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首页> 外文期刊>Development >FGF and PI3 kinase signaling pathways antagonistically modulate sex muscle differentiation in C. elegans.
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FGF and PI3 kinase signaling pathways antagonistically modulate sex muscle differentiation in C. elegans.

机译:FGF和PI3激酶信号通路拮抗调节秀丽隐杆线虫的性肌分化。

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摘要

Myogenesis in vertebrate myocytes is promoted by activation of the phosphatidyl-inositol 3'-kinase (PI3 kinase) pathway and inhibited by fibroblast growth factor (FGF) signaling. We show that hyperactivation of the Caenorhabditis elegans FGF receptor, EGL-15, similarly inhibits the differentiation of the hermaphrodite sex muscles. Activation of the PI3 kinase signaling pathway can partially suppress this differentiation defect, mimicking the antagonistic relationship between these two pathways known to influence vertebrate myogenesis. When ectopically expressed in body wall muscle precursor cells, hyperactivated EGL-15 can also interfere with the proper development of the body wall musculature. Hyperactivation of EGL-15 has also revealed additional effects on a number of fundamental processes within the postembryonic muscle lineage, such as cell division polarity. These studies provide important in vivo insights into the contribution of FGF signaling events to myogenesis.
机译:激活磷脂酰肌醇3'激酶(PI3激酶)途径促进脊椎动物肌细胞的肌发生,并抑制成纤维细胞生长因子(FGF)信号传导。我们显示秀丽隐杆线虫FGF受体,EGL-15的过度激活同样抑制了雌雄同体性肌肉的分化。 PI3激酶信号传导途径的激活可以部分抑制这种分化缺陷,从而模拟了已知影响脊椎动物肌发生的这两种途径之间的拮抗关系。当在体壁肌肉前体细胞中异位表达时,过度活化的EGL-15也可能会干扰体壁肌肉的正常发育。 EGL-15的过度激活还揭示了对胚后肌肉谱系内许多基本过程的额外影响,例如细胞分裂极性。这些研究为FGF信号事件对肌发生的贡献提供了重要的体内见解。

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