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J. Biol. Chem., Vol. 279, Issue 1, 401-406, January 2, 2004

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Polycomb Group Suppressor of Zeste 12 Links Heterochromatin Protein 1 and Enhancer of Zeste 2^*

Ken Yamamoto, Miki Sonoda, Junichi Inokuchi¶, Senji Shirasawa¶, and Takehiko Sasazuki||**

From the Division of Molecular Population Genetics, Department of Molecular Genetics, Medical Institute of Bioregulation, and Kyushu University Center of Excellence Program on Lifestyle-Related Diseases, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan and the ^¶Department of Pathology, ^||Research Institute, International Medical Center of Japan, 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655, Japan

Drosophila suppressor of zeste 12 (Su(z)12) is a Polycomb group (PcG) transcriptional repressor and is present in E(z)-ESC, a multiprotein complex with methylation activity specific for lysine 9 and 27 of histone H3. Although PcG- and heterochromatin-mediated gene silencing have been considered distinct, mutant flies of Su(z)12 showed not only homeotic transformation but also position effect variegation. We now report that the mammalian SU(Z)12 directly interacts with heterochromatin protein 1 (HP1) and PcG enhancer of zeste 2 (EZH2), the mammalian counterpart of E(z), in vitro and in vivo. Two distinct domains in SU(Z)12 are involved in these interactions, the region between the zinc finger motif and the VEFS (VRN2-EMF2-FIS2-Su(z)12) box for HP1 (amino acid residues 479–536) and the VEFS box for EZH2 (amino acid residues 600–639), which are not mutually exclusive. Interestingly this region of the VEFS box has been shown to be critical for the phenotype of the Su(z)12 mutant fly. In addition SU(Z)12 represses transcription activity in the presence of HP1 in a reporter assay. These results provide a molecular explanation for the functional link of these epigenetic silencing processes mediated by Su(z)12.

Received for publication, July 9, 2003 , and in revised form, October 1, 2003.

^* This work was supported by a grant-in-aid for scientific research (C) from the Japan Society for the Promotion of Science, by a grant-in-aid for scientific research on priority areas "Genome Biology," and by a grant from the 21st Center of Excellence Program from the Ministry of Education, Culture, Sports, Science and Technology of Japan. 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.

^** Director-General of Research Institute, International Medical Center of Japan.

To whom correspondence should be addressed. Fax: 81-92-642-4614; E-mail: kyama{at}bioreg.kyushu-u.ac.jp.

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