RhoG Promotes Neural Progenitor Cell Proliferation in Mouse Cerebral Cortex
RhoG Promotes Neural Progenitor Cell Proliferation in Mouse Cerebral Cortex
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DOI：
10.1091/mbc.e09-03-0200
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发表时间：
2009-12-01
影响因子：
3.3
通讯作者：
Katoh, Hironori
中科院分区：
文献类型：
--
作者：
Fujimoto, Satoshi;Negishi, Manabu;Katoh, Hironori
在皮质发育的早期，神经前体细胞在脑室带(VZ)扩大它们的数量，并产生神经元。虽然已经有一系列研究揭示了鼻咽癌的神经发生过程，但调控鼻咽癌增殖的分子机制在很大程度上仍不清楚。在这里，我们发现RhoG是Rho家族GTP酶家族的成员之一，在皮质发育的早期阶段就在VZ表达。在体外，RhoG基因的表达促进了鼻咽癌的增殖和溴脱氧尿嘧啶核苷(BrdU)的掺入，体内Ki67阳性细胞比例增加。相反，RNA干扰抑制RhoG的增殖，抑制BrdU的掺入，抑制Ki67阳性细胞在NPC中的比例。然而，RhoG基因敲除并不影响鼻咽癌的分化和存活。RhoG诱导的BrdU掺入需要磷脂酰肌醇3-激酶(PI3K)活性，而不需要与Elmo的相互作用。综上所述，这些结果表明，RhoG通过PI3K在皮质发育中促进鼻咽癌的增殖。
In early cortical development, neural progenitor cells (NPCs) expand their population in the ventricular zone (VZ), and produce neurons. Although a series of studies have revealed the process of neurogenesis, the molecular mechanisms regulating NPC proliferation are still largely unknown. Here we found that RhoG, a member of Rho family GTPases, was expressed in the VZ at early stages of cortical development. Expression of constitutively active RhoG promoted NPC proliferation and incorporation of bromodeoxyuridine (BrdU) in vitro, and the proportion of Ki67-positive cells in vivo. In contrast, knockdown of RhoG by RNA interference suppressed the proliferation, BrdU incorporation, and the proportion of Ki67-positive cells in NPCs. However, knockdown of RhoG did not affect differentiation and survival of NPC. The RhoG-induced promotion of BrdU incorporation required phosphatidylinositol 3-kinase (PI3K) activity but not the interaction with ELMO. Taken together, these results indicate that RhoG promotes NPC proliferation through PI3K in cortical development.