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<p>The basic helix-loop-helix transcription factors, Neurog1 and Neurod1, orchestrate spiral ganglion neuron (SGN) differentiation in the embryonic cochlea. Their knockout leads to profound SGN and hair cell (HC) loss, cochlear truncation, and hearing impairment. To investigate SGN diversification and lineage origins, we generated three knock-in mouse strains: <i>Neurod1-Cre</i>, <i>Neurod1-iCreER</i>, and <i>Neurog1-iCreER</i>. In <i>Neurod1-Cre</i>; <i>Rosa26-LSL-tdTomato</i> (Ai9) mice, in addition to SGNs, tdTomato<sup>+</sup> HCs and supporting cells were observed, displaying an apical-to-basal gradient. Tamoxifen induction at embryonic day 7.5 (E7.5) also labeled HCs in <i>Neurog1-iCreER/iCreER</i>; Ai9/+ mice at E18.5. Notably, a pure population of SGNs was traced in <i>Neurod1-iCreER/+</i>; Ai9/+ mice with tamoxifen administration from E7.5 to postnatal day 0 (P0). Dose standardization further enabled maximal SGN labeling upon induction at E12.5. These results illuminate the progenitor origins and developmental trajectories of SGNs and HCs, and establish a functional genetic tool for sorting and conditional manipulation of SGNs in auditory research.</p>

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Characteristics and Cell Lineage Tracing of Neurod1-Cre and Neurod1-iCreER Mice Targeting Cochlear Neurons

  • 期刊论文

  • 发表日期：

    2025年12月27日

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  • Zhiji Chen,
  • Xiaoqing Zhou,
  • Ting Yang,
  • Xuelai Liu,
  • Juhong Zhang,
  • Menglong Feng,
  • Shaojing Kuang,
  • Wei Yuan

摘要

The basic helix-loop-helix transcription factors, Neurog1 and Neurod1, orchestrate spiral ganglion neuron (SGN) differentiation in the embryonic cochlea. Their knockout leads to profound SGN and hair cell (HC) loss, cochlear truncation, and hearing impairment. To investigate SGN diversification and lineage origins, we generated three knock-in mouse strains: Neurod1-Cre, Neurod1-iCreER, and Neurog1-iCreER. In Neurod1-Cre; Rosa26-LSL-tdTomato (Ai9) mice, in addition to SGNs, tdTomato+ HCs and supporting cells were observed, displaying an apical-to-basal gradient. Tamoxifen induction at embryonic day 7.5 (E7.5) also labeled HCs in Neurog1-iCreER/iCreER; Ai9/+ mice at E18.5. Notably, a pure population of SGNs was traced in Neurod1-iCreER/+; Ai9/+ mice with tamoxifen administration from E7.5 to postnatal day 0 (P0). Dose standardization further enabled maximal SGN labeling upon induction at E12.5. These results illuminate the progenitor origins and developmental trajectories of SGNs and HCs, and establish a functional genetic tool for sorting and conditional manipulation of SGNs in auditory research.