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首页> 外文期刊>Development >Canonical Wnt activity regulates trunk neural crest delamination linking BMPoggin signaling with G1/S transition.
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Canonical Wnt activity regulates trunk neural crest delamination linking BMPoggin signaling with G1/S transition.

机译:规范的Wnt活性调节主干神经c分层,将BMP /头蛋白信号传导与G1 / S过渡联系起来。

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摘要

Delamination of premigratory neural crest cells depends on a balance between BMPoggin and on successful G1/S transition. Here, we report that BMP regulates G1/S transition and consequent crest delamination through canonical Wnt signaling. Noggin overexpression inhibits G1/S transition and blocking G1/S abrogates BMP-induced delamination; moreover, transcription of Wnt1 is stimulated by BMP and by the developing somites, which concomitantly inhibit noggin production. Interfering with beta-catenin and LEF/TCF inhibits G1/S transition, neural crest delamination and transcription of various BMP-dependent genes, which include Cad6B, Pax3 and Msx1, but not that of Slug, Sox9 or FoxD3. Hence, we propose that developing somites inhibit noggin transcription in the dorsal tube, resulting in activation of BMP and consequent Wnt1 production. Canonical Wnt signaling in turn stimulates G1/S transition and generation of neural crest cell motility independently of its proposed role in earlier neural crest specification.
机译:迁移前神经c细胞的分层取决于BMP /头蛋白和成功的G1 / S过渡之间的平衡。在这里,我们报告BMP通过规范Wnt信号调节G1 / S过渡和随之而来的波峰分层。头蛋白过表达抑制G1 / S过渡,阻断G1 / S消除了BMP引起的分层。此外,BMP和发育中的卵节刺激Wnt1的转录,从而抑制头蛋白的产生。干扰β-连环蛋白和LEF / TCF会抑制G1 / S过渡,神经c分层和各种BMP依赖性基因(包括Cad6B,Pax3和Msx1)的转录,但不能抑制Slug,Sox9或FoxD3的基因转录。因此,我们建议发育中的节肢动物抑制背管中的头蛋白转录,从而导致BMP活化和随后的Wnt1产生。规范的Wnt信号依次刺激G1 / S过渡和神经c细胞运动的产生,而与它在早期神经c规范中的拟议作用无关。

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