Phagocytes use their actomyosin cytoskeleton to migrate as well as to probe their environment by phagocytosis or macropinocytosis. Although migration and extracellular material uptake have been shown to be coupled in some immune cells, the mechanisms involved in such coupling are largely unknown. By combining time-lapse imaging with genetics, we here identify the lysosomal Ca2+ channel Trpml as an essential player in the coupling of cell locomotion and phagocytosis in hemocytes, the Drosophila macrophage-like immune cells. Trpml is needed for both hemocyte migration and phagocytic processing at distinct subcellular localizations: Trpml regulates hemocyte migration by controlling actomyosin contractility at the cell rear, whereas its role in phagocytic processing lies near the phagocytic cup in a myosin-independent fashion. We further highlight that Vamp7 also regulates phagocytic processing and locomotion but uses pathways distinct from those of Trpml. Our results suggest that multiple mechanisms may have emerged during evolution to couple phagocytic processing to cell migration and facilitate space exploration by immune cells.

中文翻译：

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Trpml 控制肌动球蛋白收缩性并将迁移与果蝇巨噬细胞的吞噬作用耦合

吞噬细胞利用其肌动球蛋白细胞骨架进行迁移，并通过吞噬作用或巨胞饮作用来探测其环境。尽管迁移和细胞外物质摄取已被证明在一些免疫细胞中是耦合的，但这种耦合所涉及的机制在很大程度上是未知的。通过将延时成像与遗传学相结合，我们在此确定溶酶体 Ca2+ 通道 Trpml 是血细胞（果蝇巨噬细胞样免疫细胞）中细胞运动和吞噬作用耦合的重要参与者。Trpml 对于不同亚细胞定位的血细胞迁移和吞噬过程都是必需的：Trpml 通过控制细胞后部的肌动球蛋白收缩性来调节血细胞迁移，而其在吞噬过程中的作用则以不依赖于肌球蛋白的方式位于吞噬杯附近。我们进一步强调，Vamp7 还调节吞噬过程和运动，但使用与 Trpml 不同的途径。我们的结果表明，在进化过程中可能出现了多种机制，将吞噬过程与细胞迁移结合起来，并促进免疫细胞的空间探索。