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J. Biol. Chem., Vol. 280, Issue 13, 12758-12765, April 1, 2005

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Regulation of -Catenin Signaling and Maintenance of Chondrocyte Differentiation by Ubiquitin-independent Proteasomal Degradation of -Catenin^*

Sang-Gu Hwang, Sung-Sook Yu, Je-Hwang Ryu, Hong-Bae Jeon, Yung-Joon Yoo, Soo-Hyun Eom, and Jang-Soo Chun

From the Department of Life Science, Gwangju Institute of Science and Technology, Gwangju 500-712, Korea

Accumulation of -catenin and subsequent stimulation of -catenin-T cell-factor (Tcf)/lymphoid-enhancerfactor (Lef) transcriptional activity causes dedifferentiation of articular chondrocytes, which is characterized by decreased type II collagen expression and initiation of type I collagen expression. This study examined the mechanisms of -catenin degradation, the role of -catenin in -catenin signaling, and the physiological significance of -catenin regulation of -catenin signaling in articular chondrocytes. We found that both - and -catenin accumulated during dedifferentiation of chondrocytes by escaping from proteasomal degradation. -Catenin degradation was ubiquitination-dependent, whereas -catenin was proteasomally degraded in a ubiquitination-independent fashion. The accumulated - and -catenin existed as complexes in the cytosol and nucleus. The complex formation between - and -catenin blocked proteasomal degradation of -catenin and also inhibited -catenin-Tcf/Lef transcriptional activity and the suppression of type II collagen expression associated with ectopic expression of -catenin, the inhibition of proteasome, or Wnt signaling. Collectively, our results indicate that ubiquitin-independent degradation of -catenin regulates -catenin signaling and maintenance of the differentiated phenotype of articular chondrocytes.

Received for publication, November 29, 2004 , and in revised form, January 24, 2005.

^* This work was supported by Grants R01-2003-000-10154-0 and R02-2004-000-10015-0 from the Basic Research Program of the Korea Science and Engineering Foundation and Grant M1-0104-00-0064 from the National Research Laboratory Program from the Korea Ministry of Science and Technology. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank^TM/EBI Data Bank with accession number(s) AB193105.

To whom correspondence should be addressed: Dept. of Life Science, Gwangju Institute of Science and Technology, Buk-Gu, Gwangju 500-712, Korea. Tel.: 82-62-970-2497; Fax: 82-62-970-2484, E-mail: jschun{at}gist.ac.kr.

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