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Molecular and Cellular Biology, July 2002, p. 4815-4826, Vol. 22, No. 13
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.13.4815-4826.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

JDP2, a Repressor of AP-1, Recruits a Histone Deacetylase 3 Complex To Inhibit the Retinoic Acid-Induced Differentiation of F9 Cells

Chunyuan Jin,1,2 Hongjie Li,1,2 Takehide Murata,1 Kailai Sun,2 Masami Horikoshi,3 Robert Chiu,4,5 and Kazunari K. Yokoyama1*

Gene Engineering Division, RIKEN (Institute of Physical and Chemical Research), BioResource Center, Tsukuba, Ibaraki 305-0074,1 Institute of Molecular and Cellular Bioscience, University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan,3 Department of Medical Genetics, China Medical University, Shenyang 110001, People's Republic of China,2 Dental Research Institute/Oral Biology and Medicine, School of Dentistry,4 Surgical Oncology, School of Medicine, University of California, Los Angeles, California 90095-16685

Received 5 November 2001/ Returned for modification 17 December 2001/ Accepted 25 March 2002

Up-regulation of the c-jun gene is a critical event in the retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Activating transcription factor 2 (ATF-2) and p300 cooperate in the activation of transcription of the c-jun gene during the differentiation of F9 cells. We show here that the overexpression of Jun dimerization protein 2 (JDP2), a repressor of AP-1, inhibits the transactivation of the c-jun gene by ATF-2 and p300 by recruitment of the histone deacetylase 3 (HDAC3) complex, thereby repressing the RA-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Moreover, chromatin immunoprecipitation assays showed that the JDP2/HDAC3 complex, which binds to the differentiation response element within the c-jun promoter in undifferentiated F9 cells, was replaced by the p300 complex in response to RA, with an accompanying change in the histone acetylation status of the chromatin, the initiation of transcription of the c-jun gene, and the subsequent differentiation of F9 cells. These results suggest that JDP2 may be a key factor that controls the commitment of F9 cells to differentiation and shed new light on the mechanism by which an AP-1 repressor functions.

* Corresponding author. Mailing address: Gene Engineering Division, RIKEN (The Institute of Physical and Chemical Research), BioResource Center, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan. Phone: 81-298-36-3612. Fax: 81-298-36-9120. E-mail: kazu{at}rtc.riken.go.jp.

Molecular and Cellular Biology, July 2002, p. 4815-4826, Vol. 22, No. 13
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.13.4815-4826.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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