Consequence of the loss of Sox2 in the developing brain of the mouse
Consequence of the loss of Sox2 in the developing brain of the mouse
复制标题
DOI：
10.1016/j.febslet.2008.07.011
复制
发表时间：
2008-08-06
期刊：
影响因子：
3.5
通讯作者：
Okuda, Akihiko
中科院分区：
文献类型：
--
作者：
Miyagi, Satoru;Masui, Shinji;Okuda, Akihiko
转录因子Sox2在神经干细胞和祖细胞中高水平表达。在这里，我们使用Cre-loxP系统在发育中的大脑中特异性地灭活Sox2。尽管突变动物在出生后没有存活下来，但对妊娠晚期胚胎的分析表明，Sox2的丢失会导致侧脑室扩大和神经球形成细胞数量减少。然而，尽管SOX2基因缺陷的神经干细胞的神经源性潜能减弱，但它们仍保持其多能性和自我更新能力。我们发现SOX3在发育过程中SOX2缺失的大脑中表达水平升高，可能减轻了SOX2缺失的影响。(C)2008年欧洲生化学会联合会。爱思唯尔出版公司版权所有。
The transcription factor Sox2 is expressed at high levels in neural stem and progenitor cells. Here, we inactivated Sox2 specifically in the developing brain by using Cre-loxP system. Although mutant animals did not survive after birth, analysis of late gestation embryos revealed that loss of Sox2 causes enlargement of the lateral ventricles and a decrease in the number of neurosphere-forming cells. However, although their neurogenic potential is attenuated, Sox2-deficient neural stem cells retain their multipotency and self-renewal capacity. We found that expression level of Sox3 is elevated in Sox2 null developing brain, probably mitigating the effects of loss of Sox2. (c) 2008 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.