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Molecular and Cellular Biology, July 2006, p. 5226-5236, Vol. 26, No. 14
0270-7306/06/$08.00+0     doi:10.1128/MCB.00440-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

A Feed-Forward Repression Mechanism Anchors the Sin3/Histone Deacetylase and N-CoR/SMRT Corepressors on Chromatin

Michiel Vermeulen,1 Wendy Walter,2 Xavier Le Guezennec,1 Jaehoon Kim,3 Rajeswari S. Edayathumangalam,4 Edwin Lasonder,5 Karolin Luger,4 Robert G. Roeder,3 Colin Logie,1 Shelley L. Berger,2 and Hendrik G. Stunnenberg1*

Department of Molecular Biology, Nijmegen Center for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, The Netherlands,1 Gene Expression and Regulation Program, The Wistar Institute, Philadelphia, Pennsylvania 19024,2 Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, 1230 York Avenue, New York, New York 10021,3 Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523-1870,4 Center for Molecular and Biomolecular Informatics, University Medical Centre St. Radboud, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands5

Received 13 March 2006/ Returned for modification 17 April 2006/ Accepted 28 April 2006

Transcription in eukaryotes is governed in part by histone acetyltransferase (HAT)- and histone deacetylase (HDAC)-containing complexes that are recruited via activators and repressors, respectively. Here, we show that the Sin3/HDAC and N-CoR/SMRT corepressor complexes repress transcription from histone H3- and/or H4-acetylated nucleosomal templates in vitro. Repression of histone H3-acetylated templates was completely dependent on the histone deacetylase activity of the corepressor complexes, whereas this activity was not required to repress H4-acetylated templates. Following deacetylation, both complexes become stably anchored in a repressor-independent manner to nucleosomal templates containing hypoacetylated histone H3, but not H4, resulting in dominance of repression over activation. The observed stable anchoring of corepressor complexes casts doubt on the view of a dynamic balance between readily exchangeable HAT and HDAC activities regulating transcription and implies that pathways need to be in place to actively remove HDAC complexes from hypoacetylated promoters to switch on silent genes.

* Corresponding author. Mailing address: NCMLS, Radboud University Nijmegen, Department of Molecular Biology, Geert Grooteplein Zuid 30, Nijmegen, The Netherlands. Phone: 31-3610524. Fax: 31-3610520. E-mail: h.stunnenberg{at}ncmls.ru.nl.

Molecular and Cellular Biology, July 2006, p. 5226-5236, Vol. 26, No. 14
0270-7306/06/$08.00+0     doi:10.1128/MCB.00440-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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