ArticleScientific reports2015
Sox2-CreER mice are useful for fate mapping of mature, but not neonatal, cochlear supporting cells in hair cell regeneration studies.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- The aryl hydrocarbon receptor is expressed in non-sensory cells in the cochlea and regulates hair cell survival.Frontiers in molecular neuroscience · 2026Article
- Conditional Overexpression of Neuritin in Supporting Cell Protects Cochlear Hair Cell and Delays Age-Related Hearing Loss by Enhancing Autophagy.International journal of molecular sciences · 2025Article
- Abnormal Innervation, Demyelination, and Degeneration of Spiral Ganglion Neurons as Well as Disruption of Heminodes are Involved in the Onset of Deafness in Cx26 Null Mice.Neuroscience bulletin · 2024Article
- Deletion of the Notch ligand Jagged1 during cochlear maturation leads to inner hair cell defects and hearing loss.Cell death & disease · 2022Article
- Molecular Pathways Modulating Sensory Hair Cell Regeneration in Adult Mammalian Cochleae: Progress and Perspectives.International journal of molecular sciences · 2021Review
- A cell-type-specific atlas of the inner ear transcriptional response to acoustic trauma.Cell reports · 2021Article
- Cell Type-Specific Expression Analysis of the Inner Ear: A Technical Report.The Laryngoscope · 2021Article
- GATA3 maintains the quiescent state of cochlear supporting cells by regulating p27Scientific reports · 2021Article
- Cochlear supporting cells require GAS2 for cytoskeletal architecture and hearing.Developmental cell · 2021Article
- Expression of a membrane-targeted fluorescent reporter disrupts auditory hair cell mechanoelectrical transduction and causes profound deafness.Hearing research · 2021Article
- TUB and ZNF532 Promote the Atoh1-Mediated Hair Cell Regeneration in Mouse Cochleae.Frontiers in cellular neuroscience · 2021Article
- The Notch Ligand Jagged1 Is Required for the Formation, Maintenance, and Survival of Hensen's Cells in the Mouse Cochlea.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Dibenzazepine promotes cochlear supporting cell proliferation and hair cell regeneration in neonatal mice.Cell proliferation · 2020Article
- Characterization of the transcriptomes ofAmerican journal of stem cells · 2020Article
- Multiple supporting cell subtypes are capable of spontaneous hair cell regeneration in the neonatal mouse cochlea.Development (Cambridge, England) · 2019Article
- SOX2 is required for inner ear neurogenesis.Scientific reports · 2017Article
- Cochlear hair cell regeneration after noise-induced hearing loss: Does regeneration follow development?Hearing research · 2017Review
- Quantitative Analysis of Supporting Cell Subtype Labeling Among CreER Lines in the Neonatal Mouse Cochlea.Journal of the Association for Research in Otolaryngology : JARO · 2017Article
- Gfi1Scientific reports · 2017Article
- Dual role for Sox2 in specification of sensory competence and regulation of Atoh1 function.Developmental neurobiology · 2017Article
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3 authors.
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Abstract
Studies of hair cell regeneration in the postnatal cochlea rely on fate mapping of supporting cells. Here we characterized a Sox2-CreER knock-in mouse line with two independent reporter mouse strains at neonatal and mature ages. Regardless of induction age, reporter expression was robust, with CreER activity being readily detectable in >85% of supporting cells within the organ of Corti. When induced at postnatal day (P) 28, Sox2-CreER activity was exclusive to supporting cells demonstrating its utility for fate mapping studies beyond this age. However, when induced at P1, Sox2-CreER activity was also detected in >50% of cochlear hair cells, suggesting that Sox2-CreER may not be useful to fate map a supporting cell origin of regenerated hair cells if induced at neonatal ages. Given that this model is currently in use by several investigators for fate mapping purposes, and may be adopted by others in the future, our finding that current protocols are effective for restricting CreER activity to supporting cells at mature but not neonatal ages is both significant and timely.
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