Nonmuscle myosin II generates forces that transmit tension and drive contraction in multiple tissues during dorsal closure
Nonmuscle myosin II generates forces that transmit tension and drive contraction in multiple tissues during dorsal closure
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DOI：
10.1016/j.cub.2005.11.064
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发表时间：
2005-12-20
期刊：
影响因子：
9.2
通讯作者：
Kiehart, DP
中科院分区：
文献类型：
--
作者：
Franke, JD;Montague, RA;Kiehart, DP
背景：作为胚胎发育特征的形态发生运动需要对细胞形状变化进行精确的时间和空间控制。果蝇背侧闭合是一个成熟的上皮片形态发生模型，超过60个基因的突变导致闭合缺陷。闭合需要来自不同组织的四种力精确平衡。负责产生的每一个部队的蛋白质尚未determined.Results：我们的文件背关闭在活的胚胎显示，突变在非肌肉肌球蛋白11（编码的拉链;拉链/Myoll）破坏多个组织的完整性，在关闭。我们证明，Myoll本地化是不同的，但重叠，F-肌动蛋白在suracellular荷包，而在adjacoserosa。和侧表皮均具有相似的皮质分布。在zip/Myoll突变体胚胎中，我们恢复Myoll功能，无论是普遍存在的还是特异性的，在前缘，浆膜，或侧表皮，并发现zip/Myoll功能在任何一个组织可以拯救关闭。使用一种新的转基因镶嵌方法，我们确定了前缘细胞中的超细胞荷包线的收缩性需要zip/Myoll产生的力; zip/Myoll功能负责浆膜细胞的顶端收缩; zip/Myoll对拉链很重要; zip/Myoll收缩性的缺陷导致接缝形成过程中外侧表皮片的错位。结论：我们确定zip/Myoll负责产生力，驱动每个力产生组织中细胞形状的变化，从而有助于闭合。这种高度保守的收缩蛋白可能在整个胚胎发育过程中驱动细胞片层运动。
Background: The morphogenic movements that characterize embryonic development require the precise temporal and spatial control of cell-shape changes. Drosophila dorsal closure is a well-established model for epithelial sheet morphogenesis, and mutations in more than 60 genes cause defects in closure. Closure requires that four forces, derived from distinct tissues, be precisely balanced. The proteins responsible for generating each of the forces have not been determined.Results: We document dorsal closure in living embryos to show that mutations in nonmuscle myosin 11 (encoded by zipper; zip/Myoll) disrupt the integrity of multiple tissues during closure. We demonstrate that Myoll localization is distinct from, but overlaps, F-actin in the supracellular purse string, whereas in the amnioserosa. and lateral epidermis each has similar, cortical distributions. In zip/Myoll mutant embryos, we restore Myoll function either ubiquitously or specifically in the leading edge, amnioserosa, or lateral epidermis and find that zip/Myoll function in any one tissue can rescue closure. Using a novel, transgenic mosaic approach, we establish that contractility of the supracellular purse string in leadingedge cells requires zip/Myoll-generated forces; that zip/Myoll function is responsible for the apical contraction of amnioserosa cells; that zip/Myoll is important for zipping; and that defects in zip/Myoll contractility cause the misalignment of the lateral-epidermal sheets during seam formation.Conclusions: We establish that zip/Myoll is responsible forgenerating the forces that drive cell-shape changes in each of the force-generating tissues that contribute to closure. This highly conserved contractile protein likely drives cell-sheet movements throughout phylogeny.