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由螺旋-环-螺旋抑制因子Id2调控的神经嵴特化

Neural crest specification regulated by the helix-loop-helix repressor Id2.

作者信息

Martinsen B J, Bronner-Fraser M

机构信息

B. J. Martinsen, Division of Biology, Beckman Institute 139-74, California Institute of Technology, Pasadena, CA 91125, USA.

出版信息

Science. 1998 Aug 14;281(5379):988-91. doi: 10.1126/science.281.5379.988.

DOI:10.1126/science.281.5379.988
PMID:9703514
Abstract

Vertebrate neural crest cells, derived from the neural folds, generate a variety of tissues, such as cartilage, ganglia, and cranial (intramembranous) bone. The chick homolog of the helix-loop-helix transcriptional regulator Id2 is expressed in cranial but not trunk neural folds and subsequently in some migrating cranial neural crest cells. Ectopic expression of Id2 with recombinant retroviruses converted ectodermal cells to a neural crest fate, demonstrating that proper regulation of Id2 is important for sustaining epidermal traits. In addition, overexpression of Id2 resulted in overgrowth and premature neurogenesis of the dorsal neural tube. These results suggest that Id2 may allocate ectodermal precursors into neural rather than epidermal lineages.

摘要

脊椎动物的神经嵴细胞起源于神经褶,可生成多种组织,如软骨、神经节和颅骨(膜内成骨)。螺旋-环-螺旋转录调节因子Id2的鸡同源物在颅神经褶而非躯干神经褶中表达,随后在一些迁移的颅神经嵴细胞中表达。用重组逆转录病毒异位表达Id2可将外胚层细胞转变为神经嵴命运,表明对Id2的适当调节对于维持表皮特征很重要。此外,Id2的过表达导致背神经管过度生长和过早神经发生。这些结果表明,Id2可能将外胚层前体细胞分配到神经而非表皮谱系中。

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