The apical junction of epithelial cells can generate force to control cell geometry and perform contractile processes while maintaining barrier function and adhesion. Yet, the structural basis for force generation at the apical junction is not fully understood. Here, we describe two synaptopodin-dependent actomyosin structures that are spatially, temporally, and structurally distinct. The first structure is formed by the retrograde flow of synaptopodin initiated at the apical junction, creating a sarcomeric stress fiber that lies parallel to the apical junction. Contraction of the apical stress fiber is associated with either clustering of membrane components or shortening of junctional length. Upon junction maturation, apical stress fibers are disassembled. In mature epithelial monolayer, a motorized “contractomere” capable of “walking the junction” is formed at the junctional vertex. Actomyosin activities at the contractomere produce a compressive force evident by actin filament buckling and measurement with a new α-actinin-4 force sensor. The motility of contractomeres can adjust junctional length and change cell packing geometry during cell extrusion and intercellular movement. We propose a model of epithelial homeostasis that utilizes contractomere motility to support junction rearrangement while preserving the permeability barrier.

中文翻译：

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上皮连接处的突触蛋白应力纤维和收缩小球


上皮细胞的顶端连接可以产生力来控制细胞几何形状并执行收缩过程，同时维持屏障功能和粘附。然而，心尖连接处产生力的结构基础尚未完全了解。在这里，我们描述了两种在空间、时间和结构上不同的突触蛋白依赖性肌动球蛋白结构。第一个结构是由在顶端连接处引发的突触蛋白的逆行流动形成的，产生平行于顶端连接处的肌节应力纤维。顶端应力纤维的收缩与膜成分的聚集或连接长度的缩短有关。连接成熟后，顶端应力纤维被分解。在成熟的上皮单层中，在交界顶点形成能够“行走交界处”的机动化“收缩粒”。收缩球的肌动球蛋白活动产生压缩力，通过肌动蛋白丝屈曲和使用新的 α-actinin-4 力传感器进行测量可以明显看出。收缩粒的运动可以在细胞挤出和细胞间运动过程中调节连接长度并改变细胞堆积的几何形状。我们提出了一种上皮稳态模型，利用收缩小球运动来支持连接重排，同时保留通透性屏障。