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  1. 首页
  3. 通过积极抑制许多非神经元命运来保护神经元身份
  1. 首页
  3. 通过积极抑制许多非神经元命运来保护神经元身份

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通过积极抑制许多非神经元命运来保护神经元身份

Moritz Mall1, Michael S Kareta1, Soham Chanda1,2

  • 1Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, California 94305, USA.

Nature
|April 6, 2017

在PubMed 上查看摘要

概括
此摘要是机器生成的。

Myt1-like (Myt1l) 作为主抑制剂,沉默非神经元基因以维持神经元身份并帮助细胞重编程. 这种泛神经元因子是细胞命运决定和重编程效率的关键.

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Continuous Theta Burst Stimulation of the Posterior Medial Frontal Cortex to Experimentally Reduce Ideological Threat Responses
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11:54

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07:52

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科学领域:

  • 细胞生物学
  • 发育生物学
  • 表观遗传学

背景情况:

  • 细胞重新编程需要沉默捐赠细胞程序.
  • 人们认为,特定的血统抑制剂可以调解这种沉默.
  • 通过常见的重编程因素使多种细胞程序沉默的机制尚不清楚.

研究的目的:

  • 研究Myt1-like (Myt1l) 在神经元重编程和认同中的作用.
  • 确定Myt1l如何沉默多个体系程序.
  • 探索Myt1l在神经元正常发育中的功能.

主要方法:

  • 研究了老鼠纤维细胞对神经元的重新编程.
  • 分析了Myt1l对体系程序的直接抑制.
  • 研究了Myt1l通过其N终端域招募Sin3b复合物.
  • 检查了Myt1l的基因组结合点和染色体配置.
  • 评估了Myt1l对Notch信号通路组件 (例如Hes1) 的抑制.
  • 在正在发育的小鼠大脑和初级神经元中进行了急性Myt1l敲击.

主要成果:

  • Myt1l直接抑制多样化的体系计划,保持神经元的身份.
  • Myt1l通过非特征的N终端域招募Sin3b进行抑制.
  • 在神经元和纤维细胞之间保持着开放的染色体.
  • Myt1l抑制了诺奇的信号传递,它的降低模仿了诺奇的功能增强.
  • 神经元中的Myt1l耗尽会抑制非神经元程序并损害神经元功能.

    • 结论:

    • Myt1l是一个关键的全神经抑制剂,通过沉默非神经程序来维持神经元的身份.
    • 在发育过程中,Myt1l使神经元能够逃脱Notch激活.
    • Myt1l的"多而不是一个"抑制机制对于细胞命运的维护至关重要,并可能对其他细胞类型的重编程有用.