Transformation from morula to blastocyst is a defining event of preimplantation embryo development. During this transition, the embryo must establish a paracellular permeability barrier to enable expansion of the blastocyst cavity. Here, using live imaging of mouse embryos, we reveal an actin-zippering mechanism driving this embryo sealing. Preceding blastocyst stage, a cortical F-actin ring assembles at the apical pole of the embryo's outer cells. The ring structure forms when cortical actin flows encounter a network of polar microtubules that exclude F-actin. Unlike stereotypical actin rings, the actin rings of the mouse embryo are not contractile, but instead, they expand to the cell-cell junctions. Here, they couple to the junctions by recruiting and stabilizing adherens and tight junction components. Coupling of the actin rings triggers localized myosin II accumulation, and it initiates a tension-dependent zippering mechanism along the junctions that is required to seal the embryo for blastocyst formation.

中文翻译：

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扩大的肌动蛋白环使小鼠胚胎形成胚泡形成拉链。

从桑ula到胚泡的转化是植入前胚胎发育的决定性事件。在此过渡过程中，胚胎必须建立细胞旁通透性屏障，以使胚泡腔扩大。在这里，使用小鼠胚胎的实时成像，我们揭示了驱动该胚胎封闭的肌动蛋白拉链机制。在胚泡期之前，皮质F-肌动蛋白环在胚胎外部细胞的顶极组装。当皮质肌动蛋白流遇到排除F-肌动蛋白的极性微管网络时，形成环结构。与典型的肌动蛋白环不同，小鼠胚胎的肌动蛋白环不收缩，而是扩展到细胞-细胞连接处。在这里，它们通过募集并稳定附着物和紧密的连接组件而耦合到连接处。