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Xmc mediates Xctr1-independent morphogenesis in Xenopus laevis.

机译:Xmc介导非洲爪蟾Xctr1独立的形态发生。

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摘要

In the frog, Xenopus laevis, fibroblast growth factor (FGF) signaling is required for both mesoderm formation and the morphogenetic movements that drive the elongation of the notochord, a dorsal mesodermal derivative; the coordination of these distinct roles is mediated by the Xenopus Ctr1 (Xctr1) protein: maternal Xctr1 is required for mesodermal differentiation, while the subsequent loss of Xctr1 promotes morphogenesis. The signaling cascade activated by FGF in the presence of Ctr1 has been well characterized; however, the Xctr1-independent, FGF-responsive network remains poorly defined. We have identified Xenopus Marginal Coil (Xmc) as a gene whose expression is highly enriched following Xctr1 knockdown. Zygotic initiation of Xmc expression in vivo coincides with a decrease in maternal Xctr1 transcripts; moreover, Xmc loss-of-function inhibits Xctr1 knockdown-mediated elongation of FGF-treated animal cap explants, implicating Xmc as a key effector of Xctr1-independent gastrular morphogenesis.
机译:在青蛙非洲爪蟾中,成纤维细胞生长因子(FGF)信号是中胚层形成和驱动背脊线(中背皮衍生物)伸长的形态发生运动所必需的。这些不同角色的协调是由非洲爪蟾Ctr1(Xctr1)蛋白介导的:中胚层分化需要母体Xctr1,而随后Xctr1的缺失会促进形态发生。在Ctr1存在下被FGF激活的信号级联反应已被很好地表征。但是,Xctr1独立,FGF反应网络仍然定义不清。我们已经确定非洲爪蟾边缘线圈(Xmc)作为其基因在Xctr1敲除后高度富集的基因。体内Xmc表达的合子启动与母体Xctr1转录物的减少相吻合。此外,Xmc功能丧失抑制Xctr1敲低介导的FGF处理的动物帽外植体的伸长,暗示Xmc是Xctr1依赖性胃小形态发生的关键效应子。

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