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Originally published In Press as doi:10.1074/jbc.M110747200 on January 11, 2002

J. Biol. Chem., Vol. 277, Issue 11, 8847-8853, March 15, 2002
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Cyclin D1 Represses the Basic Helix-Loop-Helix Transcription Factor, BETA2/NeuroD*

Christelle RatineauDagger §, Mary W. PetryDagger , Hiroyuki Mutoh, and Andrew B. Leiter||

From the Division of Gastroenterology, GRASP Digestive Disease Center, New England Medical Center/Tufts University School of Medicine, Boston, Massachusetts 02111

Expression of the hormone secretin in enteroendocrine cells is restricted to the nondividing villus compartment of the intestine, implying that terminal differentiation is linked to cell cycle arrest and that differentiation is repressed in actively proliferating cells. We have shown previously that the basic helix-loop-helix protein, BETA2/NeuroD, induces cell cycle withdrawal in addition to increasing secretin gene expression. A number of transcription factors important for differentiation are repressed by D cyclins. Repression by D cyclins appears to be independent of its effects on the cell cycle. We show that cyclin D1 represses BETA2/NeuroD-dependent transcription of the secretin gene. Examination of cyclin box mutants shows that repression is unrelated to Cdk4 activation. Although cyclin D1 and BETA2 associate in vivo, they do not directly interact. Cyclin D1 may be recruited to BETA2 by binding to the C-terminal domain of the p300 coactivator, downstream from the BETA2-binding site. In the small intestine, cyclin D1 expression occurs only in the actively proliferating crypts of Lieberkuhn but not in villi. Thus repression by cyclin D1 may serve to prevent secretin gene transcription from occurring in relatively immature epithelial progenitor cells.

* This work was supported in part by National Institutes of Health Grants DK43673 and DK52870 (to A. B. L.), the GRASP Digestive Disease Center Grant P30-DK34928, and by a grant from the Harold Whitworth Pierce Charitable Trust and The Medical Foundation, Inc. (Boston) (to H. M.).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.

Dagger Both authors contributed equally to this work.

§ Present address: INSERM U45, Hôpital Edouard Herriot Pavillon Hbis, 69437 Lyon Cedex 03, France.

Present address: Jichi Medical School, Gastroenterology Division, Yakushiji 3311-1, Minamikawachimachi, Kawachi-gun, Tochigi-ken 329-0498, Japan.

|| To whom correspondence should be addressed: Division of Gastroenterology, 218, New England Medical Center, 750 Washington St., Boston, MA 02111. Tel.: 617-636-8337; Fax: 617-636-4207; E-mail: aleiter@lifespan.org.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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