The role of the Ets domain transcription factor erm in modulating differentiation of neural crest stem cells
The role of the Ets domain transcription factor erm in modulating differentiation of neural crest stem cells
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DOI：
10.1006/dbio.2002.0795
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发表时间：
2002-10-01
影响因子：
2.7
通讯作者：
Sommer, L
中科院分区：
文献类型：
--
作者：
Paratore, C;Brugnoli, G;Sommer, L
转录因子Erm是Ets结构域蛋白Pea3亚家族的成员，其在多能神经嵴细胞、外周神经元和卫星神经胶质中表达。还没有确定机构风险管理在开发过程中的具体作用。我们解决了Erm的功能，在神经嵴发育的一个显性负性形式的Erm的强制表达。Erm在神经嵴细胞中的功能抑制干扰神经元的命运决定，而祖细胞的存活和增殖不受影响。与此相反，在神经嵴干细胞中阻断Erm功能并不影响其采用胶质细胞命运的能力，这与胶质细胞诱导信号无关。此外，胶质细胞的存活和分化是正常的。然而，在神经胶质细胞中的增殖率急剧下降，这表明Erm在控制细胞周期进程中的神经胶质特异性作用。因此，与参与神经发生的晚期步骤的Pea3亚家族的其他成员相比，Erm.似乎是早期神经嵴发育所必需的。此外，我们的数据点多，谱系特异性作用的Erm神经嵴干细胞及其衍生物，这表明Erm的功能是依赖于细胞的内在和外在的背景。(C)2002 Elsevier Science（美国）。
The transcription factor Erm is a member of the Pea3 subfamily of Ets domain proteins that is expressed in multipotent neural crest cells, peripheral neurons, and satellite glia. A specific role of Erm during development has not yet been established. We addressed the function of Erm in neural crest development by forced expression of a dominant-negative form of Erm. Functional inhibition of Erm in neural crest cells interfered with neuronal fate decision, while progenitor survival and proliferation were not affected. In contrast, blocking Erm function in neural crest stem cells did not influence their ability to adopt a glial fate, independent of the glia-inducing signal. Furthermore, glial survival and differentiation were normal. However, the proliferation rate was drastically diminished in glial cells, suggesting a glia-specific role of Erm in controlling cell cycle progression. Thus, in contrast to other members of the Pea3 subfamily that are involved in late steps of neurogenesis, Erm. appears to be required in early neural crest development. Moreover, our data point to multiple, lineage-specific roles of Erm in neural crest stem cells and their derivatives, suggesting that Erm function is dependent on the cell intrinsic and extrinsic context. (C) 2002 Elsevier Science (USA).