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Kinesin superfamily protein Kif26b links Wnt5a-Ror signaling to the control of cell and tissue behaviors in vertebrates. | LitMetric

AI Article Synopsis

  • - The Wnt5a-Ror signaling pathway is vital for processes like embryonic development, reproduction, and tissue regeneration, yet its specific molecular functions are not fully understood.
  • - Researchers discovered that the protein Kif26b is a key target of the Wnt5a-Ror pathway, which affects its stability and degradation through a process unrelated to the traditional Wnt/β-catenin pathway.
  • - Disrupting Kif26b function led to significant developmental issues such as malformations and loss of germ cells, emphasizing Kif26b's role in linking Wnt5a-Ror signaling to important cellular behaviors in vertebrates.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5590807PMC
http://dx.doi.org/10.7554/eLife.26509DOI Listing

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