Notch1 control of oligodendrocyte differentiation in the spinal cord.
Notch1 control of oligodendrocyte differentiation in the spinal cord.
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NOTCH1控制脊髓中的少突胶质细胞分化。
DOI：
10.1083/jcb.200202002
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发表时间：
2002-08-19
影响因子：
7.8
通讯作者：
Mantei, Ned
中科院分区：
文献类型：
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作者：
Genoud, Stephane;Lappe-Siefke, Corinna;Goebbels, Sandra;Radtke, Freddy;Aguet, Michel;Scherer, Steven S;Suter, Ueli;Nave, Klaus-Armin;Mantei, Ned
我们选择性地抑制Notch 1信号在少突胶质细胞前体（OPCs）使用Cre/loxP系统在转基因小鼠中的作用，研究Notch 1在少突胶质细胞（OL）的发育和分化。OPCs的早期发育在脊髓中表现正常。然而，在胚胎第17.5天，观察到过早的OL分化和异位不成熟的OL存在于灰质。出生时，Notch 1突变动物的OL凋亡强烈增加。在大脑中也观察到过早的OL分化，表明Notch 1是中枢神经系统各个区域OL分化的正确空间和时间调节所必需的。这些发现确立了Notch 1在哺乳动物体内OPC发育的后期步骤中的广泛功能。
We have selectively inhibited Notch1 signaling in oligodendrocyte precursors (OPCs) using the Cre/loxP system in transgenic mice to investigate the role of Notch1 in oligodendrocyte (OL) development and differentiation. Early development of OPCs appeared normal in the spinal cord. However, at embryonic day 17.5, premature OL differentiation was observed and ectopic immature OLs were present in the gray matter. At birth, OL apoptosis was strongly increased in Notch1 mutant animals. Premature OL differentiation was also observed in the cerebrum, indicating that Notch1 is required for the correct spatial and temporal regulation of OL differentiation in various regions of the central nervous system. These findings establish a widespread function of Notch1 in the late steps of mammalian OPC development in vivo.