Edwards K A, Kiehart D P
Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.
Development. 1996 May;122(5):1499-511. doi: 10.1242/dev.122.5.1499.
Morphogenesis is characterized by orchestrated changes in the shape and position of individual cells. Many of these movements are thought to be powered by motor proteins. However, in metazoans, it is often difficult to match specific motors with the movements they drive. The nonmuscle myosin II heavy chain (MHC encoded by zipper is required for cell sheet movements in Drosophila embryos. To determine if myosin II is required for other processes, we examined the phenotypes of strong and weak larval lethal mutations in spaghetti squash (sqh), which encodes the nonmuscle myosin II regulatory light chain (RLC). sqh mutants can be rescued to adulthood by daily induction of a sqh cDNA transgene driven by the hsp70 promoter. By transiently ceasing induction of the cDNA, we depleted RLC at specific times during development. When RLC is transiently depleted in larvae, the resulting adult phenotypes demonstrate that RLC is required in a stage-specific fashion for proper development of eye and leg imaginal discs. When RLC is depleted in adult females, oogenesis is reversibly disrupted. Without RLC induction, developing egg chambers display a succession of phenotypes that demonstrate roles for myosin II in morphogenesis of the interfollicular stalks, three morphologically and mechanistically distinct types of follicle cell migration, and completion of nurse cell cytoplasm transport (dumping). Finally, we show that in sqh mutant tissues, MHC is abnormally localized in punctate structures that do not contain appreciable amounts of filamentous actin or the myosin tail-binding protein p127. This suggests that sqh mutant phenotypes are chiefly caused by sequestration of myosin into inactive aggregates. These results show that myosin II is responsible for a surprisingly diverse array of cell shape changes throughout development.
形态发生的特征是单个细胞的形状和位置发生协调变化。许多此类运动被认为是由马达蛋白驱动的。然而，在后生动物中，通常很难将特定的马达蛋白与其驱动的运动相匹配。果蝇胚胎中细胞片层运动需要由拉链基因编码的非肌肉肌球蛋白II重链（MHC）。为了确定肌球蛋白II是否参与其他过程，我们研究了编码非肌肉肌球蛋白II调节轻链（RLC）的南瓜基因（sqh）中强、弱幼虫致死突变体的表型。通过由hsp70启动子驱动的sqh cDNA转基因的每日诱导，sqh突变体可以存活至成年。通过暂时停止cDNA的诱导，我们在发育的特定时间耗尽了RLC。当幼虫中的RLC被暂时耗尽时，所产生的成年表型表明RLC以阶段特异性方式是眼和腿成虫盘正常发育所必需的。当成年雌性中的RLC被耗尽时，卵子发生被可逆地破坏。在没有RLC诱导的情况下，发育中的卵室表现出一系列表型，这些表型表明肌球蛋白II在滤泡间柄的形态发生、三种形态和机制上不同类型的滤泡细胞迁移以及滋养细胞细胞质运输（倾倒）的完成中发挥作用。最后，我们表明在sqh突变组织中，MHC异常定位于点状结构中，这些结构不含有大量的丝状肌动蛋白或肌球蛋白尾部结合蛋白p127。这表明sqh突变体表型主要是由肌球蛋白隔离到无活性聚集体中引起的。这些结果表明，肌球蛋白II在整个发育过程中负责一系列惊人多样的细胞形状变化。
