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FAM83F regulates canonical Wnt signalling through an interaction with CK1α.

Karen Dunbar1, Rebecca A Jones2, Kevin Dingwell2

  • 1Medical Research Council Protein Phosphorylation and Ubiquitylation Unit (MRC-PPU), School of Life Sciences, University of Dundee, Sir James Black Centre, Dundee, UK.

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The FAM83F protein enhances Wnt signaling, crucial for embryonic development and colorectal cancer (CRC). It interacts with CK1α at the plasma membrane, activating this key pathway.

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Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Cancer Research

Background:

  • The function of the FAM83F protein remains largely unknown, similar to other FAM83 family members.
  • Wnt signaling is a critical pathway involved in embryonic development and various cancers, including colorectal cancer (CRC).

Purpose of the Study:

  • To elucidate the function of the FAM83F protein.
  • To investigate the role of FAM83F in Wnt signaling activation and its implications in CRC.

Main Methods:

  • Overexpression and ablation studies in Xenopus embryos and human CRC cells.
  • Analysis of FAM83F farnesylation and its interaction with CK1α.
  • CRISPR/Cas9 genome editing to create farnesyl-deficient FAM83F mutants.

Main Results:

  • FAM83F overexpression activates Wnt signaling, while its ablation attenuates it in CRC cells.
  • FAM83F is farnesylated and interacts with CK1α at the plasma membrane, which is essential for Wnt pathway activation.
  • FAM83F acts upstream of GSK-3β, and its plasma membrane localization is critical for Wnt signaling modulation.

Conclusions:

  • FAM83F is a novel activator of the Wnt signaling pathway.
  • FAM83F's interaction with CK1α at the plasma membrane is essential for its function in Wnt signaling.
  • FAM83F plays a significant role in Wnt signaling, with potential implications for colorectal cancer therapeutics.