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Molecular and Cellular Biology, June 2007, p. 4347-4354, Vol. 27, No. 12
0270-7306/07/$08.00+0     doi:10.1128/MCB.01640-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Chibby Promotes Adipocyte Differentiation through Inhibition of ß-Catenin Signaling{triangledown}

Feng-Qian Li,1 Amar M. Singh,4 Adaobi Mofunanya,1,2 Damon Love,1,3 Naohiro Terada,4 Randall T. Moon,5 and Ken-Ichi Takemaru1*

Department of Pharmacology,1 Graduate Program in Genetics,2 Graduate Program in Molecular and Cellular Pharmacology, SUNY at Stony Brook, Stony Brook, New York 11794,3 Department of Pathology, University of Florida, Gainesville, Florida 32610,4 Department of Pharmacology, HHMI, Institute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, Washington 981955

Received 1 September 2006/ Returned for modification 16 October 2006/ Accepted 24 March 2007

The canonical Wnt/ß-catenin signaling pathway plays diverse roles in embryonic development and disease. Activation of this pathway, likely by Wnt-10b, has been shown to inhibit adipogenesis in cultured 3T3-L1 preadipocytes and in mice. Here, we report that the ß-catenin antagonist Chibby (Cby) is required for adipocyte differentiation. Cby is expressed in adipose tissue in mice, and Cby protein levels increase during adipogenic differentiation of 3T3-L1 cells. Ectopic expression of Cby induces spontaneous differentiation of these cells into mature adipocytes to an extent similar to that of dominant-negative Tcf-4. In contrast, depletion of Cby by RNA interference potently blocks adipogenesis of 3T3-L1 and mouse embryonic stem cells. In support of this, embryonic fibroblasts obtained from Cby-deficient embryos display attenuated differentiation to the adipogenic lineage. Mechanistically, Cby promotes adipocyte differentiation, in part by inhibiting ß-catenin, since gain or loss of function of Cby influences ß-catenin signaling in 3T3-L1 cells. Our results therefore establish Cby as a novel proadipogenic factor required for adipocyte differentiation.

* Corresponding author. Mailing address: SUNY at Stony Brook, Department of Pharmacology, BST 7-169 Nicolls Rd., Stony Brook, NY 11794-8651. Phone: (631) 444-7976. Fax: (631) 444-3218. E-mail: takemaru{at}pharm.sunysb.edu

{triangledown} Published ahead of print on 2 April 2007.

Molecular and Cellular Biology, June 2007, p. 4347-4354, Vol. 27, No. 12
0270-7306/07/$08.00+0     doi:10.1128/MCB.01640-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Rashid, S., Pilecka, I., Torun, A., Olchowik, M., Bielinska, B., Miaczynska, M. (2009). Endosomal Adaptor Proteins APPL1 and APPL2 Are Novel Activators of {beta}-Catenin/TCF-mediated Transcription. J. Biol. Chem. 284: 18115-18128 [Abstract] [Full Text]  
  • Li, F.-Q., Mofunanya, A., Harris, K., Takemaru, K.-I. (2008). Chibby cooperates with 14-3-3 to regulate {beta}-catenin subcellular distribution and signaling activity. JCB 181: 1141-1154 [Abstract] [Full Text]  


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