Migrasomes, vesicular organelles generated on the retraction fibers of migrating cells, play a crucial role in migracytosis, mediating intercellular communication. The cargoes determine the functional specificity of migrasomes. Migrasomes harbor numerous intraluminal vesicles, a pivotal component of their cargoes. The mechanism underlying the transportation of these intraluminal vesicles to the migrasomes remains enigmatic. In this study, we identified that Rab10 and Caveolin-1 (CAV1) mark the intraluminal vesicles in migrasomes. Transport of Rab10-CAV1 vesicles to migrasomes required the motor protein Myosin Va and adaptor proteins RILPL2. Notably, the phosphorylation of Rab10 by the kinase LRRK2 regulated this process. Moreover, CSF-1 can be transported to migrasomes through this mechanism, subsequently fostering monocyte–macrophage differentiation in skin wound healing, which served as a proof of the physiological importance of this transporting mechanism.

中文翻译：

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Rab10-CAV1 介导的腔内囊泡转运至迁移体


迁移体是在迁移细胞的回缩纤维上产生的囊泡细胞器，在迁移细胞作用、介导细胞间通讯中发挥着至关重要的作用。货物决定了迁移体的功能特异性。迁移体含有大量的腔内囊泡，这是其货物的关键组成部分。这些腔内囊泡运输至迁移体的机制仍然是个谜。在这项研究中，我们发现 Rab10 和 Caveolin-1 (CAV1) 标记了迁移体中的管腔内囊泡。 Rab10-CAV1 囊泡转运至迁移体需要运动蛋白肌球蛋白 Va 和接头蛋白 RILPL2。值得注意的是，激酶 LRRK2 对 Rab10 的磷酸化调节了这一过程。此外，CSF-1可以通过这种机制转运至迁移体，随后促进皮肤伤口愈合中的单核细胞-巨噬细胞分化，这证明了这种转运机制的生理重要性。