Cytoskeletal dynamics and supracellular organisation of cell shape fluctuations during dorsal closure
Cytoskeletal dynamics and supracellular organisation of cell shape fluctuations during dorsal closure
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DOI：
10.1242/dev.045872
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发表时间：
2010-08-15
期刊：
影响因子：
4.6
通讯作者：
Gorfinkiel, Nicole
中科院分区：
文献类型：
--
作者：
Blanchard, Guy B.;Murugesu, Sughashini;Gorfinkiel, Nicole
在果蝇背侧闭合（DC）过程中，羊膜（AS）细胞形状的波动为理解收缩上皮提供了一个理想的系统，无论是从细胞机制方面还是从单个细胞的活动如何产生组织行为方面。通过定量图像分析，我们发现细胞顶端形状的波动是由内侧细胞骨架驱动的，有周期性的收缩肌凝蛋白和肌动蛋白穿过细胞顶端。形状变化大多是各向异性的，相邻的细胞经常（但是短暂的）组织成平行变形的弦。在DC的早期阶段，长周期长度的形状波动不会产生净组织收缩。周期长度随着净组织收缩的开始而缩短，随后是波动幅度的衰减。最终，随着as细胞迅速收缩，波动变得无法检测。这些转变伴随着顶端肌凝蛋白的增加，在细胞-细胞连接处和中间，后者最终形成一个连贯的，但仍然是动态的，跨越细胞的薄片。肌凝蛋白活性或肌动蛋白聚合增加的突变体通过改变肌凝蛋白的亚细胞定位表现出细胞早衰收缩。粗脉突变体胚胎在前缘肌动蛋白索上表现出缺陷，其波动衰减时间与野生型相似，表明衰减是AS的自主特性。我们的研究结果表明，细胞形状波动是顶端肌凝蛋白水平低和增加的细胞的特性，并且中间和连接肌凝蛋白群体联合起来收缩AS细胞顶端并驱动DC。
Fluctuations in the shape of amnioserosa (AS) cells during Drosophila dorsal closure (DC) provide an ideal system with which to understand contractile epithelia, both in terms of the cellular mechanisms and how tissue behaviour emerges from the activity of individual cells. Using quantitative image analysis we show that apical shape fluctuations are driven by the medial cytoskeleton, with periodic foci of contractile myosin and actin travelling across cell apices. Shape changes were mostly anisotropic and neighbouring cells were often, but transiently, organised into strings with parallel deformations. During the early stages of DC, shape fluctuations with long cycle lengths produced no net tissue contraction. Cycle lengths shortened with the onset of net tissue contraction, followed by a damping of fluctuation amplitude. Eventually, fluctuations became undetectable as AS cells contracted rapidly. These transitions were accompanied by an increase in apical myosin, both at cell-cell junctions and medially, the latter ultimately forming a coherent, but still dynamic, sheet across cells. Mutants with increased myosin activity or actin polymerisation exhibited precocious cell contraction through changes in the subcellular localisation of myosin. thickveins mutant embryos, which exhibited defects in the actin cable at the leading edge, showed similar timings of fluctuation damping to the wild type, suggesting that damping is an autonomous property of the AS. Our results suggest that cell shape fluctuations are a property of cells with low and increasing levels of apical myosin, and that medial and junctional myosin populations combine to contract AS cell apices and drive DC.