Galectin and Myc enable cochlear progenitor expansion in vitro and in vivo
- 1Stanford University
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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BibTeX
@misc{kubota2026galectin,
title = {{Galectin and Myc enable cochlear progenitor expansion in vitro and in vivo}},
author = {M. Kubota and J. M. Abitbol and P. K. Lee and M. S. Matern and S. Bustos Barocio and T. A. Jan and A. Cheng and S. Heller},
howpublished = {bioRxiv},
year = {2026},
month = jun,
doi = {10.64898/2026.06.03.729765},
url = {https://www.biorxiv.org/content/10.64898/2026.06.03.729765v2},
note = {CC BY},
}
RIS
TY - UNPB
TI - Galectin and Myc enable cochlear progenitor expansion in vitro and in vivo
AU - M. Kubota
AU - J. M. Abitbol
AU - P. K. Lee
AU - M. S. Matern
AU - S. Bustos Barocio
AU - T. A. Jan
AU - A. Cheng
AU - S. Heller
PY - 2026
DA - 2026/06/03
PB - bioRxiv
DO - 10.64898/2026.06.03.729765
UR - https://www.biorxiv.org/content/10.64898/2026.06.03.729765v2
AB - 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.
ER -