Assembly and positioning of actomyosin rings by contractility and planar cell polarity.
Assembly and positioning of actomyosin rings by contractility and planar cell polarity.
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DOI：
10.7554/elife.09206
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发表时间：
2015-10-21
期刊：
影响因子：
7.7
通讯作者：
Jiang D
中科院分区：
文献类型：
--
作者：
Sehring IM;Recho P;Denker E;Kourakis M;Mathiesen B;Hannezo E;Dong B;Jiang D
肌动球蛋白细胞骨架是形态发生中的主要力产生机制，因此对细胞骨架定位的鲁棒空间控制是必不可少的。在这份报告中，我们表明，肌动球蛋白收缩性和平面细胞极性（PCP）在有丝分裂后的玻璃海鞘脊索细胞的相互作用，自组装和重新定位肌动球蛋白环，细胞伸长发挥着至关重要的作用。有趣的是，随着收缩力的增加，在向中心迁移之前，环总是在细胞的前缘形成，反映了皮层的一种新的动力学特性。我们的药物和基因操作揭示了收缩性和PCP之间的拔河比赛，收缩性使皮质流向赤道，PCP试图重新定位它们。我们开发了一个简单的模型，物理力量的基础上，这拔河比赛，定量再现我们的结果。因此，我们提出了一个定量的框架解剖收缩性和PCP的自组装和重新定位的细胞骨架结构，这应该是适用于其他形态发生事件的相对贡献。DOI：http://dx.doi.org/10.7554/eLife.09206.001动物细胞可以移动，细胞移动在发育的早期阶段特别重要，此时发育中的胚胎迅速改变形状。这些运动依赖于由一种叫做肌动蛋白的蛋白质组成的纤维网络。就像动物的骨骼一样，这个网络为细胞提供了一个内部支架，并支持细胞的运动。另一种称为肌球蛋白的蛋白质与肌动蛋白密切合作，并作为驱动这些运动的马达。为了研究细胞运动如何促进发育，科学家们经常求助于简单的管状海洋动物，称为海squares。这些看起来很奇怪的生物是人类和其他有脊髓的动物的远亲。所有这些相关的生物在其发育的最早阶段都发育出一种长的杆状结构，称为脊索，这对形成神经系统至关重要。研究海鞘脊索的发育比其他动物更容易，因为海鞘的脊索仅由40个排成一列的细胞组成。现在，Sehring等人提供了关于塑造海鞘中脊索细胞的力量的新细节。实验使用显微镜和荧光标记来观察细胞伸长形成杆状脊索时发生的情况，脊索从动物的前部延伸到后部。这表明，在每个细胞的前端附近形成了一个由肌动蛋白和肌球蛋白组成的环，然后迁移到细胞的中间，沿着沿着伸展。然后，Sehring等人用一种阻断肌球蛋白运动能力的药物处理这些细胞。在这些细胞中，肌动蛋白-肌球蛋白环仍然卡在细胞的前部。在后期处理细胞，也就是说，当环已经到达中心时，导致中心环移回细胞的前端。此外，当用肌球蛋白阻断药物处理一种细胞没有明显前部或后部的突变海鞘时，环最终出现在细胞中的随机位置。总之，这些结果表明，肌动蛋白-肌球蛋白环的位置是由细胞前端的拉力和环本身的肌球蛋白驱动力之间的拔河决定的。这些发现揭示了一个确定细胞内骨架位置的一般规律。未来的研究将询问细胞的前端如何吸引和拉动环，以及这对组织生长和器官形成意味着什么。DOI：http://dx.doi.org/10.7554/eLife.09206.002
The actomyosin cytoskeleton is a primary force-generating mechanism in morphogenesis, thus a robust spatial control of cytoskeletal positioning is essential. In this report, we demonstrate that actomyosin contractility and planar cell polarity (PCP) interact in post-mitotic Ciona notochord cells to self-assemble and reposition actomyosin rings, which play an essential role for cell elongation. Intriguingly, rings always form at the cells′ anterior edge before migrating towards the center as contractility increases, reflecting a novel dynamical property of the cortex. Our drug and genetic manipulations uncover a tug-of-war between contractility, which localizes cortical flows toward the equator and PCP, which tries to reposition them. We develop a simple model of the physical forces underlying this tug-of-war, which quantitatively reproduces our results. We thus propose a quantitative framework for dissecting the relative contribution of contractility and PCP to the self-assembly and repositioning of cytoskeletal structures, which should be applicable to other morphogenetic events. DOI: http://dx.doi.org/10.7554/eLife.09206.001 Animal cells can move, and cell movements are particularly important during the early stages of development, when the developing embryo rapidly changes shape. These movements depend on a network of fibers made up of a protein called actin. Just like an animal's skeleton, this network provides an internal scaffold for the cell and supports the cell's movements. Another protein called myosin works closely with actin and acts as a motor that drives these movements. To study how cellular movements contribute to development, scientists often turn to simple, tube-like sea animals called sea squirts. These strange-looking creatures are distant relatives of humans and other animals with a spinal cord. All of these related creatures develop a long, rod-shaped structure called the notochord during the earliest stages of their development that is critical for forming the nervous system. Studying the development of the notochord is easier in sea squirts than other animals because the sea squirt's notochord is made up of just 40 cells arranged in a single file. Now, Sehring et al. provide new details about the forces that shape the notochord cells in sea squirts. The experiments used microscopes and fluorescent markers to see what happens as the cells elongate to form the rod-like notochord, which stretches from the front to the back of the animal. This revealed that a ring made of actin and myosin forms near the front end of each cell and then migrates to the middle of the cell, stretching it along the way. Sehring et al. then treated the cells with a drug that blocks myosin's motor-like ability. In these cells, the actin–myosin ring remains stuck in the front of the cell. Treating the cells at a later stage, that is, when the rings had already arrived at the center, led to the central rings moving back to the front end of the cell. Furthermore, when a mutant sea squirt that had cells without a distinct front or back was treated with the myosin-blocking drug, the ring ended up at random places in the cells. Together, these results suggest that the placement of the actin–myosin ring is determined by a tug-of-war between the pull of the front end of the cell and the myosin-driven force of the ring itself. These findings reveal a general rule that can determine the position of cell's inner skeleton. Future studies will ask how the front end of the cell attracts and pulls the ring, and what this means for tissue growth and organ formation. DOI: http://dx.doi.org/10.7554/eLife.09206.002