AI Article Synopsis

  • Angiogenesis is the process where endothelial cells grow and move towards signals that promote new blood vessel formation, regulated by pathways like Wnt planar cell polarity (PCP) and proteins such as Dishevelled (Dvl) and Daam1.
  • Kif26b, a kinesin protein, works with Daam1 to help endothelial cells sprout and migrate in an organized direction by reorganizing microtubules.
  • Depleting either Kif26b or Daam1 disrupts the polarization of cells and their ability to maintain proper front-rear orientation, but introducing Kif26b can correct some of the defects caused by Daam1 depletion, highlighting their cooperative role in cell communication and structure during

Article Abstract

Angiogenesis involves the coordinated growth and migration of endothelial cells (ECs) toward a proangiogenic signal. The Wnt planar cell polarity (PCP) pathway, through the recruitment of Dishevelled (Dvl) and Dvl-associated activator of morphogenesis (Daam1), has been proposed to regulate cell actin cytoskeleton and microtubule (MT) reorganization for oriented cell migration. Here we report that Kif26b--a kinesin--and Daam1 cooperatively regulate initiation of EC sprouting and directional migration via MT reorganization. First, we find that Kif26b is recruited within the Dvl3/Daam1 complex. Using a three-dimensional in vitro angiogenesis assay, we show that Kif26b and Daam1 depletion impairs tip cell polarization and destabilizes extended vascular processes. Kif26b depletion specifically alters EC directional migration and mislocalized MT organizing center (MTOC)/Golgi and myosin IIB cell rear enrichment. Therefore the cell fails to establish a proper front-rear polarity. Of interest, Kif26b ectopic expression rescues the siDaam1 polarization defect phenotype. Finally, we show that Kif26b functions in MT stabilization, which is indispensable for asymmetrical cell structure reorganization. These data demonstrate that Kif26b, together with Dvl3/Daam1, initiates cell polarity through the control of PCP signaling pathway-dependent activation.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4791138PMC
http://dx.doi.org/10.1091/mbc.E14-08-1332DOI Listing

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