一个表观遗传抑制剂TRIM66决定了单一的嗅觉受体表达,神经活动和嗅觉行为
Hongqiang Bao1,2, Rong Liu1,2, Yalei Kong1,2
1Department of Otolaryngology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Nature communications
|December 12, 2025
概括
研究人员确定TRIM66是嗅觉受体基因选择中的关键抑制剂. 在嗅觉感官神经元 (OSN) 中删除Trim66会破坏嗅觉受体基因的沉默,影响嗅觉处理和行为.
科学领域:
- 神经科学是一个神经科学.
- 遗传学 是一个遗传学.
- 分子生物学分子生物学
背景情况:
- 嗅觉受体 (OR) 基因选择是一种复杂的单基因和单基因表达过程.
- 不成熟的嗅觉感官神经元 (OSN) 表达多个OR基因,在成熟过程中静止除了一个外的所有OR基因.
- 控制这种沉默的分子机制和抑制器在很大程度上是未知的.
研究的目的:
- 确定负责沉默额外嗅觉受体基因的分子抑制剂.
- 阐明嗅觉受体基因表达从多基因转变为单基因的机制.
- 为了研究受损嗅觉受体基因沉默的功能后果.
主要方法:
- 在小鼠模型中利用了Trim66的遗传删除.
- 在单个成熟的嗅觉感官神经元 (OSN) 中分析了基因表达.
- 研究了TRIM66与嗅觉受体增强剂的分子相互作用.
主要成果:
- TRIM66被确定为嗅觉受体基因表达的关键抑制剂.
- 删除Trim66导致在成熟的OSN中保留多个OR基因.
- TRIM66与嗅觉受体增强剂结合并抑制它们,使额外的OR基因沉默.
- 删除Trim66导致了嗅觉信息处理和先天性行为的重大缺陷.
结论:
- TRIM66是从多基因到单基因嗅觉受体表达过渡的关键分子参与者.
- 在适当的嗅觉感官神经元功能和行为中,TRIM66介导的抑制是必不可少的.
- 这项研究确定了理解嗅觉基因选择调节的缺失环节.
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