在发育中的新皮质中,Srsf1和Elavl1通过控制TrkC受体异型表达来对神经元命运选择产生敌对作用
A Ioana Weber1,2, Srinivas Parthasarathy1, Ekaterina Borisova1,3
1Charité Universitätsmedizin Berlin, Institute of Cell Biology and Neurobiology, Charitéplatz 1, 10117 Berlin, Germany.
Nucleic acids research
|September 12, 2023
概括
研究人员发现了两个RNA结合蛋白Srsf1和Elavl1通过调节TrkC受体拼接来控制新皮质中神经元的发育. 这一发现阐明了在大脑发育过程中如何产生特定的神经元类型.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 发展生物学 发展生物学
背景情况:
- 新皮质负责较高的认知功能,具有多层结构,具有多样化的神经元亚型.
- 神经原生细胞 (NPC) 在复杂的,不完全理解的分子指导下产生这些神经元.
- TrkC受体的替代拼接,特别是TrkC-T1异型,会影响皮质外投射神经元 (CFuPN) 的命运.
研究的目的:
- 研究TrkC受体异型在新皮层发育中的细胞类型特定调节.
- 确定控制TrkC-T1和TrkC-TK+异型之间的平衡的分子机制.
- 阐明Srsf1和Elavl1在确定神经元亚型,特别是CFuPN和状投射神经元 (CPN) 命运中的作用.
主要方法:
- 对TrkC受体的替代拼接和转录稳定性的分析.
- 研究RNA结合蛋白Srsf1和Elavl1.1的对抗作用.
- 在体内研究以确定Srsf1和Elavl1对神经皮层发育中的神经元命运决定的影响.
主要成果:
- 在TrkC-T1和TrkC-TK+异型之间的平衡是细胞类型特异的新皮质发育.
- Srsf1和Elavl1对抗性地调节了TrkC-T1与TrkC-TK+的比例.
- 在体内,Srsf1促进CFuPN命运,而Elavl1促进CPN命运.
结论:
- 新皮质中Srsf1和Elavl1的时空表达决定了神经元的命运选择.
- 这些蛋白调节TrkC的替代拼接和转录稳定性,影响神经元亚型的产生.
- 这项研究增强了在新皮层发育过程中体内替代拼接的机制理解.
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