Several cytoskeleton-associated proteins and signaling pathways work in concert to regulate actin cytoskeleton remodeling, cell adhesion, and migration. Although the leukocyte-specific protein 1 (LSP1) has been shown to interact with the actin cytoskeleton, its function in the regulation of actin cytoskeleton dynamics is, as yet, not fully understood. We have recently demonstrated that the bimolecular complex between LSP1 and myosin1e controls actin cytoskeleton remodeling during phagocytosis. In this study, we show that LSP1 downregulation severely impairs cell migration, lamellipodia formation, and focal adhesion dynamics in macrophages. Inhibition of the interaction between LSP1 and myosin1e also impairs these processes resulting in poorly motile cells, which are characterized by few and small lamellipodia. Furthermore, cells in which LSP1-myosin1e interaction is inhibited are typically associated with inefficient focal adhesion turnover. Collectively, our findings show that the LSP1-myosin1e bimolecular complex plays a pivotal role in the regulation of actin cytoskeleton remodeling and focal adhesion dynamics required for cell migration.

中文翻译：

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LSP1-myosin1e双分子复合物调节粘着斑动力学和细胞迁移

几种细胞骨架相关蛋白和信号通路协同工作以调节肌动蛋白细胞骨架重塑、细胞粘附和迁移。尽管已显示白细胞特异性蛋白 1 (LSP1) 与肌动蛋白细胞骨架相互作用，但其在调节肌动蛋白细胞骨架动力学方面的功能尚未完全了解。我们最近证明了 LSP1 和 myosin1e 之间的双分子复合物控制吞噬作用过程中肌动蛋白细胞骨架的重塑。在这项研究中，我们表明 LSP1 下调严重损害巨噬细胞中的细胞迁移、片状伪足形成和粘着斑动力学。抑制 LSP1 和肌球蛋白 1e 之间的相互作用也会损害这些过程，导致运动性差的细胞，其特征是片状伪足少而小。此外，LSP1-myosin1e 相互作用被抑制的细胞通常与低效的粘着斑周转有关。总的来说，我们的研究结果表明，LSP1-myosin1e 双分子复合物在调节肌动蛋白细胞骨架重塑和细胞迁移所需的粘着斑动力学方面发挥着关键作用。