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bioRxiv · 10.64898/2026.06.03.729765

Galectin and Myc enable cochlear progenitor expansion in vitro and in vivo

Kubota, M.·Abitbol, J. M.·Lee, P. K.·Matern, M. S.·Bustos Barocio, S.·Jan, T. A.·Cheng, A.·Heller, S.
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Abstract

The neonatal cochlear epithelium harbors regenerative capacity, attributable to the transient greater epithelial ridge (GER). After injury, GER cells re-enter the cell cycle, migrate into the damaged organ of Corti, and differentiate into sensory or supporting cells in vivo; in culture, they proliferate to form inner ear organoids. The mechanisms underlying this competence remain unclear. Here, we generated organoids from mouse GER cells and performed single-cell transcriptomics at organoid initiation. Analysis revealed extracellular matrix reorganization with prominent involvement of galectins. Pharmacological inhibition reduced organoid growth, whereas overexpression of galectin-1 or Myc enhanced growth, identifying both factors as regulators of cochlear progenitor expansion. Moreover, Myc overexpression conferred organoid-forming capacity in post-neonatal cochlear epithelial cells after hearing onset, thereby extending the time window for regenerative competence. In vivo, organ of Corti ablation induced galectin-1 upregulation and GER proliferation, suppressed by galectin-1 blockade, establishing a model to rekindle proliferative potential in mature cochlear cells.

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Kubota, M., Abitbol, J. M., Lee, P. K., Matern, M. S., Bustos Barocio, S., Jan, T. A., Cheng, A., Heller, S.. 2026-06-07. Galectin and Myc enable cochlear progenitor expansion in vitro and in vivo. https://doi.org/10.64898/2026.06.03.729765

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