Sehring Ivonne M, Recho Pierre, Denker Elsa, Kourakis Matthew, Mathiesen Birthe, Hannezo Edouard, Dong Bo, Jiang Di
Sars International Centre for Marine Molecular Biology, University of Bergen, Bergen, Norway.
Department of Physico-Chemistry of Living Matter, Institut Curie, Paris, France.
Elife. 2015 Oct 21;4:e09206. doi: 10.7554/eLife.09206.
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.
肌动球蛋白细胞骨架是形态发生过程中主要的力产生机制,因此对细胞骨架定位进行稳健的空间控制至关重要。在本报告中,我们证明了在有丝分裂后的海鞘脊索细胞中,肌动球蛋白收缩性与平面细胞极性(PCP)相互作用,以自组装和重新定位肌动球蛋白环,这对细胞伸长起着至关重要的作用。有趣的是,随着收缩性增加,环总是在细胞前缘形成,然后向中心迁移,这反映了皮层的一种新的动态特性。我们的药物和基因操作揭示了收缩性(使皮层流朝向赤道定位)与PCP(试图重新定位皮层流)之间的拔河效应。我们建立了一个关于这种拔河效应背后物理力的简单模型,该模型定量地重现了我们的结果。因此,我们提出了一个定量框架,用于剖析收缩性和PCP对细胞骨架结构自组装和重新定位的相对贡献,该框架应适用于其他形态发生事件。