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J. Biol. Chem., Vol. 281, Issue 10, 6608-6615, March 10, 2006

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Down-regulation of Histone Deacetylases Stimulates Adipocyte Differentiation^*

From the Department of Biological Sciences and Research Center for Functional Cellulomics, Seoul National University, Seoul 151-742, South Korea

Specific cell type differentiation is driven by programmed regulation of gene expression, which is the result of coordinated modulation of the transcription machinery and chromatin-remodeling factors. We present evidence here that the down-regulation of histone deacetylases is an important process during adipocyte differentiation. In 3T3-L1 cells, histone hyperacetylation was selectively induced at the promoter regions of adipogenic genes during adipocyte differentiation. Interestingly, this was accompanied by a dramatic decrease in the expression level of several histone deacetylases including HDAC1, -2, and -5 and a reduction in overall histone deacetylase enzyme activity. Inhibition of histone deacetylase activity using sodium butyrate resulted in stimulation of adipogenic gene expression and adipocyte differentiation. Consistently, HDAC1 knock-down promoted adipogenesis whereas HDAC1 overexpression attenuated adipocyte differentiation in 3T3-L1 cells. Together, these results suggest that the regulation of not only adipogenic transcription factors, but also chromatin-modifying enzymes is crucial for the execution of bona fide adipogenesis.

Received for publication, August 15, 2005 , and in revised form, November 3, 2005.

^* This work was supported in part by grants from Stem Cell Research Center of the 21st Century Frontier Research Program (SC13150), Research Center for Functional Cellulomics of Science Research Center Program, and the National Research Laboratory Program of Korea Science and Engineering Foundation. 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 on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1-S3.

¹ Both authors contributed equally to this work.

² Supported by BK21 Research Fellowships from the Ministry of Education and Human Resources Development.

³ To whom correspondence should be addressed: Dept. of Biological Sciences, Research Center for Functional Cellulomics, Seoul National University, San 56-1, Sillim-Dong, Gwanak-Gu, Seoul, South Korea 151-742. Tel.: 82-2-880-5852; Fax: 82-2-878-5852; E-mail: jaebkim{at}snu.ac.kr.

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