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Originally published In Press as doi:10.1074/jbc.M006626200 on September 7, 2000

J. Biol. Chem., Vol. 275, Issue 50, 39458-39465, December 15, 2000
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Regulation of Apoptosis and Cell Cycle Progression by MCL1
DIFFERENTIAL ROLE OF PROLIFERATING CELL NUCLEAR ANTIGEN*

Kenichi FujiseDagger §, Di ZhangDagger , Juinn-lin Liu||, and Edward T. H. YehDagger §

From the Dagger  Research Center for Cardiovascular Diseases, Institute of Molecular Medicine for Prevention of Human Diseases, § Divisions of Cardiology and Molecular Medicine, Department of Internal Medicine, University of Texas Health Science Center, Houston, and || Department of Neuro-oncology, M. D. Anderson Cancer Center, Houston, Texas 77030

MCL1 (ML1 myeloid cell leukemia 1), a Bcl-2 (B- cell lymphoma-leukemia 2) homologue, is known to function as an anti-apoptotic protein. Here we show in vitro and in vivo that MCL1 interacts with the cell cycle regulator, proliferating cell nuclear antigen (PCNA). This finding prompted us to investigate whether MCL1, in addition to its anti-apoptotic function, has an effect on cell cycle progression. A bromodeoxyuridine uptake assay showed that the overexpression of MCL1 significantly inhibited the cell cycle progression through the S-phase. The S-phase of the cell cycle is also known to be regulated by PCNA. A mutant of MCL1 that lacks PCNA binding (MCL1Delta 4A) could not inhibit cell cycle progression as effectively as wild type MCL1. In contrast, MCL1Delta 4A retained its anti-apoptotic function in HeLa cells when challenged by Etoposide. In addition, the intracellular localization of MCL1Delta 4A was identical to that of wild type MCL1. An in vitro pull-down assay suggested that MCL1 is the only Bcl-2 family protein to interact with PCNA. In fact, MCL1, not other Bcl-2 family proteins, contained the PCNA-binding motif described previously. Taken together, MCL1 is a regulator of both apoptosis and cell cycle progression, and the cell cycle regulatory function of MCL1 is mediated through its interaction with PCNA.

* This work was supported in part by National Institutes of Health Mentored Scientist Development Award KO8, 1KO8 HL04015-01.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.

To whom correspondence should be addressed: 6431 Fannin St., Suite 4200, Houston, TX 77030. Tel.: 713-500-6661; Fax: 713-500-6647; E-mail: Kenichi.Fujise@uth.tmc.edu.

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