一个PRDM16-CtBP1/2复合体与HDAC1/2相互作用,调节神经发生的转录程序,并指导皮质神经元迁移
Sophie Warren1, Bader El Farran1, Sungyun Kang1
1Department of Biology, Indiana University, Bloomington, IN 47405, USA.
概括
基因组甲基转移酶PRDM16与CtBP1/2相互作用,以调节皮质神经发生和神经元迁移. 减少PRDM16相互作用可能导致神经发育缺陷.
科学领域:
- 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.
- 发展生物学 发展生物学
背景情况:
- 增强剂的染色体调节对细胞命运和分化至关重要.
- 神经干细胞中增强剂调节的机制尚未完全理解.
- PRDM16是一种对皮质神经元定位至关重要的基因组甲基转移酶.
研究的目的:
- 研究PRDM16在皮层神经发生和神经元迁移中的作用.
- 阐明PRDM16如何与染色质修饰酶和转录因子相互作用.
- 了解神经发育缺陷在PRDM16的分子基础.
主要方法:
- 共同免疫沉以确定蛋白质相互作用.
- 染色素免疫沉以研究增强剂占用率.
- 对基因表达和神经元分化标记物的分析.
主要成果:
- PRDM16与CtBP1和CtBP2相互作用,控制皮质神经发生和上层神经元迁移.
- PRDM16,CtBP1/2,HDAC1,HDAC2和LSD1是共同调节的增强剂.
- CTCF促进了对皮质增强剂的CtBP1/2招募.
- 减少PRDM16与染色体调节者的相互作用与神经发育缺陷有关.
结论:
- PRDM16,CtBP1/2,以及相关的染色质调节剂对于皮质正常发育至关重要.
- 在PRDM16介导的染色质调节中出现的障碍,可能导致神经发育障碍.
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