ArticleFrontiers of medicine2019
Tprn is essential for the integrity of stereociliary rootlet in cochlear hair cells in mice.
Article in Frontiers of medicine, 2019. 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, 14 citations in OpenAlex.
- Taperin bundles F-actin at stereocilia pivot points enabling optimal lifelong mechanosensitivity.The Journal of cell biology · 2025Article
- Evidence of early genomic selection in Holstein Friesian across African and European ecosystems.BMC genomics · 2025Article
- Cochlear Implantation Outcomes in Genotyped Subjects with Sensorineural Hearing Loss.Journal of the Association for Research in Otolaryngology : JARO · 2025Article
- Dominant effect of a single amino acid mutation in the motor domain of myosin VI on hearing in mice.Experimental animals · 2025Article
- 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
- Reducing Taperin Expression Restores Hearing in Grxcr2 Mutant Mice.Neuroscience · 2022Article
- Investigation of the effects of downregulation of jumping translocation breakpoint (JTB) protein expression in MCF7 cells for potential use as a biomarker in breast cancer.American journal of cancer research · 2022Article
- AJournal of medical genetics · 2020Article
- Stereocilia Rootlets: Actin-Based Structures That Are Essential for Structural Stability of the Hair Bundle.International journal of molecular sciences · 2020Review
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tprn encodes the taperin protein, which is concentrated in the tapered region of hair cell stereocilia in the inner ear. In humans, TPRN mutations cause autosomal recessive nonsyndromic deafness (DFNB79) by an unknown mechanism. To determine the role of Tprn in hearing, we generated Tprn-null mice by clustered regularly interspaced short palindromic repeat/Cas9 genome-editing technology from a CBA/CaJ background. We observed significant hearing loss and progressive degeneration of stereocilia in the outer hair cells of Tprn-null mice starting from postnatal day 30. Transmission electron microscopy images of stereociliary bundles in the mutant mice showed some stereociliary rootlets with curved shafts. The central cores of the stereociliary rootlets possessed hollow structures with surrounding loose peripheral dense rings. Radixin, a protein expressed at stereocilia tapering, was abnormally dispersed along the stereocilia shafts in Tprn-null mice. The expression levels of radixin and β-actin significantly decreased.We propose that Tprn is critical to the retention of the integrity of the stereociliary rootlet. Loss of Tprn in Tprn-null mice caused the disruption of the stereociliary rootlet, which resulted in damage to stereociliary bundles and hearing impairments. The generated Tprn-null mice are ideal models of human hereditary deafness DFNB79.
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