SOX10 抑制出生後小鼠耳蝸中異位感覺斑塊的形成

// SOX10 restricts the formation of ectopic sensory patches in the postnatal mouse cochlea

出生時於Sox10rtTA/+小鼠以多西環素誘導激活Notch，耳蜗非感覺細胞沿管腔增生並再入細胞週期，產生異位前感覺（prosensory）斑，並出現類毛細胞與支持細胞身分改變｜前感覺標記（如Sox2）誘導能力與Notch活性呈劑量相關｜缺失一個Sox10等位基因提高表現型滲透率，顯示Notch–SOX10協同調控內耳細胞命運，具再生與修復應用潛力

// They tested whether activating Notch signaling in the neonatal mouse cochlea (using a doxycycline‑inducible Notch system in Sox10rtTA/+ knock‑in mice) can reinitiate prosensory specification. Notch activation at birth caused hyperplasia and cell‑cycle reentry of non‑sensory cells along the cochlear duct, producing ectopic prosensory patches with hair cell–like cells and altered supporting‑cell identities. Competence to induce prosensory markers (e.g., Sox2) scaled with Notch level, and loss of one Sox10 allele increased phenotype penetrance, showing Notch–SOX10 interactions regulate cellular identity in the developing inner ear.

Published 2026年9月1日