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J Biol Chem, Vol. 275, Issue 1, 651-656, January 7, 2000

A Mechanism of Repression by Acute Myeloid Leukemia-1, the Target of Multiple Chromosomal Translocations in Acute Leukemia*

Bart LutterbachDagger §, Jennifer J. WestendorfDagger §, Bryan LinggiDagger §, Stuart Isaacpar , Edward Seto**, and Scott W. HiebertDagger §Dagger Dagger

From the Dagger  Departments of Biochemistry and Medicine, and the § Vanderbilt Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, the par  Department of Biology, Bethel College, North Newton, Kansas 67117, and the ** H. Lee Moffitt Cancer Center and Research Institute, University of South Florida, Tampa, Florida 33612

AML1 is one of the most frequently translocated genes in human leukemia. Here we demonstrate that acute myeloid leukemia-1 (AML-1) (Runx-1) represses transcription from a native promoter, p21Waf1/Cip1. Unexpectedly, this repression did not require interactions with the Groucho co-repressor. To define the mechanism of repression, we asked whether other co-repressors could interact with AML-1. We demonstrate that AML-1 interacts with the mSin3 co-repressors. Moreover, endogenous AML-1 associated with endogenous mSin3A in mammalian cells. A deletion mutant of AML-1 that did not interact with mSin3A failed to repress transcription. The AML-1/mSin3 association suggests a mechanism of repression for the chromosomal translocation fusion proteins that disrupt AML-1.

* This work was supported in part by NCI Grants RO1-AG13726, RO1-CA64140, and RO1-CA77274 from the National Institutes of Health, by American Chemical Society Grants JFRA-591 (to S. W. H.) and F32-CA77167 (to J. J. W.), by Center Grant CA68485 from the NCI, National Institutes of Health, and by Grant MCB9631067 from the National Science Foundation (to E. S.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Fellow of the Leukemia Society of America and supported by Grant 5669-99 from the Leukemia Society of America.

Dagger Dagger To whom correspondence should be addressed: Dept. of Biochemistry, Vanderbilt Cancer Center, Vanderbilt University School of Medicine, Medical Research Bldg. II, Rm. 512, 23rd and Pierce, Nashville, TN 37232. Tel.: 615-936-3582; Fax: 615-936-1790; E-mail: scott.hiebert@mcmail.vanderbilt.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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