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首页> 外文期刊>Development >Mouse embryos lacking Smad1 signals display defects in extra-embryonic tissues and germ cell formation.
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Mouse embryos lacking Smad1 signals display defects in extra-embryonic tissues and germ cell formation.

机译：缺少Smad1信号的小鼠胚胎在胚外组织和生殖细胞形成中表现出缺陷。

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The Smad proteins are important intracellular mediators of the transforming growth factor beta (TGFbeta) family of secreted growth factors. Smad1 is an effector of signals provided by the bone morphogenetic protein (BMP) sub-group of TGFbeta molecules. To understand the role of Smad1 in mouse development, we have generated a Smad1 loss-of-function allele using homologous recombination in ES cells. Smad1-/- embryos die by 10.5 dpc because they fail to connect to the placenta. Mutant embryos are first recognizable by 7.0 dpc, owing to a characteristic localized outpocketing of the visceral endoderm at the posterior embryonic/extra-embryonic junction, accompanied by a dramatic twisting of the epiblast and nascent mesoderm. Chimera analysis reveals that these two defects are attributable to a requirement for Smad1 in the extra-embryonic tissues. By 7.5 dpc, Smad1-deficient embryos show a marked impairment in allantois formation. By contrast, the chorion overproliferates, is erratically folded within the extra-embryonic space and is impeded in proximal migration. BMP signals are known to be essential for the specification and proliferation of primordial germ cells. We find a drastic reduction of primordial germ cells in Smad1-deficient embryos, suggesting an essential role for Smad1-dependent signals in primordial germ cell specification. Surprisingly, despite the key involvement of BMP signaling in tissues of the embryo proper, Smad1-deficient embryos develop remarkably normally. An examination of the expression domains of Smad1, Smad5 and Smad8 in early mouse embryos show that, while Smad1 is uniquely expressed in the visceral endoderm at 6.5 dpc, in other tissues Smad1 is co-expressed with Smad5 and/or Smad8. Collectively, these data have uncovered a unique function for Smad1 signaling in coordinating the growth of extra-embryonic structures necessary to support development within the uterine environment.
机译：Smad蛋白是分泌型生长因子的转化生长因子β（TGFbeta）家族的重要细胞内介体。 Smad1是由TGFbeta分子的骨形态发生蛋白（BMP）子组提供的信号的效应子。为了了解Smad1在小鼠发育中的作用，我们使用ES细胞中的同源重组产生了Smad1功能丧失的等位基因。 Smad1-/-胚胎死于10.5 dpc，因为它们无法连接到胎盘。由于在后胚/胚外接合处内脏内胚层的特征性局部突出，并伴随着表皮细胞和新生中胚层的剧烈扭曲，因此突变胚首先可被识别为7.0 dpc。嵌合体分析显示这两个缺陷可归因于胚外组织对Smad1的需求。通过7.5 dpc，Smad1缺陷型胚胎在尿囊形成中显示出明显的损伤。相比之下，绒毛膜过度增殖，在胚外空间内呈不规则折叠状态，并阻碍了近端迁移。已知BMP信号对于原始生殖细胞的规范和增殖至关重要。我们发现Smad1基因缺陷的胚胎中原始生殖细胞的急剧减少，表明原始生殖细胞规范中Smad1依赖性信号的重要作用。出人意料的是，尽管BMP信号传导主要参与了正常胚胎的组织，但Smad1缺陷型胚胎却能正常发育。对早期小鼠胚胎中Smad1，Smad5和Smad8表达域的检查表明，虽然Smad1在内脏内胚层中的表达为6.5 dpc，但在其他组织中Smad1与Smad5和/或Smad8共表达。总体而言，这些数据揭示了Smad1信号传导在协调支持子宫环境内发育所必需的胚外结构生长方面的独特功能。

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