PDF(Pubmed)
Abstract：
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.
摘要：
迁徙者,在迁移细胞的回缩纤维上产生的囊泡细胞器，在迁徙过程中起着至关重要的作用，介导细胞间通讯。货物决定了迁移体的功能特异性。Migrasomes藏有许多管腔内囊泡，他们货物的关键组成部分。这些腔内囊泡运输到迁移体的潜在机制仍然是神秘的。在这项研究中,我们发现Rab10和Caveolin-1（CAV1）标记了迁移体中的腔内囊泡。Rab10-CAV1囊泡向迁移体的转运需要运动蛋白肌球蛋白Va和衔接蛋白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到迁移体，随后促进皮肤伤口愈合中的单核细胞-巨噬细胞分化，这证明了这种运输机制的生理重要性。
