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Molecular and Cellular Biology, April 2003, p. 2942-2952, Vol. 23, No. 8
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.8.2942-2952.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Novel SWI/SNF Chromatin-Remodeling Complexes Contain a Mixed-Lineage Leukemia Chromosomal Translocation Partner

Zuqin Nie,1 Zhijiang Yan,1 Everett H. Chen,2 Salvatore Sechi,3,{dagger} Chen Ling,1 Sharleen Zhou,4 Yutong Xue,1 Dafeng Yang,1 Darryl Murray,1 Emi Kanakubo,1 Michael L. Cleary,2 and Weidong Wang1*

Laboratory of Genetics,1 Research Resources Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224,3 Department of Pathology, Stanford University, Stanford, California 94305,2 Howard Hughes Medical Institute, University of California, Berkeley, California 947204

Received 18 October 2002/ Returned for modification 10 December 2002/ Accepted 21 January 2003

The SWI/SNF family of chromatin-remodeling complexes has been discovered in many species and has been shown to regulate gene expression by assisting transcriptional machinery to gain access to their sites in chromatin. Several complexes of this family have been reported for humans. In this study, two additional complexes are described that belong to the same SWI/SNF family. These new complexes contain as many as eight subunits identical to those found in other SWI/SNF complexes, and they possess a similar ATP-dependent nucleosome disruption activity. But unlike known SWI/SNFs, the new complexes are low in abundance and contain an extra subunit conserved between human and yeast SWI/SNF complexes. This subunit, ENL, is a homolog of the yeast SWI/SNF subunit, ANC1/TFG3. Moreover, ENL is a fusion partner for the gene product of MLL that is a common target for chromosomal translocations in human acute leukemia. The resultant MLL-ENL fusion protein associates and cooperates with SWI/SNF complexes to activate transcription of the promoter of HoxA7, a downstream target essential for oncogenic activity of MLL-ENL. Our data suggest that human SWI/SNF complexes show considerable heterogeneity, and one or more may be involved in the etiology of leukemia by cooperating with MLL fusion proteins.

* Corresponding author. Mailing address: Laboratory of Genetics, National Institute on Aging, National Institutes of Health, 333 Cassell Dr., TRIAD Center Room 4000, Baltimore, MD 21224. Phone: (410) 558-8334. Fax: (410) 558-8331. E-mail: wangw{at}grc.nia.nih.gov.

{dagger} Present address: National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, Bethesda, MD 20892-5460.

Molecular and Cellular Biology, April 2003, p. 2942-2952, Vol. 23, No. 8
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.8.2942-2952.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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