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在大脑发育过程中,SNIP1和PRC2协调神经母细胞的细胞命运

Yurika Matsui¹, Mohamed Nadhir Djekidel², Katherine Lindsay¹

¹Department of Developmental Neurobiology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA.

Nature communications

|August 8, 2023

概括

Smad核相互作用蛋白1 (SNIP1) 对于神经前体细胞的存活和大脑发育至关重要. SNIP1调节细胞死亡和生存途径,影响神经发生和大脑结构.

科学领域:

发展生物学发展生物学
神经科学是一个神经科学.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

细胞死亡是对发育至关重要的编程过程,但其机制仍然不清楚.
神经前体细胞的存活和神经发生对于正确的大脑形成至关重要.

研究的目的:

研究Smad核相互作用蛋白1 (SNIP1) 在神经前体细胞存活和大脑发育中的作用.
阐明SNIP1在神经发生过程中影响细胞命运决定的分子机制.

主要方法:

研究了SNIP1在神经前代细胞和发育中的大脑中的作用.
分析了由SNIP1.1.介导的亡诱导,基因调节和表观遗传修饰 (H3K27me3).
研究了SNIP1,TGFβ,NFκB信号传输和Polycomb复合体PRC2.2之间的相互作用.

主要成果:

SNIP1促进神经前体细胞的存活和神经发生,这对大脑发育至关重要.
减少SNIP1导致大脑发育不良以及增加酶9依赖性亡.
在TGFβ和NFκB的影响下,SNIP1调节参与细胞存活和神经发生的基因.
在特定的基因位置上,SNIP1促进了Polycomb复杂的PRC2占用和H3K27me3的周转.
PRC2 枯竭部分挽救了遗传程序,并减少了 SNIP1 枯竭的大脑中的亡.

结论:

SNIP1是大脑发育的组成部分,通过促进神经前体细胞存活和神经发生.
SNIP1的功能包括通过通过PRC2和H3K27me3.3对目标基因的表观遗传控制来调节细胞生存/死亡途径.
通过SNIP1对PRC2和H3K27标记的局部特异性调节,在发育中的大脑中切换细胞存活和死亡.

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