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哺乳动物神经胚形成的遗传基础。

The genetic basis of mammalian neurulation.

作者信息

Copp Andrew J, Greene Nicholas D E, Murdoch Jennifer N

机构信息

Neural Development Unit, Institute of Child Health, University College London, London WC1N 1EH, UK.

出版信息

Nat Rev Genet. 2003 Oct;4(10):784-93. doi: 10.1038/nrg1181.

DOI:10.1038/nrg1181
PMID:13679871
Abstract

More than 80 mutant mouse genes disrupt neurulation and allow an in-depth analysis of the underlying developmental mechanisms. Although many of the genetic mutants have been studied in only rudimentary detail, several molecular pathways can already be identified as crucial for normal neurulation. These include the planar cell-polarity pathway, which is required for the initiation of neural tube closure, and the sonic hedgehog signalling pathway that regulates neural plate bending. Mutant mice also offer an opportunity to unravel the mechanisms by which folic acid prevents neural tube defects, and to develop new therapies for folate-resistant defects.

摘要

80多个突变小鼠基因会破坏神经胚形成,从而能够深入分析潜在的发育机制。尽管许多基因变异体仅得到了初步研究,但已经可以确定有几个分子途径对正常神经胚形成至关重要。这些途径包括神经管闭合起始所需的平面细胞极性途径,以及调节神经板弯曲的音猬因子信号通路。突变小鼠还为揭示叶酸预防神经管缺陷的机制以及开发针对叶酸抵抗性缺陷的新疗法提供了机会。

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