Interestingly, the homodimeric kinesin-2 subunit Kif17, which cooperates with Kif3a in ciliary transport of C. Yet, several lines of evidence suggest that kinesin-2 mediated transport occurs outside cilia: Expression of mutant Kif3a in cultured Xenopus cells blocked vesicle transport from the ER to the Golgi preventing pigment dispersion, and deletion of the kinesin-2 component Kap3 was associated with decreased transport of N-cadherin to the cell periphery.

Several Hedgehog (HH) components localize to cilia and this organelle plays a central role in the activation of the HH pathway which could explain the similarities in HH and cilia phenotypes. The constitutive deletion of Kif3a in mice results in severely disordered mesoderm development reminiscent of defective hedgehog signalling and in mid-embryonic lethality. Kinesin-2 has been mostly studied in cilia where it functions to carry protein complexes along the microtubular axoneme from the base to the tip of the cilium in a process termed intraflagellar transport (IFT) that is required for cilia formation. Hetero-trimeric Kinesin-2 consists of the two motor subunits Kif3a/Kif3b and the cargo-binding protein Kap3. Kif3a is a subunit of hetero-trimeric Kinesin-2, a microtubule (MT) plus-end directed motor protein. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Д¬ompeting interests: The authors have declared that no competing interests exist. BB is supported by a junior career development grant (J3) of the Interdisciplinary Center of Clinical Research at the University of Erlangen-Nuremberg. GW is supported by the DFG KFO 201, and by the European Community's Seventh Framework Program (grant agreement number 241955, SYSCILIA). This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ДЇunding: This work was supported by DFG grants KU 1504 (EWK), SFB 592 Z2 (RN) and BIOSS cluster of excellence 294 (RN, EWK, GW). Received: NovemAccepted: MaPublished: May 1, 2013Д¬opyright: В© 2013 Boehlke et al. Zegers, NCMLS, Radboud University Nijmegen Medical Center, Netherlands (2013) Kif3a Guides Microtubular Dynamics, Migration and Lumen Formation of MDCK Cells. These data uncover that Kif3a regulates the microtubular cytoskeleton in the cell periphery and imply that extra-ciliary Kif3a has an unexpected function in morphogenesis.Д¬itation: Boehlke C, Kotsis F, Buchholz B, Powelske C, Eckardt K-U, Walz G, et al. Loss of Kif3a retarded lateral membrane specification and completely prevented the formation of three-dimensional spheres in collagen. Microtubules at the leading edge of Kif3a depleted cells failed to grow perpendicularly into the leading edge and microtubular dynamics were dampened in Kif3a depleted cells. Here we show that tetracycline inducible depletion of Kif3a in MDCK cells slows epithelial cell migration. Outside cilia, Kinesin-2 mediated transport has been implicated in vesicle and N-cadherin transport, but it is unknown if and how extraciliary Kif3a affects basic cellular functions such as migration or the formation of multicellular structures. The microtubular motor Kinesin-2 and its subunit Kif3a are essential for the formation of primary cilia, an organelle implicated in a wide spectrum of developmental abnormalities.

Tubular lumen