The armadillo protein p0071 controls KIF3 motor transport

Author:

Becher Alexander1ORCID,Eiseler Tim1ORCID,Porzner Marc1,Walther Paul2,Keil René3,Bobrovich Susanne1,Hatzfeld Mechthild3,Seufferlein Thomas1ORCID

Affiliation:

1. Department of Internal Medicine I, Ulm University, Albert-Einstein-Allee 23, 89081 Ulm, Germany

2. Central Facility for Electron Microscopy, Ulm University, Albert-Einstein-Allee 11, 89081, Ulm, Germany

3. Institute of Molecular Medicine, Division of Pathobiochemistry, Martin-Luther-University of Halle-Wittenberg, D-06114 Halle, Germany

Abstract

We here report a novel function of the armadillo protein p0071 during KIF3/kinesin-2-mediated transport. Secretion of chromogranin A and matrix metallopeptidase 9 from pancreatic neuroendocrine tumor cells or pancreatic cancer cells, respectively, was substantially reduced following knockdown of p0071. Vesicle tracking indicated impaired directional persistence of vesicles upon p0071 depletion. This suggests a disturbed balance between plus- and minus-end directed microtubule transport in cells lacking p0071. P0071 directly interacts with the KIF3/kinesin-2 motor subunit KIF3B. Our data indicate that p0071 also interacts with the kinesin cargo adaptor protein KAP3 acting as a stabilizing linker between KIF3B and its KAP3 cargo binding entity. Thus, p0071 is required for directional vesicle movement and secretion of different KIF3-transported carriers, regulating the transport of intracellular membrane vesicles along microtubules.

Funder

Deutsche Forschungsgemeinschaft

Publisher

The Company of Biologists

Subject

Cell Biology

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