Converse control of oligodendrocyte and astrocyte lineage development by Sonic hedgehog in the chick spinal cord
Converse control of oligodendrocyte and astrocyte lineage development by Sonic hedgehog in the chick spinal cord
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DOI：
10.1016/j.ydbio.2004.02.015
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发表时间：
2004-06-15
影响因子：
2.7
通讯作者：
Cochard, P
中科院分区：
文献类型：
--
作者：
Agius, E;Soukkarieh, C;Cochard, P
在发育中的脊髓中，少突胶质细胞祖细胞（oligodendrocyte progenitor，OLP）起源于腹侧神经上皮，并且该谱系的特化取决于腹侧中线细胞产生的Sonic hedgehog（Shh）的诱导活性。另一方面，已经表明OLP身份是通过转录因子olig2和nka2.2的共表达获得的。虽然最初表达在相邻的非重叠区域的腹侧神经上皮，这些转录因子成为共表达在pMN域的时间OLP规范通过背侧延伸的Nkx2.2域。在这里，我们表明，Shh足以促进神经上皮细胞中Olig2和Nkx2.2的共表达。此外，Shh活性对于这种共表达是必要的，因为阻断Shh信号传导完全废除Olig2表达并阻碍Nkx2.2的背侧延伸。虽然Shh在这些阶段会影响神经上皮细胞增殖，但Nkx2.2结构域的背侧延伸不是由于祖细胞增殖，而是由于腹侧神经上皮的重复模式化。最后，Shh不仅刺激OLP规范，但也同时限制了腹侧延伸的星形胶质细胞祖细胞（AP）域，减少星形胶质细胞的发展。我们建议，规范不同的胶质细胞谱系是一个选择的结果，取决于嘘信号。(C)2004年爱思唯尔公司All rights reserved.
In the developing spinal cord, oligodendrocyte progenitors (OLPs) originate from the ventral neuroepithelium and the specification of this lineage depends on the inductive activity of Sonic hedgehog (Shh) produced by ventral midline cells. On the other hand, it has been shown that OLP identity is acquired by the coexpression of the transcription factors olig2 and nka2.2. Although initially expressed in adjacent nonoverlapping domains of the ventral neuroepithelium, these transcription factors become coexpressed in the pMN domain at the time of OLP specification through dorsal extension of the Nkx2.2 domain. Here we show that Shh is sufficient to promote the coexpression of Olig2 and Nkx2.2 in neuroepithelial cells. In addition, Shh activity is necessary for this coexpression since blocking Shh signalling totally abolishes Olig2 expression and impedes dorsal extension of Nkx2.2. Although Shh at these stages affects neuroepithelial cell proliferation, the dorsal extension of the Nkx2.2 domain is not due to progenitor proliferation but to repatteming of the ventral neuroepithelium. Finally, Shh not only stimulates OLP specification but also simultaneously restricts the ventral extension of the astrocyte progenitor (AP) domain and reduces astrocyte development. We propose that specification of distinct glial lineages is the result of a choice that depends on Shh signalling. (C) 2004 Elsevier Inc. All rights reserved.