Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA.
Curr Biol. 2010 Feb 9;20(3):253-8. doi: 10.1016/j.cub.2009.12.021. Epub 2010 Jan 21.
Coordinated apical constriction (AC) in epithelial sheets drives tissue invagination [1, 2] and is required for diverse morphogenetic movements such as gastrulation [3], neurulation [4, 5], and organogenesis [6]. We showed previously that actomyosin contractility drives AC in Xenopus laevis bottle cells [7]; however, it remained unclear whether it does so in concert with other processes. Here we report that endocytosis-driven membrane remodeling is required for efficient AC. We found endosomes exclusively in bottle cells in the early gastrula. Disrupting endocytosis with dominant-negative dynamin or rab5 perturbed AC, with a significant decrease in constriction rate late in the process, suggesting that endocytosis operates downstream of actomyosin contractility to remove excess membrane. Additionally, disrupting endocytosis during neurulation inhibits AC in hingepoint cells, resulting in neural tube closure defects. Thus, membrane remodeling during AC could be a general mechanism to achieve efficient invagination in embryos.
上皮片层的协调顶端收缩（AC）驱动组织内陷[1,2]，并且是各种形态发生运动所必需的，例如原肠胚形成[3]、神经胚形成[4,5]和器官发生[6]。我们之前已经表明，肌动球蛋白收缩力驱动非洲爪蟾瓶状细胞中的 AC[7]；然而，尚不清楚它是否与其他过程协同作用。在这里，我们报告说内吞作用驱动的膜重塑对于有效的 AC 是必需的。我们发现早期原肠胚中只有瓶状细胞中存在内体。用显性负性 dynamin 或 rab5 破坏内吞作用会扰乱 AC，在过程后期收缩率显著降低，这表明内吞作用在肌动球蛋白收缩力之后起作用，以去除多余的膜。此外，在神经胚形成期间破坏内吞作用会抑制铰接点细胞中的 AC，导致神经管闭合缺陷。因此，AC 期间的膜重塑可能是胚胎中实现有效内陷的一般机制。
