Frat is dispensable for canonical Wnt signaling in mammals
Abstract
Wnt-signal transduction through β-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.
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Footnotes
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Supplemental material is available at http://www.genesdev.org.
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Article published online ahead of print. Article and publication date are at http://www.genesdev.org/cgi/doi/10.1101/gad.326705.
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↵4 Corresponding author.
↵4 E-MAIL a.berns{at}nki.nl; FAX 31-20-512-2011.
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- Accepted December 17, 2004.
- Received September 29, 2004.
- Cold Spring Harbor Laboratory Press