ArticlePloS one2013
Expression and function of scleraxis in the developing auditory system.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Advances in biomarkers for differential diagnosis of autoimmune and autoinflammatory inner ear disorders.Molecular biology reports · 2026Review
- The Notch ligand Jagged1 plays a dual role in cochlear hair cell regeneration.Nature communications · 2025Article
- Cryosectioning and Immunostaining Mouse Inner Ear Tissue: From Embryonic to Adult Stages.Journal of visualized experiments : JoVE · 2025Article
- Cochlear transcript diversity and its role in auditory functions implied by an otoferlin short isoform.Nature communications · 2023Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
A study of genes expressed in the developing inner ear identified the bHLH transcription factor Scleraxis (Scx) in the developing cochlea. Previous work has demonstrated an essential role for Scx in the differentiation and development of tendons, ligaments and cells of chondrogenic lineage. Expression in the cochlea has been shown previously, however the functional role for Scx in the cochlea is unknown. Using a Scx-GFP reporter mouse line we examined the spatial and temporal patterns of Scx expression in the developing cochlea between embryonic day 13.5 and postnatal day 25. Embryonically, Scx is expressed broadly throughout the cochlear duct and surrounding mesenchyme and at postnatal ages becomes restricted to the inner hair cells and the interdental cells of the spiral limbus. Deletion of Scx results in hearing impairment indicated by elevated auditory brainstem response (ABR) thresholds and diminished distortion product otoacoustic emission (DPOAE) amplitudes, across a range of frequencies. No changes in either gross cochlear morphology or expression of the Scx target genes Col2A, Bmp4 or Sox9 were observed in Scx(-/-) mutants, suggesting that the auditory defects observed in these animals may be a result of unidentified Scx-dependent processes within the cochlea.
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Registered trials
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