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骨形态发生蛋白信号传导抑制小鼠胚胎中的过早神经分化。

BMP signalling inhibits premature neural differentiation in the mouse embryo.

作者信息

Di-Gregorio Aida, Sancho Margarida, Stuckey Daniel W, Crompton Lucy A, Godwin Jonathan, Mishina Yuji, Rodriguez Tristan A

机构信息

Molecular Embryology Group, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London W12 ONN, UK.

出版信息

Development. 2007 Sep;134(18):3359-69. doi: 10.1242/dev.005967. Epub 2007 Aug 15.

Abstract

The specification of a subset of epiblast cells to acquire a neural fate constitutes the first step in the generation of the nervous system. Little is known about the signals required for neural induction in the mouse. We have analysed the role of BMP signalling in this process. We demonstrate that prior to gastrulation, Bmp2/4 signalling via Bmpr1a maintains epiblast pluripotency and prevents precocious neural differentiation of this tissue, at least in part by maintaining Nodal signalling. We find that during gastrulation, BMPs of the 60A subgroup cooperate with Bmp2/4 to maintain pluripotency. The inhibition of neural fate by BMPs is independent of FGF signalling, as inhibition of FGF signalling between 5.5 and 7.5 days post-coitum does not block neural differentiation in the mouse embryo. Together, our results demonstrate that inhibition of BMP signalling has a central role during neural induction in mammals and suggest that FGFs do not act as neural inducers in the post-implantation mouse embryo.

摘要

上胚层细胞的一个亚群被指定获得神经命运是神经系统生成的第一步。关于小鼠神经诱导所需的信号,我们知之甚少。我们分析了BMP信号在此过程中的作用。我们证明,在原肠胚形成之前,通过Bmpr1a的Bmp2/4信号维持上胚层的多能性,并至少部分通过维持Nodal信号来防止该组织过早的神经分化。我们发现,在原肠胚形成期间,60A亚组的BMP与Bmp2/4协同维持多能性。BMP对神经命运的抑制独立于FGF信号,因为在交配后5.5至7.5天抑制FGF信号不会阻断小鼠胚胎中的神经分化。总之,我们的结果表明,抑制BMP信号在哺乳动物神经诱导过程中起核心作用,并表明FGF在植入后小鼠胚胎中不作为神经诱导因子起作用。

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