Pulsatile cell-autonomous contractility drives compaction in the mouse embryo
Pulsatile cell-autonomous contractility drives compaction in the mouse embryo
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DOI：
10.1038/ncb3185
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发表时间：
2015-07-01
影响因子：
21.3
通讯作者：
Hiiragi, Takashi
中科院分区：
文献类型：
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作者：
Maitre, Jean-Leon;Niwayama, Ritsuya;Hiiragi, Takashi
哺乳动物胚胎开始形态发生与压实，这是必不可少的指定的第一谱系的囊胚。8细胞阶段的小鼠胚胎通过以Cdh 1依赖的方式扩大其细胞-细胞接触而紧凑。因此提出Cdh 1粘附分子产生驱动压实的力。使用微量吸管抽吸映射所有的紧张局势在发育中的胚胎，我们表明，压实主要是由一个两倍的张力增加在细胞介质界面。我们发现，主要的力发生器的压实是肌动球蛋白皮质，这引起了脉冲收缩开始在8细胞阶段。值得注意的是，当细胞脱离粘附接触时，收缩以周期性皮层波的形式出现。与此一致，mzCdh 1（-/-）胚胎的张力映射表明，Cdh 1通过重定向收缩远离细胞-细胞接触而起作用。我们的研究提供了一个框架，以了解早期哺乳动物胚胎发生和进化保守的脉冲收缩的原始观点。
Mammalian embryos initiate morphogenesis with compaction, which is essential for specifying the first lineages of the blastocyst. The 8-cell-stage mouse embryo compacts by enlarging its cell-cell contacts in a Cdh1-dependent manner. It was therefore proposed that Cdh1 adhesion molecules generate the forces driving compaction. Using micropipette aspiration to map all tensions in a developing embryo, we show that compaction is primarily driven by a twofold increase in tension at the cell-medium interface. We show that the principal force generator of compaction is the actomyosin cortex, which gives rise to pulsed contractions starting at the 8-cell stage. Remarkably, contractions emerge as periodic cortical waves when cells are disengaged from adhesive contacts. In line with this, tension mapping of mzCdh1(-/-) embryos suggests that Cdh1 acts by redirecting contractility away from cell-cell contacts. Our study provides a framework to understand early mammalian embryogenesis and original perspectives on evolutionary conserved pulsed contractions.