In:
The Journal of Neuroscience, Society for Neuroscience
Abstract:
Early B-cell factor 1 (EBF1) is a basic helix-loop-helix transcription factor essential for the differentiation of various tissues. Our single-cell RNA sequencing data suggest that Ebf1 is expressed in the sensory epithelium of the mouse inner ear. Here, we found that the murine Ebf1 gene and its protein are expressed in the prosensory domain of the inner ear, medial region of the cochlear duct floor, otic mesenchyme, and cochleo-vestibular ganglion. Ebf1 deletion in mice results in incomplete formation of the spiral limbus and scala tympani, increased number of cells in the organ of Corti and Kölliker's organ, and aberrant course of the spiral ganglion axons. Ebf1 deletion in the mouse cochlear epithelia caused the proliferation of SOX2-positive cochlear cells at E13.5, indicating that EBF1 suppresses the proliferation of the prosensory domain and cells of Kölliker's organ to facilitate the development of appropriate numbers of hair and supporting cells. Furthermore, mice with deletion of cochlear epithelium-specific Ebf1 showed poor postnatal hearing function. Our results suggest that Ebf1 is essential for normal auditory function in mammals. Significance statement The elaborate cellular organization and three-layered luminal structure of the mammalian cochlea are essential for normal sound perception, but the developmental process of these structures is not fully understood. The present study revealed the roles of the basic helix-loop-helix type transcription factor Ebf1 in the development of the cochlea. Ebf1 was widely expressed in the inner ear, regulated the proper number of cochlear hair and supporting cells, and was involved in developing scala tympani and spiral limbus. As a result, Ebf1 was necessary for the development of normal hearing. These results suggest the essential roles of Ebf1 in the whole cochlear development and contribute to understanding a part of the complex cochlear development process.
Type of Medium:
Online Resource
ISSN:
0270-6474
,
1529-2401
DOI:
10.1523/JNEUROSCI.1060-23.2023
Language:
English
Publisher:
Society for Neuroscience
Publication Date:
2024
detail.hit.zdb_id:
1475274-8
SSG:
12
Permalink