Frat is dispensable for canonical Wnt signaling in mammals

Genes Dev. 2005 Feb 15;19(4):425-30. doi: 10.1101/gad.326705. Epub 2005 Jan 28.


Wnt-signal transduction through beta-catenin is thought to require the inhibition of GSK3 by Frat/GBP. To investigate the role of Frat in mammalian development, we have generated mice with targeted mutations in all three murine Frat homologs. We show that Frat is normally expressed at sites of active Wnt signaling. Surprisingly, Frat-deficient mice do not display gross abnormalities. Moreover, canonical Wnt signaling in primary cells is unaffected by the loss of Frat. These studies show that Frat is not an essential component of the canonical Wnt pathway in higher organisms, despite the strict requirement of Frat/GBP for maternal Wnt signaling in Xenopus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Blotting, Western
  • Carrier Proteins / genetics
  • Carrier Proteins / physiology*
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • Intercellular Signaling Peptides and Proteins / metabolism*
  • Mice
  • Mice, Knockout
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / physiology*
  • Proto-Oncogene Proteins
  • Signal Transduction / physiology*
  • Wnt Proteins


  • Adaptor Proteins, Signal Transducing
  • Carrier Proteins
  • Frat1 protein, mouse
  • Frat2 protein, mouse
  • Intercellular Signaling Peptides and Proteins
  • Neoplasm Proteins
  • Peg12 protein, mouse
  • Proto-Oncogene Proteins
  • Wnt Proteins