Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Dr. Aiguader, 88, Barcelona 08003, Spain.
Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona 08028, Spain.
Dev Cell. 2018 Nov 19;47(4):453-463.e3. doi: 10.1016/j.devcel.2018.10.025.
During epithelial contraction, cells generate forces to constrict their surface and, concurrently, fine-tune the length of their adherens junctions to ensure force transmission. While many studies have focused on understanding force generation, little is known on how junctional length is controlled. Here, we show that, during amnioserosa contraction in Drosophila dorsal closure, adherens junctions reduce their length in coordination with the shrinkage of apical cell area, maintaining a nearly constant junctional straightness. We reveal that junctional straightness and integrity depend on the endocytic machinery and on the mechanosensitive activity of the actomyosin cytoskeleton. On one hand, upon junctional stretch and decrease in E-cadherin density, actomyosin relocalizes from the medial area to the junctions, thus maintaining junctional integrity. On the other hand, when junctions have excess material and ruffles, junction removal is enhanced, and high junctional straightness and tension are restored. These two mechanisms control junctional length and integrity during morphogenesis.
在上皮细胞收缩过程中，细胞会产生力来收缩其表面，并同时微调黏着连接的长度，以确保力的传递。虽然许多研究都集中在理解力的产生上，但对于如何控制连接长度知之甚少。在这里，我们表明，在果蝇背腹闭合过程中羊浆膜的收缩过程中，黏着连接会与顶端细胞面积的收缩相协调而缩短，从而保持几乎恒定的连接直线度。我们揭示了连接的直线度和完整性取决于内吞作用机制以及肌动球蛋白细胞骨架的机械敏感性活性。一方面，在连接拉伸和 E-钙黏蛋白密度降低时，肌动球蛋白从中央区域重新分布到连接点，从而维持连接的完整性。另一方面，当连接点有多余的物质和褶皱时，连接点的去除会增强，并且高连接直线度和张力会得到恢复。这两个机制在形态发生过程中控制连接的长度和完整性。
