Gap closure is a common morphogenetic process. In mammals, failure to close the embryonic hindbrain neuropore (HNP) gap causes fatal anencephaly. We observed that surface ectoderm cells surrounding the mouse HNP assemble high-tension actomyosin purse strings at their leading edge and establish the initial contacts across the embryonic midline. Fibronectin and laminin are present, and tensin 1 accumulates in focal adhesion-like puncta at this leading edge. The HNP gap closes asymmetrically, faster from its rostral than caudal end, while maintaining an elongated aspect ratio. Cell-based physical modeling identifies two closure mechanisms sufficient to account for tissue-level HNP closure dynamics: purse-string contraction and directional cell motion implemented through active crawling. Combining both closure mechanisms hastens gap closure and produces a constant rate of gap shortening. Purse-string contraction reduces, whereas crawling increases gap aspect ratio, and their combination maintains it. Closure rate asymmetry can be explained by asymmetric embryo tissue geometry, namely a narrower rostral gap apex, whereas biomechanical tension inferred from laser ablation is equivalent at the gaps’ rostral and caudal closure points. At the cellular level, the physical model predicts rearrangements of cells at the HNP rostral and caudal extremes as the gap shortens. These behaviors are reproducibly live imaged in mouse embryos. Thus, mammalian embryos coordinate cellular- and tissue-level mechanics to achieve this critical gap closure event.

间隙闭合是一种常见的形态发生过程。在哺乳动物中，胚胎后脑神经孔（HNP）间隙未能闭合会导致致命的无脑畸形。我们观察到小鼠 HNP 周围的表面外胚层细胞在其前缘组装高张力肌动球蛋白荷包，并在胚胎中线建立初始接触。存在纤连蛋白和层粘连蛋白，张力蛋白 1 积聚在该前缘的粘着斑状斑点中。 HNP 间隙不对称地闭合，从头端比从尾端闭合得更快，同时保持细长的纵横比。基于细胞的物理模型确定了两种足以解释组织水平 HNP 闭合动态的闭合机制：荷包收缩和通过主动爬行实现的定向细胞运动。结合两种闭合机制可加速间隙闭合并产生恒定的间隙缩短率。荷包收缩会减少，而爬行会增加间隙纵横比，它们的组合可以维持该间隙纵横比。闭合率不对称可以通过不对称的胚胎组织几何形状来解释，即较窄的吻端间隙顶点，而从激光消融推断出的生物力学张力在间隙的吻端和尾端闭合点处是相等的。在细胞水平上，物理模型预测随着间隙的缩短，HNP 头端和尾端的细胞会发生重新排列。这些行为在小鼠胚胎中可重复地实时成像。因此，哺乳动物胚胎协调细胞和组织水平的力学来实现这一关键的间隙闭合事件。