Abscission is a complex cellular process that is required for mitotic division. It is well-established that coordinated and localized changes in actin and microtubule dynamics are vital for cytokinetic ring formation, as well as establishment of the abscission site. Actin cytoskeleton reorganization during abscission would not be possible without the interplay between Rab11- and Rab35-containing endosomes and their effector proteins, whose roles in regulating endocytic pathways at the cleavage furrow have now been studied extensively. Here, we identified Rab14 as a novel regulator of cytokinesis. We demonstrate that depletion of Rab14 causes either cytokinesis failure or significantly prolongs division time. We show that Rab14 contributes to the efficiency of recruiting Rab11-endosomes to the ICB microtubules and that Rab14 knockout leads to inhibition of actin clearance at the abscission site. Finally, we demonstrate that Rab14 binds to microtubule minus-end interacting MACF2/CAMSAP3 complex and that this binding affects targeting of endosomes to the ICB microtubules. Collectively, our data identified Rab14 and MACF2/CAMSAP3 as proteins that regulate actin depolymerization and endosome targeting during cytokinesis.

脱落是有丝分裂所需的复杂细胞过程。众所周知，肌动蛋白和微管动力学的协调和局部变化对于细胞因子环的形成以及脱落位点的建立至关重要。如果没有含有 Rab11 和 Rab35 的内涵体及其效应蛋白之间的相互作用，在脱落过程中肌动蛋白细胞骨架的重组是不可能的，其在调节卵裂沟内吞途径中的作用现已得到广泛研究。在这里，我们将 Rab14 鉴定为胞质分裂的新型调节剂。我们证明 Rab14 的消耗会导致胞质分裂失败或显着延长分裂时间。我们表明，Rab14 有助于将 Rab11 内体募集到 ICB 微管的效率，并且 Rab14 敲除会抑制脱落位点的肌动蛋白清除。最后，我们证明 Rab14 与微管负端相互作用的 MACF2/CAMSAP3 复合物结合，并且这种结合会影响内体对 ICB 微管的靶向。总的来说，我们的数据将 Rab14 和 MACF2/CAMSAP3 鉴定为在胞质分裂过程中调节肌动蛋白解聚和内体靶向的蛋白质。