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Cell Logist. 2014 Jan 1;4(1):e28928. Epub 2014 May 6.

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

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Department of Cell and Developmental Biology; School of Medicine; Anschutz Medical Campus; University of Colorado Denver; Aurora, CO USA.
Department of Nephrology; University Hospital; Freiburg, Germany ; BIOSS Centre for Biological Signaling Studies; Albert-Ludwigs-Universität Freiburg; Freiburg, Germany.


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.


AMIS; FIP5; Kinesin-2; apical trafficking; lumen formation; tubulogenesis

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