The transition from radial glial to intermediate progenitor cell is inhibited by FGF signaling during corticogenesis.
The transition from radial glial to intermediate progenitor cell is inhibited by FGF signaling during corticogenesis.
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DOI：
10.1523/jneurosci.3844-09.2009
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发表时间：
2009-11-18
期刊：
影响因子：
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通讯作者：
Hébert JM
中科院分区：
文献类型：
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作者：
Kang W;Wong LC;Shi SH;Hébert JM
在皮质发生过程中，放射状胶质干细胞的自我更新与其后代祖细胞的产生之间的平衡对于产生新皮质的正确大小和细胞组成至关重要。人们对干细胞向祖细胞转变的调控机制知之甚少。 FGF 通常与促进神经前体细胞的增殖有关，但尚不清楚它们如何在体内对干细胞、祖细胞或两者发挥作用。在这里，三个 FGF 受体基因在皮质神经发生过程中同时被删除。在这些突变体中，由于从未定型状态向分化程度更高的状态的转变增加，放射状胶质细胞被耗尽，最初导致祖细胞增加，但最终导致皮层变小。然而，祖细胞本身的增殖率并没有改变。这些结果表明，FGF 通常会抑制皮质生成过程中放射状胶质细胞向祖细胞的转变。
During corticogenesis, the balance between the self renewal of radial glial stem cells and the production of their descendent progenitor cells is essential in generating the correct size and cell composition of the neocortex. How the stem to progenitor cell transition is regulated is poorly understood. FGFs are commonly implicated in promoting proliferation of neural precursor cells, but it is unclear how they exert their effects on stem cells, progenitor cells, or both in vivo. Here, three FGF receptor genes are simultaneously deleted during cortical neurogenesis. In these mutants, radial glia are depleted due to an increased transition from an uncommitted state to a more differentiated one, initially causing an increase in progenitors, but ultimately resulting in a smaller cortex. The proliferation rate of progenitors themselves, however, is unchanged. These results indicate that FGFs normally repress the radial glia to progenitor cell transition during corticogenesis.