Published 2 September 2003. doi:10.1083/jcb.200307181
© The Rockefeller University Press,
0021-9525/2003/9/753 $5.00
The Journal of Cell Biology, Volume 162, Number 5, 753-756
When Wnts antagonize Wnts
Gilbert Weidinger and
Randall T. Moon
Howard Hughes Medical Institute and Department of Pharmacology, University of Washington School of Medicine, Seattle, WA 98195
Address correspondence to Randall T. Moon, Department of Pharmacology, University of Washington, Box 357370, Seattle, WA 98195. Tel.: (206) 543-1722. Fax: (206) 543-0858. email: rtmoon{at}u.washington.edu
Secreted Wnt ligands appear to activate a variety of signaling pathways. Two papers in this issue now present genetic evidence that "noncanonical" Wnt signaling inhibits the "canonical" Wnt/ß-catenin pathway. Westfall et al. (2003a) show that zebrafish embryos lacking maternal Wnt-5 function are dorsalized due to ectopic activation of ß-catenin, whereas Topol et al. (2003) report that chondrogenesis in the distal mouse limb bud depends on inhibition of Wnt/ß-catenin signaling by a paralogue of Wnt-5. These studies present the first genetic confirmation of the previous hypothesis that vertebrate Wnt signaling pathways can act in an antagonistic manner.
Abbreviations used in this paper: JNK, c-jun NH2-terminal kinase; PCP, planar cell polarity; PI, phosphatidylinositol; PKC, protein kinase C.

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