Authors
Lama Khalaily, Shahar Kasirer, Rotem Domb, Mi Zhou, Buwei Shao, Shahar Taiber, Ran Elkon, Litao Tao, David Sprinzak, Karen B Avraham
Published in
Science advances. Volume 12. Issue 25. Pages eaed3887. Jun 19, 2026. Epub Jun 17, 2026.
Abstract
Regeneration enables organisms to repair damaged tissues, yet this capacity is notably limited in the cochlear sensory epithelium, essential for sound detection. A major cause of hearing loss arises from the irreversible loss of sensory hair cells (HCs) in the cochlea. While supporting cells (SCs) have a latent ability to transdifferentiate into HCs, this regenerative potential is rapidly lost after development. Using live imaging and single-cell multiomics of cochlear explants, we uncovered the cellular and molecular heterogeneity underlying the limited regenerative capacity of the neonatal mouse cochlea. Notch repression broadly silenced key SC genes, yet only a rare subpopulation of Deiters' cells (DC), termed transdifferentiating DCs (tDCs), initiated the transdifferentiation into HC fate. These cells underwent coordinated transcriptional and enhancer remodeling, linking epigenetic priming with morphological plasticity, while other SCs remained refractory despite robust Notch targets down-regulation. Our study provides a molecular definition of an early induced transitional DC to HC state, revealing Notch inhibition as a selective trigger that unmasks rare regenerative competence.
PMID:
42308318
Bibliographic data and abstract were imported from PubMed on 18 Jun 2026.
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