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Nucleic Acids Research, 2000, Vol. 28, No. 8 1707-1713
© 2000 Oxford University Press

Transcriptional repression by the insulator protein CTCF involves histone deacetylases

Marcus Lutz, Les J. Burke, Guillermo Barreto, Frauke Goeman, Heiko Greb, Rüdiger Arnold, Holger Schultheiß, Alexander Brehm1, Tony Kouzarides1, Victor Lobanenkov2 and Rainer Renkawitz*

Genetisches Institut der Justus-Liebig-Universität, Heinrich-Buff-Ring 58–62, 35392 Giessen, Germany, 1Wellcome/CRC Institute for Development and Cancer Biology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK and 2National Institute of Allergy and Infectious Diseases, National Institutes of Health, Molecular Pathology Section, Building 7, Room 303, MSC-0760 Bethesda, MD 20892-0760, USA

The highly conserved zinc-finger protein, CTCF, is a candidate tumor suppressor protein that binds to highly divergent DNA sequences. CTCF has been connected to multiple functions in chromatin organization and gene regulation including chromatin insulator activity and transcriptional enhancement and silencing. Here we show that CTCF harbors several autonomous repression domains. One of these domains, the zinc-finger cluster, silences transcription in all cell types tested and binds directly to the co-repressor SIN3A. Two distinct regions of SIN3A, the PAH3 domain and the extreme C-terminal region, bind independently to this zinc-finger cluster. Analysis of nuclear extract from HeLa cells revealed that CTCF is also capable of retaining functional histone deacetylase activity. Furthermore, the ability of regions of CTCF to retain deacetylase activity correlates with the ability to bind to SIN3A and to repress gene activity. We suggest that CTCF driven repression is mediated in part by the recruitment of histone deacetylase activity by SIN3A.

* To whom correspondence should be addressed. Tel: +49 641 99 35460; Fax: +49 641 99 35469; Email: rainer.renkawitz@gen.bio.uni-giessen.de


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