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J. Biol. Chem., Vol. 278, Issue 51, 51638-51645, December 19, 2003

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Mi-2 Associates with BRG1 and RET Finger Protein at the Distinct Regions with Transcriptional Activating and Repressing Abilities^*

Yohei Shimono, Hideki Murakami, Kumi Kawai, Paul A. Wade¶, Kaoru Shimokata||, and Masahide Takahashi**

From the Departments of Pathology and ^||Internal Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan, Department of Molecular Pathology, Center for Neural Disease and Cancer, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan, and ^¶Department of Pathology, Emory University, Atlanta, Georgia 30322

Mi-2 is the main component of the nucleosome remodeling and deacetylase complex and plays an important role in epigenetic transcriptional repression. Here we show that the amino-terminal and carboxyl-terminal regions of Mi-2 have distinct transcriptional activities and bind to BRG1, a component of the SWI/SNF complex, and the RET finger protein (RFP), respectively. Analysis by luciferase reporter assay revealed that the amino-terminal region of Mi-2 has a strong transactivating ability, whereas its carboxyl-terminal region has transcriptional repressive activity. Co-localization and association of Mi-2, RFP, and histone deacetylase 1 suggested that these proteins cooperate in transcriptional repression. Furthermore, the functional importance of the association of Mi-2 and RFP was confirmed by using Rfp^–/– fibroblasts. On the other hand, we demonstrated that Mi-2 and BRG1 were associated with each other and that the bromodomain region of BRG1 strongly suppressed transactivation by the amino-terminal region of Mi-2. The findings that Mi-2 interacts with both transactivating and repressing proteins and directly associates with another chromatin remodeling protein, BRG1, provide new insight into the formation of multiprotein supercomplex involved in transcriptional regulation.

Received for publication, August 19, 2003 , and in revised form, September 18, 2003.

^* This work was supported in part by grants-in-aid for the Center of Excellence Research, Scientific Research on Priority Areas Cancer and Scientific Research (A) from the Ministry of Education, Culture, Sports, Science and Technology of Japan (to M. T.). 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.

^** To whom correspondence should be addressed: Dept. of Pathology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. Tel.: 81-52-744-2093; Fax: 81-52-744-2098; E-mail: mtakaha{at}med.nagoya-u.ac.jp.

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