Vertex sliding drives intercalation by radial coupling of adhesion and actomyosin networks during Drosophila germband extension.
Vertex sliding drives intercalation by radial coupling of adhesion and actomyosin networks during Drosophila germband extension.
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DOI：
10.7554/elife.34586
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发表时间：
2018-07-09
期刊：
影响因子：
7.7
通讯作者：
Loerke D
中科院分区：
文献类型：
--
作者：
Vanderleest TE;Smits CM;Xie Y;Jewett CE;Blankenship JT;Loerke D
Oriented cell intercalation is an essential developmental process that shapes tissue morphologies through the directional insertion of cells between their neighbors. Previous research has focused on properties of cell–cell interfaces, while the function of tricellular vertices has remained unaddressed. Here, we identify a highly novel mechanism in which vertices demonstrate independent sliding behaviors along cell peripheries to produce the topological deformations responsible for intercalation. Through systematic analysis, we find that the motion of vertices connected by contracting interfaces is not physically coupled, but instead possess strong radial coupling. E-cadherin and Myosin II exist in previously unstudied populations at cell vertices and undergo oscillatory cycles of accumulation and dispersion that are coordinated with changes in cell area. Additionally, peak enrichment of vertex E-cadherin/Myosin II coincides with interface length stabilization. Our results suggest a model in which asymmetric radial force balance directs the progressive, ratcheted motion of individual vertices to drive intercalation. Cells need to come together to form tissues of different shapes and sizes. Cells can move about in different ways to shape the tissues. For example, a process called cell intercalation is vital for creating elongated structures like the spinal cord and inner ear. In intercalation, a cell slots itself between neighboring cells to lengthen tissues in one direction. Most of the work to understand cell intercalation has examined the interfaces that form between two neighboring cells. But there are points called vertices where three cells make contact with each other. Vanderleest, Smits et al. have now used microscopy and computational analysis to examine these contact points, known as vertices, in fruit flies. It was thought that vertices that are connected by a single interface coordinate how they move. However, Vanderleest, Smits et al. now show that these connected vertices move independently of each other. Instead, the movements of unconnected vertices on opposite sides of the cell show coordination. Vanderleest, Smits et al. also found that two proteins build up at the vertices in the early stages of intercalation. One of these, called E-cadherin, enables cells to stick to each other. The other protein, called Myosin II, helps E-cadherin to localize to the vertices and also enables cells to contract. These results suggest that the vertices help to guide intercalation and changes in cell shape. Tracking the vertices over time revealed that they slide around the surface of the cells. During this sliding the total length of the interfaces that meet at the vertex remains the same – so as one becomes shorter, neighboring interfaces will become longer. This creates a zipper-like movement of the vertices that tugs the cells into line and suggests a new mechanism by which interconnected cells can change shape. Future work will focus on identifying the molecules that specify these unique vertex behaviors.
