ArticleProceedings of the National Academy of Sciences of the United States of America2015
The RNA-binding protein LIN28B regulates developmental timing in the mammalian cochlea.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
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- Temporal single-cell atlas of full-length Huntington's disease mouse model defines stage-specific signatures of corticostriatal dysfunction.bioRxiv : the preprint server for biology · 2026Article
- The RNA-binding protein TRIM71 is essential for hearing in humans and mice and times auditory sensory organ development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Analysis of miRNAs from Inner Ear Organoid-Derived Extracellular Vesicles.Journal of the Association for Research in Otolaryngology : JARO · 2025Article
- AAV-Sparcl1 promotes hair cell regeneration by increasing supporting cell plasticity.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- AAV-regulatedMolecular therapy. Nucleic acids · 2024Article
- Roles of supporting cells in the maintenance and regeneration of the damaged inner ear: A literature review.Journal of otology · 2024Review
- EBF1 Limits the Numbers of Cochlear Hair and Supporting Cells and Forms the Scala Tympani and Spiral Limbus during Inner Ear Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Hair Cell Regeneration: From Animals to Humans.Clinical and experimental otorhinolaryngology · 2024Review
- Stem Cell-Based Hair Cell Regeneration and Therapy in the Inner Ear.Neuroscience bulletin · 2024Review
- TRIM71 reactivation enhances the mitotic and hair cell-forming potential of cochlear supporting cells.EMBO reports · 2023Article
- Rps14 upregulation promotes inner ear progenitor proliferation and hair cell regeneration in the neonatal mouse cochlea.Cell proliferation · 2023Article
- Future Pharmacotherapy for Sensorineural Hearing Loss by Protection and Regeneration of Auditory Hair Cells.Pharmaceutics · 2023Review
- The role of LIN28B in tumor progression and metastasis in solid tumor entities.Oncology research · 2023Review
- Emerging Roles of RNA-Binding Proteins in Inner Ear Hair Cell Development and Regeneration.International journal of molecular sciences · 2022Review
- Hearing loss: The final frontier of pharmacology.Pharmacology research & perspectives · 2022Review
- Follistatin promotes LIN28B-mediated supporting cell reprogramming and hair cell regeneration in the murine cochlea.Science advances · 2022Article
- Hippo-Yap/Taz signalling in zebrafish regeneration.NPJ Regenerative medicine · 2022Review
- Cochlear Development; New Tools and Approaches.Frontiers in cell and developmental biology · 2022Review
- Research Progress on the Mechanism of Cochlear Hair Cell Regeneration.Frontiers in cellular neuroscience · 2021Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
Proper tissue development requires strict coordination of proliferation, growth, and differentiation. Strict coordination is particularly important for the auditory sensory epithelium, where deviations from the normal spatial and temporal pattern of auditory progenitor cell (prosensory cell) proliferation and differentiation result in abnormal cellular organization and, thus, auditory dysfunction. The molecular mechanisms involved in the timing and coordination of auditory prosensory proliferation and differentiation are poorly understood. Here we identify the RNA-binding protein LIN28B as a critical regulator of developmental timing in the murine cochlea. We show that Lin28b and its opposing let-7 miRNAs are differentially expressed in the auditory sensory lineage, with Lin28b being highly expressed in undifferentiated prosensory cells and let-7 miRNAs being highly expressed in their progeny-hair cells (HCs) and supporting cells (SCs). Using recently developed transgenic mouse models for LIN28B and let-7g, we demonstrate that prolonged LIN28B expression delays prosensory cell cycle withdrawal and differentiation, resulting in HC and SC patterning and maturation defects. Surprisingly, let-7g overexpression, although capable of inducing premature prosensory cell cycle exit, failed to induce premature HC differentiation, suggesting that LIN28B's functional role in the timing of differentiation uses let-7 independent mechanisms. Finally, we demonstrate that overexpression of LIN28B or let-7g can significantly alter the postnatal production of HCs in response to Notch inhibition; LIN28B has a positive effect on HC production, whereas let-7 antagonizes this process. Together, these results implicate a key role for the LIN28B/let-7 axis in regulating postnatal SC plasticity.
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