Wnt-5a inhibits the canonical Wnt pathway by promoting GSK-3–independent β-catenin degradation

Topol , Lilia; Jiang , Xueyuan; Choi , Hosoon; Garrett-Beal , Lisa; Carolan , Peter J.; Yang , Yingzi

doi:10.1083/jcb.200303158

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Article| September 02 2003

Wnt-5a inhibits the canonical Wnt pathway by promoting GSK-3–independent β-catenin degradation

Lilia Topol,

Lilia Topol

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

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Xueyuan Jiang,

Xueyuan Jiang

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

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Hosoon Choi,

Hosoon Choi

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

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Lisa Garrett-Beal,

Lisa Garrett-Beal

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

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Peter J. Carolan,

Peter J. Carolan

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

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Yingzi Yang

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

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Author and Article Information

Lilia Topol

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

Xueyuan Jiang

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

Hosoon Choi

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

Lisa Garrett-Beal

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

Peter J. Carolan

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

Yingzi Yang

Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

Address correspondence to Yingzi Yang, Genetic Disease Research Branch, National Human Genome Research Institute, NIH, 49 Convent Dr., Room 4A68, Bethesda, MD 20892. Tel: (301) 402-2034. Fax: (301) 402-2170. email: [email protected]

Xueyuan Jiang's present address is Dept. of Biochemistry and State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing 210093, People's Republic of China.

Abbreviations used in this paper: AER, apical ectodermal ridge; CEF, chick embryonic fibroblast; CsA, Cyclosporin A.

Received: March 25 2003

Accepted: June 23 2003

Online ISSN: 1540-8140

Print ISSN: 0021-9525

2003

J Cell Biol (2003) 162 (5): 899–908.

https://doi.org/10.1083/jcb.200303158

Wnts are secreted signaling molecules that can transduce their signals through several different pathways. Wnt-5a is considered a noncanonical Wnt as it does not signal by stabilizing β-catenin in many biological systems. We have uncovered a new noncanonical pathway through which Wnt-5a antagonizes the canonical Wnt pathway by promoting the degradation of β-catenin. This pathway is Siah2 and APC dependent, but GSK-3 and β-TrCP independent. Furthermore, we provide evidence that Wnt-5a also acts in vivo to promote β-catenin degradation in regulating mammalian limb development and possibly in suppressing tumor formation.

2003

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Wnt-5a inhibits the canonical Wnt pathway by promoting GSK-3–independent β-catenin degradation

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