在上皮管腔形成过程中,运动蛋白-2介导根尖内体运输。

Cellular logistics Pub Date : 2014-01-01 Epub Date: 2014-05-06 DOI:10.4161/cl.28928
Dongying Li, E Wolfgang Kuehn, Rytis Prekeris
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引用次数: 27

摘要

顶管腔的形成是管状器官上皮形态发生的关键步骤。适当的运输和靶向根尖蛋白到根尖膜起始点(AMIS)在建立孤立的中央管腔中起着至关重要的作用。FIP5是一种与rab11相互作用的蛋白,在细胞分裂过程中,它是一个重要的调节因子,指导顶核内体沿着微管向AMIS运输。然而,在管腔形成过程中,究竟是哪种分子马达在运输fip5阳性的顶核内体,以及这一过程是如何调节的,目前尚不清楚。在这项研究中,我们证明了FIP5与微管马达(kinein -2)的相互作用是FIP5-核内体运动和这些核内体在顶管起始过程中从中心体运送到卵裂沟所必需的。运动蛋白-2的缺失破坏了顶端蛋白对AMIS的靶向,导致MDCK囊肿形成多个管腔。我们的数据为根尖管腔形成过程中依赖fip5的根尖运输的分子机制提供了更多的细节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Kinesin-2 mediates apical endosome transport during epithelial lumen formation.

Apical lumen formation is a key step during epithelial morphogenesis of tubular organs. Appropriate transport and targeting of apical proteins to the apical membrane initiation site (AMIS) plays a crucial role in establishing a solitary, central lumen. FIP5, a Rab11-interacting protein, is an important regulator that directs apical endosome trafficking along microtubules toward the AMIS during cytokinesis. However, it is unknown which molecular motor(s) transports FIP5-positive apical endosomes during lumen initiation, and how this process is regulated. In this study, we demonstrate that the interaction of FIP5 with the microtubule motor, Kinesin-2, is required for the movement of FIP5-endosomes and delivery of these endosomes from centrosomes to the cleavage furrow during apical lumen initiation. Loss of Kinesin-2 disrupts targeting of apical proteins to the AMIS and results in multiple lumen formation in MDCK cysts. Our data provide more details to the molecular mechanism of FIP5-dependent apical trafficking during apical lumen formation.

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