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Molecular and Cellular Biology, June 2006, p. 4652-4663, Vol. 26, No. 12
0270-7306/06/$08.00+0     doi:10.1128/MCB.02193-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

MafG Sumoylation Is Required for Active Transcriptional Repression

Hozumi Motohashi,1* Fumiki Katsuoka,1 Chika Miyoshi,1,2 Yasuhiro Uchimura,3 Hisato Saitoh,3 Claire Francastel,4 James Douglas Engel,5 and Masayuki Yamamoto1,2

Graduate School of Comprehensive Human Sciences and Center for Tsukuba Advanced Research Alliance, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba 305-8577, Japan,1 ERATO Environmental Response Project, Japan Science and Technology Corporation, 1-1-1 Tennoudai, Tsukuba 305-8577, Japan,2 Department of Regeneration Medicine, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan,3 Institut National de la Santé et de la Recherche Médicale U474, Institut Cochin de Génétique Moléculaire, Paris 75014, France,4 Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan 48109-06165

Received 14 November 2005/ Returned for modification 22 December 2005/ Accepted 1 April 2006

A straightforward mechanism for eliciting transcriptional repression would be to simply block the DNA binding site for activators. Such passive repression is often mediated by transcription factors that lack an intrinsic repressor activity. MafG is a bidirectional regulator of transcription, a repressor in its homodimeric state but an activator when heterodimerized with p45. Here, we report that MafG is conjugated to SUMO-2/3 in vivo. To clarify the possible physiological role(s) for sumoylation in regulating MafG activity, we evaluated mutant and wild-type MafG in transgenic mice and cultured cells. Whereas sumoylation-deficient MafG activated p45-dependent transcription normally and did not affect heterodimer activity, repression by the sumoylation-deficient MafG mutant was severely compromised in vivo. Furthermore, the SUMO-dependent repression activity of MafG was sensitive to histone deacetylase inhibition. Thus, repression by MafG is not achieved through simple passive repression by competing for the activator binding site but requires sumoylation, which then mediates transcriptional repression through recruitment of a repressor complex containing histone deacetylase activity.

* Corresponding author. Mailing address: Center for TARA, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba 305-8577, Japan. Phone: 81-29-853-7320. Fax: 81-29-853-7318. E-mail: hozumim{at}tara.tsukuba.ac.jp.

Molecular and Cellular Biology, June 2006, p. 4652-4663, Vol. 26, No. 12
0270-7306/06/$08.00+0     doi:10.1128/MCB.02193-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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