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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Postgastrulation Smad2-deficient embryos show defects in embryo turning and anterior morphogenesis
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Postgastrulation Smad2-deficient embryos show defects in embryo turning and anterior morphogenesis

机译：妊娠后Smad2缺陷型胚胎在胚胎转向和前部形态发生方面表现出缺陷

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摘要

SMAD2 is a member of the transforming growth factor #beta# and activin-signaling pathway. To examine the role of Smad2 in postgas- trulation development, we independently generated mice with a null mutation in this gene. Smad2-deficient embryos die around day 7.5 of gestation because of failure of gastrulatian and failure to establish an anteror-posterior (A-P) axis. Expressian of the homeobox gene Hex (the earliest known marker of the A-P polarity and the prospec- tive head organizer) was found to be missing in Smad2-deficient embryos. Homozygous mutant embryos and embryonic stem cells formed mesoderm derivatives revealing that mesoderm induction is SMAD2 independent. In the presence of wild-type extraembryonic tissues, Smad2-deficient embryos developed beyond 7.5 and up to 10.5 days postcoitum, demonstrating a requirement for SMAD2 in extraembryonic tissues for the generation of an A-P axis and gastru- lation. The rescued postgastrulation embryos showed malformation of head structures, abnormal embryo turning, and cyclopia. Our results show that smad2 expression is required at several stages during embryogenesis.
机译：SMAD2是转化生长因子＃beta＃和激活素信号通路的成员。为了检查Smad2在胃后发育中的作用，我们独立产生了在该基因中具有无效突变的小鼠。缺乏Smad2的胚胎会在妊娠7.5天左右死亡，这是因为其胃下肌衰竭和无法建立前后轴（A-P）。发现在Smad2缺陷的胚胎中缺少同源盒基因Hex的Expressian（最早的已知A-P极性标记和预期的头部组织者）。纯合子突变体胚胎和胚胎干细胞形成中胚层衍生物，表明中胚层诱导是SMAD2独立的。在存在野生型胚外组织的情况下，Smad2缺陷型胚胎发育超过7.5天，并在分娩后长达10.5天，这表明胚外组织中对SMAD2的需求导致了A-P轴的产生和胃的塑形。被救出的胎后胚胎显示出头部结构畸形，异常的胚胎转向和睫状体。我们的结果表明，smad2表达在胚胎发生的多个阶段是必需的。

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