会聚延伸(CE)需要平面细胞极性(PCP)蛋白1,2和肌动蛋白细胞骨架的协调作用,3,4,5,6,但这种关系仍未完全理解。例如,PCP信号传导定向肌动球蛋白收缩,而PCP蛋白的极化定位也需要肌动球蛋白7,8此外,肌动蛋白调节Septins在肌动蛋白组织中起关键作用9,并与青蛙的PCP和CE有关,老鼠,和fish5,6,10,11,12,但只执行PCP依赖细胞行为的子集。Septin丢失概括了在核心PCP破坏后看到的严重的组织水平CE缺陷,但留下了明显的细胞极性完整性。这些结果突出了一个普遍的事实,即细胞运动需要不同但整合的肌动蛋白群体的协调作用,例如迁移细胞中的薄片和薄片足虫13或参与根尖收缩的细胞中的内侧和交界肌动蛋白群体。14,15在非洲爪螨中胚层CE的背景下,三个这样的肌动蛋白群体很重要,称为“节点和电缆”系统的表面网格,4,16,17,18深层细胞-细胞连接处的收缩网络,6,19和中等取向的富含肌动蛋白的突起,表面和深度都存在。4,19,20,21这里,我们利用独特的“二维”节点和电缆系统的适应性来探测PCP蛋白之间的关系,Septins,和这个肌动蛋白网络的极化。我们发现PCP蛋白Vangl2和Prickle2和Septins共定位在节点,节点和电缆系统显示一个神秘的,PCP和Septin依赖性前后(AP)极性在其组织和动力学。
Convergent extension (CE) requires the coordinated action of the planar cell polarity (PCP) proteins1,2 and the actin cytoskeleton,3,4,5,6 but this relationship remains incompletely understood. For example, PCP signaling orients actomyosin contractions, yet actomyosin is also required for the polarized localization of PCP proteins.7,8 Moreover, the actin-regulating Septins play key roles in actin organization9 and are implicated in PCP and CE in frogs, mice, and fish5,6,10,11,12 but execute only a subset of PCP-dependent cell behaviors. Septin loss recapitulates the severe tissue-level CE defects seen after core PCP disruption yet leaves overt cell polarity intact.5 Together, these results highlight the general fact that cell movement requires coordinated action by distinct but integrated actin populations, such as lamella and lamellipodia in migrating cells13 or medial and junctional actin populations in cells engaged in apical constriction.14,15 In the context of Xenopus mesoderm CE, three such actin populations are important, a superficial meshwork known as the \"node-and-cable\" system,4,16,17,18 a contractile network at deep cell-cell junctions,6,19 and mediolaterally oriented actin-rich protrusions, which are present both superficially and deeply.4,19,20,21 Here, we exploited the amenability of the uniquely \"two-dimensional\" node and cable system to probe the relationship between PCP proteins, Septins, and the polarization of this actin network. We find that the PCP proteins Vangl2 and Prickle2 and Septins co-localize at nodes, and that the node and cable system displays a cryptic, PCP- and Septin-dependent anteroposterior (AP) polarity in its organization and dynamics.