Actin cortex controls cell migration Cell migration is mainly controlled by local actin polymerization–driven membrane protrusion. However, a second structural mechanism might also regulate membrane protrusions and directed migration: changes in the density of the attachment between the plasma membrane and the underlying F-actin cortex, a parameter related to membrane tension. Many types of attachment and signaling mechanisms are known to alter the density of membrane-proximal cortical actin. Bisaria et al. designed a membrane-proximal F-actin (MPA) reporter that could directly measure local changes in the density of MPA in living cells. Levels of MPA were surprisingly low toward the front of migrating cells despite an opposing high overall concentration of F-actin in the same front region. The researchers propose that MPA density can integrate different signaling processes to direct local membrane protrusions and stabilize cell polarity during cell migration. Science, this issue p. 1205 Membrane protrusion and cell migration are directed by local decreases in the density of filamentous actin close to the cell membrane. Cell migration is driven by local membrane protrusion through directed polymerization of F-actin at the front. However, F-actin next to the plasma membrane also tethers the membrane and thus resists outgoing protrusions. Here, we developed a fluorescent reporter to monitor changes in the density of membrane-proximal F-actin (MPA) during membrane protrusion and cell migration. Unlike the total F-actin concentration, which was high in the front of migrating cells, MPA density was low in the front and high in the back. Back-to-front MPA density gradients were controlled by higher cofilin-mediated turnover of F-actin in the front. Furthermore, nascent membrane protrusions selectively extended outward from areas where MPA density was reduced. Thus, locally low MPA density directs local membrane protrusions and stabilizes cell polarization during cell migration.

中文翻译：

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近膜 F-肌动蛋白限制局部膜突出并指导细胞迁​​移

肌动蛋白皮层控制细胞迁移 细胞迁移主要受局部肌动蛋白聚合驱动的膜突出控制。然而，第二种结构机制也可能调节膜突出和定向迁移：质膜和底层 F-肌动蛋白皮层之间附着密度的变化，这是一个与膜张力相关的参数。已知许多类型的附着和信号机制会改变近膜皮质肌动蛋白的密度。比萨里亚等人。设计了一种近膜 F-肌动蛋白 (MPA) 报告基因，可以直接测量活细胞中 MPA 密度的局部变化。尽管在同一前沿区域中 F-肌动蛋白的总体浓度相对较高，但在迁移细胞的前沿的 MPA 水平却出奇地低。研究人员提出，MPA 密度可以整合不同的信号过程，以在细胞迁移过程中引导局部膜突出并稳定细胞极性。科学，这个问题 p。1205 细胞膜突出和细胞迁移是由靠近细胞膜的丝状肌动蛋白密度的局部降低引起的。细胞迁移是由局部膜突出通过 F-肌动蛋白在前端的定向聚合驱动的。然而，紧邻质膜的 F-肌动蛋白也束缚了膜，从而阻止了向外突出。在这里，我们开发了一种荧光报告器来监测膜突出和细胞迁移过程中膜近端 F-肌动蛋白 (MPA) 密度的变化。与迁移细胞前部高的总 F-肌动蛋白浓度不同，MPA 密度前部低而后部高。从后到前的 MPA 密度梯度受前部 F-肌动蛋白更高的 cofilin 介导的周转控制。此外，新生的膜突起选择性地从 MPA 密度降低的区域向外延伸。因此，局部低 MPA 密度引导局部膜突起并在细胞迁移过程中稳定细胞极化。