Mcidas和GemC1/Lynkeas指定胚胎放射状胶质细胞。

Neurogenesis (Austin, Tex.) Pub Date : 2016-04-27 eCollection Date: 2016-01-01 DOI:10.1080/23262133.2016.1172747
Christina Kyrousi, Maria-Eleni Lalioti, Eleni Skavatsou, Zoi Lygerou, Stavros Taraviras
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引用次数: 12

摘要

室管膜细胞是位于成年哺乳动物脑侧脑室壁上的多纤毛细胞,是成体神经干细胞所在的室管膜下区生态位的关键组成部分。室管膜细胞通过其运动纤毛的运动控制脑室系统内的脑脊液流动,并从中获得控制成体神经干细胞自我更新和分化决定的分泌分子和形态因子。多纤毛室管膜细胞在出生后完全分化,但它们是在胚胎发生中后期从放射状胶质细胞群体中分化出来的。在这里,我们讨论了最近的研究结果,表明两种新分子Mcidas和GemC1/Lynkeas是室管膜细胞径向胶质特化的关键分子。这两种蛋白最初被描述为细胞周期调节因子,揭示了与gemini的序列相似性。它们在胚胎发生过程中在室管膜细胞谱系的放射状胶质细胞中表达,而过表达和敲除实验表明,它们是室管膜细胞生成的充分和必要条件。我们认为Mcidas和GemC1/Lynkeas是分子级联的关键组成部分,该分子级联促进放射状胶质细胞向c-Myb和FoxJ1上游的多管室膜细胞谱系的命运承诺。
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Mcidas and GemC1/Lynkeas specify embryonic radial glial cells.

Ependymal cells are multiciliated cells located in the wall of the lateral ventricles of the adult mammalian brain and are key components of the subependymal zone niche, where adult neural stem cells reside. Through the movement of their motile cilia, ependymal cells control the cerebrospinal fluid flow within the ventricular system from which they receive secreted molecules and morphogens controlling self-renewal and differentiation decisions of adult neural stem cells. Multiciliated ependymal cells become fully differentiated at postnatal stages however they are specified during mid to late embryogenesis from a population of radial glial cells. Here we discuss recent findings suggesting that 2 novel molecules, Mcidas and GemC1/Lynkeas are key players on radial glial specification to ependymal cells. Both proteins were initially described as cell cycle regulators revealing sequence similarity to Geminin. They are expressed in radial glial cells committed to the ependymal cell lineage during embryogenesis, while overexpression and knock down experiments showed that are sufficient and necessary for ependymal cell generation. We propose that Mcidas and GemC1/Lynkeas are key components of the molecular cascade that promotes radial glial cells fate commitment toward multiciliated ependymal cell lineage operating upstream of c-Myb and FoxJ1.

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