基因敲除
耳蜗
条件基因敲除
听力损失
细胞生物学
毛细胞
生物
基因表达
内耳
功能(生物学)
基因剔除小鼠
医学
基因
科尔蒂器官
感觉系统
动物模型
神经科学
基因敲除
载体(分子生物学)
HEK 293细胞
基因表达调控
体内
细胞
体外
报告基因
表达式(计算机科学)
基因沉默
作者
Maryna V. Ivanchenko,Kevin T. Booth,K. Domenica Karavitaki,Larisa M. Antonellis,M. Aurel Nagy,Cole W. Peters,Spencer Price,Yaqiao Li,Anton Lytvyn,Andrew Ward,Eric C. Griffith,Siniša Hrvatin,Michael E. Greenberg,David P. Corey
标识
DOI:10.1038/s41467-025-66110-2
摘要
Mutations in the GJB2 gene cause DFNB1, the most common hereditary hearing loss. GJB2 is expressed by cochlear epithelial cells and fibrocytes, but not by sensory hair cells or neurons. Attempts to treat DFNB1 mouse models with gene therapy have not substantially restored function, as inappropriate expression in hair cells and neurons might compromise their electrical activity. Here, we use ATAC-seq to identify candidate gene regulatory elements (GREs) that can drive cell-type-specific expression of GJB2. HA-tagged GJB2, delivered to a conditional knockout mouse with AAV vectors carrying GREs, is expressed by the appropriate cells, prevents degeneration, and rescues hearing by only 10-20 dB. In a Gjb2 partial knockdown model, a vector lacking HA prevents degeneration and completely restores hearing. In cynomolgus monkey cochleas, human GJB2.HA delivered with similar vectors is located in the appropriate cell types and causes little or no compromise of hearing sensitivity. Together, these findings suggest that GRE-mediated expression of GJB2 can prevent hearing loss in DFNB1 patients.
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