In:
eLife, eLife Sciences Publications, Ltd, Vol. 6 ( 2017-09-08)
Abstract:
Wnt5a-Ror signaling constitutes a developmental pathway crucial for embryonic tissue morphogenesis, reproduction and adult tissue regeneration, yet the molecular mechanisms by which the Wnt5a-Ror pathway mediates these processes are largely unknown. Using a proteomic screen, we identify the kinesin superfamily protein Kif26b as a downstream target of the Wnt5a-Ror pathway. Wnt5a-Ror, through a process independent of the canonical Wnt/β-catenin-dependent pathway, regulates the cellular stability of Kif26b by inducing its degradation via the ubiquitin-proteasome system. Through this mechanism, Kif26b modulates the migratory behavior of cultured mesenchymal cells in a Wnt5a-dependent manner. Genetic perturbation of Kif26b function in vivo caused embryonic axis malformations and depletion of primordial germ cells in the developing gonad, two phenotypes characteristic of disrupted Wnt5a-Ror signaling. These findings indicate that Kif26b links Wnt5a-Ror signaling to the control of morphogenetic cell and tissue behaviors in vertebrates and reveal a new role for regulated proteolysis in noncanonical Wnt5a-Ror signal transduction.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.26509.001
DOI:
10.7554/eLife.26509.002
DOI:
10.7554/eLife.26509.003
DOI:
10.7554/eLife.26509.004
DOI:
10.7554/eLife.26509.005
DOI:
10.7554/eLife.26509.007
DOI:
10.7554/eLife.26509.006
DOI:
10.7554/eLife.26509.008
DOI:
10.7554/eLife.26509.011
DOI:
10.7554/eLife.26509.012
DOI:
10.7554/eLife.26509.009
DOI:
10.7554/eLife.26509.010
DOI:
10.7554/eLife.26509.013
DOI:
10.7554/eLife.26509.014
DOI:
10.7554/eLife.26509.016
DOI:
10.7554/eLife.26509.017
DOI:
10.7554/eLife.26509.018
DOI:
10.7554/eLife.26509.015
DOI:
10.7554/eLife.26509.019
DOI:
10.7554/eLife.26509.023
DOI:
10.7554/eLife.26509.024
DOI:
10.7554/eLife.26509.020
DOI:
10.7554/eLife.26509.021
DOI:
10.7554/eLife.26509.022
DOI:
10.7554/eLife.26509.025
DOI:
10.7554/eLife.26509.026
DOI:
10.7554/eLife.26509.027
DOI:
10.7554/eLife.26509.028
DOI:
10.7554/eLife.26509.029
DOI:
10.7554/eLife.26509.030
DOI:
10.7554/eLife.26509.031
DOI:
10.7554/eLife.26509.033
DOI:
10.7554/eLife.26509.034
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2017
detail.hit.zdb_id:
2687154-3