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少突胶质细胞转录因子1(olig1)的表达可识别斑马鱼中正在发育的少突胶质细胞,且需要刺猬信号通路和Notch信号通路。

olig1 Expression identifies developing oligodendrocytes in zebrafish and requires hedgehog and notch signaling.

作者信息

Schebesta Michael, Serluca Fabrizio C

机构信息

Developmental and Molecular Pathways, Novartis Institutes for Biomedical Research, Cambridge, Massachusetts 02139, USA.

出版信息

Dev Dyn. 2009 Apr;238(4):887-98. doi: 10.1002/dvdy.21909.

Abstract

Myelin, the isolating sheath around large diameter axons, is formed in the central nervous system (CNS) by oligodendrocytes. We isolated the zebrafish ortholog of olig1, a bHLH transcription factor, and describe the origin and development of oligodendrocytes in the zebrafish brain. Olig1:mem-eGFP transgenic animals demonstrate the highly dynamic nature of oligodendrocyte membrane processes, providing a tool for studying in vivo oligodendrocyte development. Formation of oligodendrocytes and initiation of olig1 expression are under the control of long-range hedgehog and notch signaling while maintenance of olig1 expression only depends on hedgehog. Over-expression of olig1 did not affect myelin formation in the brain and combined over-expression of olig1 and olig2 could not rescue loss of hedgehog signaling, indicating that critical factors other than olig1 and olig2 are necessary. Lastly, knockdown of Olig1 in an Olig2-sensitized background did result in defects in CNS myelination, indicating a functional overlap between Olig1 and Olig2 proteins.

摘要

髓磷脂是围绕大直径轴突的绝缘鞘,在中枢神经系统(CNS)中由少突胶质细胞形成。我们分离出了少突胶质细胞转录因子1(olig1)的斑马鱼直系同源物,并描述了斑马鱼大脑中少突胶质细胞的起源和发育。Olig1:mem-eGFP转基因动物展示了少突胶质细胞膜突起的高度动态特性,为研究体内少突胶质细胞发育提供了一个工具。少突胶质细胞的形成和olig1表达的起始受远程刺猬信号通路和Notch信号通路的控制,而olig1表达的维持仅依赖于刺猬信号通路。olig1的过表达不影响大脑中的髓磷脂形成,olig1和olig2的联合过表达不能挽救刺猬信号通路缺失的情况,这表明除了olig1和olig2之外,其他关键因子也是必需的。最后,在Olig2敏感背景下敲低Olig1确实导致了中枢神经系统髓鞘形成缺陷,这表明Olig1和Olig2蛋白之间存在功能重叠。

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