SoxD proteins influence multiple stages of oligodendrocyte development and modulate SoxE protein function
SoxD proteins influence multiple stages of oligodendrocyte development and modulate SoxE protein function
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DOI：
10.1016/j.devcel.2006.08.011
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发表时间：
2006-11-01
影响因子：
11.8
通讯作者：
Wegner, Michael
中科院分区：
文献类型：
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作者：
Stolt, C. Claus;Schlierf, Anita;Wegner, Michael
髓磷脂形成的少突胶质细胞是研究中枢神经系统特异性事件、谱系进展和终末分化的转录调控的极好模型。在这里，我们发现dsox转录因子Sox5和Sox6共同和细胞自主调节小鼠脊髓少突胶质细胞发育的几个阶段。它们抑制规范和终端分化并影响迁移模式。因此，少突胶质细胞前体和终分化少突胶质细胞在缺乏两种Sox蛋白的脊髓中出现早熟。Sox5和Sox6与E组Sox蛋白Sox9和Sox10具有相反的功能，促进少突胶质细胞的特化和末端分化。遗传和分子证据表明，Sox5和Sox6直接干扰E组Sox蛋白的功能。我们的研究揭示了不同组Sox蛋白之间复杂的调控网络，这对于少突胶质细胞发育的正常进展至关重要。
The myelin-forming oligodendrocytes are an excellent model to study transcriptional regulation of specification events, lineage progression, and terminal differentiation in the central nervous system. Here, we show that the group D Sox transcription factors Sox5 and Sox6 jointly and cell-autonomously regulate several stages of oligodendrocyte development in the mouse spinal cord. They repress specification and terminal differentiation and influence migration patterns. As a consequence, oligodendrocyte precursors and terminally differentiating oligodendrocytes appear precociously in spinal cords deficient for both Sox proteins. Sox5 and Sox6 have opposite functions than the group E Sox proteins Sox9 and Sox10, which promote oligodendrocyte specification and terminal differentiation. Both genetic as well as molecular evidence suggests that Sox5 and Sox6 directly interfere with the function of group E Sox proteins. Our studies reveal a complex regulatory network between different groups of Sox proteins that is essential for proper progression of oligodendrocyte development.