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mTORC1的过度活化阻断了通过TFE3-NuRD关联的干细胞命运过渡
Peizhi Li1,2, Shuhui Xu1,3, Xinyu Wu1
1Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences; Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, Guangzhou, 510530, China.
EMBO reports
|January 20, 2026
概括
拉巴胺素复合体1 (mTORC1) 过激活的机械标通过促进TFE3核转位来阻止干细胞重编程. 然后TFE3招募NuRD来抑制关键基因,揭示了控制细胞命运的共享机制.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 干细胞生物学 干细胞生物学
背景情况:
- 拉巴胺素复合体1 (mTORC1) 的机械标是细胞生长和新陈代谢的中央调节者,集成营养和生长因子信号.
- 失调的mTORC1信号破坏干细胞平衡,损害细胞命运过渡,影响发育,衰老和癌症等疾病.
- 以前的研究表明mTORC1过度激活阻断多能性退出和体细胞重编程,但潜在的转录机制尚不清楚.
研究的目的:
- 阐明mTORC1过度激活控制干细胞转换期间基因转录的分子机制.
- 研究TFE3在调解mTORC1在多能性退出和体细胞重编程过程中诱导的转录阻塞中的作用.
主要方法:
- 使用了老鼠和人类原始胚胎干细胞.
- 调查了TFE3.3的核转移情况.
- 分析了NuRD核心压力复合物的招募.
- 研究了对细胞命运过渡至关重要的基因的抑制.
主要成果:
- 证明TFE3调解了在重编程过程中mTORC1过度激活引起的转录阻塞.
- 表明TFE3在mTORC1过度激活时转移到核中,阻止多能性退出.
- 证实TFE3招募NuRD核心压缩复合体,在多能性退出和重编程过程中抑制细胞命运转换所必需的基因.
结论:
- 发现了mTORC1和TFE3参与调节干细胞身份和命运的共享机制.
- 突出了TFE3作为转录调节器在控制细胞命运过渡中的双重作用.
- 表明这种调节途径在发育,衰老和瘤发生方面的潜在影响.
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