Vulnerability in Dominant Non-Syndromic Hearing Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ThemedRxiv : the preprint server for health sciences · 2025Article
- Infrared light stimulates the cochlea through a mechanical displacement detected and amplified by hair cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Kölliker's Organ Functions as a Developmental Hub in Mouse Cochlea Regulating Spiral Limbus and Tectorial Membrane Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Endolymphatic hydrops and cochlear synaptopathy after noise exposure are distinct sequelae of hair cell stereociliary bundle trauma.Scientific reports · 2024Article
- Targeting the NLRP3 inflammasome in cochlear macrophages protects against hearing loss in chronic suppurative otitis media.Journal of neuroinflammation · 2024Article
- Chemokine Receptor CCR2 Is Protective toward Outer Hair Cells in Chronic Suppurative Otitis Media.ImmunoHorizons · 2024Article
- The impact of targeted ablation of one row of outer hair cells and Deiters' cells on cochlear amplification.Journal of neurophysiology · 2022Article
- PRDM16 expression and function in mammalian cochlear development.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Overturning the mechanisms of cochlear amplification via area deformations of the organ of Corti.The Journal of the Acoustical Society of America · 2022Article
- Unloading outer hair cell bundles in vivo does not yield evidence of spontaneous oscillations in the mouse cochlea.Hearing research · 2022Article
- Spontaneous otoacoustic emissions are biomarkers for mice with tectorial membrane defects.Hearing research · 2021Article
- Article
- Congenital Deafness and Recent Advances Towards Restoring Hearing Loss.Current protocols · 2021Article
- In Vivo Cochlear imaging provides a tool to study endolymphatic hydrops.Journal of vestibular research : equilibrium & orientation · 2021Article
- Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure.Frontiers in cell and developmental biology · 2021Article
- The release of surface-anchored α-tectorin, an apical extracellular matrix protein, mediates tectorial membrane organization.Science advances · 2019Article
- The Tectorial Membrane: Mechanical Properties and Functions.Cold Spring Harbor perspectives in medicine · 2019Review
- Organ of Corti vibration within the intact gerbil cochlea measured by volumetric optical coherence tomography and vibrometry.Journal of neurophysiology · 2018Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Most forms of hearing loss are associated with loss of cochlear outer hair cells (OHCs). OHCs require the tectorial membrane (TM) for stereociliary bundle stimulation (forward transduction) and active feedback (reverse transduction). Alpha tectorin is a protein constituent of the TM and the C1509G mutation in alpha tectorin in humans results in autosomal dominant hearing loss. We engineered and validated this mutation in mice and found that the TM was shortened in heterozygous Tecta(C1509G/+) mice, reaching only the first row of OHCs. Thus, deficient forward transduction renders OHCs within the second and third rows non-functional, producing partial hearing loss. Surprisingly, both Tecta(C1509G/+) and Tecta(C1509G/C1509G) mice were found to have increased reverse transduction as assessed by sound- and electrically-evoked otoacoustic emissions. We show that an increase in prestin, a protein necessary for electromotility, in all three rows of OHCs underlies this phenomenon. This mouse model demonstrates a human hearing loss mutation in which OHC function is altered through a non-cell-autonomous variation in prestin.
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