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Mash1/Ascl1突变体中神经元分化的延迟。

Delays in neuronal differentiation in Mash1/Ascl1 mutants.

作者信息

Pattyn Alexandre, Guillemot François, Brunet Jean-François

机构信息

CNRS UMR 8542, Département de Biologie, Ecole normale supérieure, 75005 Paris, France.

出版信息

Dev Biol. 2006 Jul 1;295(1):67-75. doi: 10.1016/j.ydbio.2006.03.008. Epub 2006 May 4.

Abstract

The inactivation of a developmental transcription factor may lead to the complete absence of a specific cell type. More commonly, though, it only partially impairs its generation. The modalities of this partial effect have rarely been documented in any detail. Here, we report a novel function for the bHLH transcription factor Ascl1/Mash1 in the generation of the nucleus of the solitary tract (nTS). In Mash1(-/-) late embryos, the nTS is markedly atrophic. Tracing back the origin of this atrophy, we show that nTS precursors appear in the mutants 1 day later than in the wild type and then accumulate at a slower pace. We also show that the previously reported atrophy of the sympathetic chain in Mash1 mutants is similarly preceded by a delay of 1 to 2 days in the appearance of differentiated ganglionic cells. Finally, we provide evidence that the acceleration imposed by Mash1, regardless of the production of post-mitotic cells, affects differentiation itself, both generic and type-specific.

摘要

一种发育转录因子的失活可能导致特定细胞类型完全缺失。不过,更常见的情况是,它只会部分损害该细胞类型的生成。这种部分效应的具体形式鲜有详细记录。在此,我们报告了bHLH转录因子Ascl1/Mash1在孤束核(nTS)生成过程中的一种新功能。在Mash1基因敲除的晚期胚胎中,nTS明显萎缩。追溯这种萎缩的起源,我们发现nTS前体细胞在突变体中出现的时间比野生型晚1天,然后以较慢的速度积累。我们还表明,之前报道的Mash1突变体中交感神经链的萎缩同样在分化的神经节细胞出现时提前1至2天出现延迟。最后,我们提供证据表明,Mash1所施加的加速作用,无论有丝分裂后细胞的产生情况如何,都会影响分化本身,包括一般分化和特定类型分化。

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