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音猬因子对体节分化和增殖的体内调节

In vivo regulation of somite differentiation and proliferation by Sonic Hedgehog.

作者信息

Marcelle C, Ahlgren S, Bronner-Fraser M

机构信息

Division of Biology, Beckman Institute 139-74, Pasadena, California 91125, USA.

出版信息

Dev Biol. 1999 Oct 15;214(2):277-87. doi: 10.1006/dbio.1999.9389.

Abstract

In vertebrates, somite differentiation is mediated in part by Sonic Hedgehog (Shh), secreted by the notochord and the floor plate. However, Shh-null mice display close to normal expression of molecular markers for dermomytome, myotome, and sclerotome, indicating that Shh might not be required for their initial induction. In this paper, we have addressed the capacity of Shh to regulate in vivo the expression of the somite differentiation markers Pax-1, MyoD, and Pax-3 after separation of paraxial mesoderm from axial structures. We show that Pax-1, which is lost under these experimental conditions, is rescued by Shh. In contrast, Shh maintains, but cannot induce MyoD expression, while Pax-3 expression is independent of the presence of axial structures or Shh. Finally, we demonstrate that Shh is a potent mitogen for somitic cells, supporting the idea that it may serve to expand subpopulations of cells within the somite.

摘要

在脊椎动物中,体节分化部分由脊索和底板分泌的音猬因子(Shh)介导。然而,Shh基因敲除小鼠的皮肌节、肌节和生骨节分子标记物表达接近正常,这表明Shh可能不是其初始诱导所必需的。在本文中,我们研究了在将轴旁中胚层与轴向结构分离后,Shh在体内调节体节分化标记物Pax-1、MyoD和Pax-3表达的能力。我们发现,在这些实验条件下丢失的Pax-1可被Shh挽救。相比之下,Shh维持但不能诱导MyoD表达,而Pax-3表达与轴向结构或Shh的存在无关。最后,我们证明Shh是体节细胞的一种有效促有丝分裂原,支持了它可能用于扩大体节内细胞亚群的观点。

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