Mcidas and GemC1/Lynkeas specify embryonic radial glial cells.
Mcidas and GemC1/Lynkeas specify embryonic radial glial cells.
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DOI：
10.1080/23262133.2016.1172747
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发表时间：
2016-01-01
期刊：
影响因子：
--
通讯作者：
Taraviras, Stavros
中科院分区：
文献类型：
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作者：
Kyrousi, Christina;Lalioti, Maria-Eleni;Taraviras, Stavros
室管膜细胞是位于成年哺乳动物脑侧脑室壁的多纤毛细胞，是成体神经干细胞所在的室管膜下区龛的关键组成部分。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，室管膜细胞从脑室系统接收分泌的分子和形态发生素，所述分泌的分子和形态发生素控制成体神经干细胞的自我更新和分化决定。多纤毛室管膜细胞在出生后阶段完全分化，然而它们在胚胎发生的中期至晚期由放射状胶质细胞群分化而来。在这里，我们讨论了最近的研究结果表明，2种新的分子，Mcidas和GemC 1/Lynkeas是放射状胶质细胞向室管膜细胞分化的关键参与者。这两种蛋白质最初被描述为细胞周期调节因子，揭示了与Geminin的序列相似性。它们在胚胎发生期间定向为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，这对于室管膜细胞的产生是充分和必要的。我们认为Mcidas和GemC 1/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FoxJ 1上游多纤毛室管膜细胞谱系的命运承诺。
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.