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J. Biol. Chem., Vol. 280, Issue 35, 30916-30923, September 2, 2005

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Jumonji Regulates Cardiomyocyte Proliferation via Interaction with Retinoblastoma Protein^*

Jooyoung Jung, Tae-gyun Kim, Gary E. Lyons, Hyeong-Reh C. Kim, and Youngsook Lee¶

From the Department of Anatomy, University of Wisconsin Medical School, Madison, Wisconsin 53706 and Department of Pathology, Wayne State University, Detroit, Michigan 48201

Jumonji (JMJ) can function as a transcriptional repressor and plays critical roles in embryonic development including heart development in mice. Although JMJ has been suggested to play a role in cell growth, the molecular mechanisms have not been resolved. The present data demonstrate that JMJ interacts with the retinoblastoma protein (Rb), one of the master regulatory genes of cell cycle. JMJ potentiates the repression function of Rb on E2F activities, leading to reduced cell cycle progression. The transcriptional repression domain of JMJ is critical for the interaction with Rb as well as repression of cell cycle. The physiological relevance of the association between Rb and JMJ was assessed in cardiomyocytes. Primary cardiomyocytes cultured from homozygous jmj knock-out mouse embryos (jmj mutants) show increased cell mitosis in a cardiomyocyte-specific manner. Reporter gene analyses demonstrate that promoter activities of cyclin D1, cyclin D2, and Cdc2 are up-regulated in jmj mutant cardiomyocytes. These data suggest that JMJ down-regulates the cell growth via interaction with Rb, which would provide important insights into the cardiac defects observed in jmj mutant mice.

Received for publication, December 22, 2004 , and in revised form, February 10, 2005.

^* This study was supported in part by National Institutes of Health Grant 69050 and American Heart Association Grant 0030002N (to Y. L.), NCI, National Institutes of Health Grant CA64139 (to H.-R. C. K.), and an American Heart Association grant (to G. E. L.). The costs of publication of this article were defrayed in part by the payment of page charges. This 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: Dept. of Anatomy, University of Wisconsin Medical School, 1300 University Ave., Madison, WI 53706. Tel.: 608-265-6352; Fax: 608-262-7306; E-mail: youngsooklee{at}facstaff.wisc.edu.

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