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Originally published In Press as doi:10.1074/jbc.M200192200 on April 8, 2002

J. Biol. Chem., Vol. 277, Issue 25, 22304-22313, June 21, 2002
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Direct Involvement of CREB-binding Protein/p300 in Sequence-specific DNA Binding of Virus-activated Interferon Regulatory Factor-3 Holocomplex*

Wakako SuharaDagger , Mitsutoshi YoneyamaDagger , Issay Kitabayashi§, and Takashi FujitaDagger

From the Dagger  Department of Tumor Cell Biology, Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo 113-8613 and the § Chromatin Function in Leukemogenesis Project, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan

Infections of bacteria and viruses induce host defense reactions known as innate responses including the activation of interferon regulatory factor-3 (IRF-3), critical for the activation of type I interferon system. Upon immediate early signals triggered by the infection, IRF-3 is phosphorylated and a homodimer results. The homodimer complexes with the coactivator CREB-binding protein (CBP)/p300 in the nucleus; thus, holocomplex of IRF-3 competent in DNA binding is generated. We showed CBP/p300 to be indispensable for the DNA binding activity of the holocomplex and to aid the binding through direct interaction with the DNA. We demonstrated that p300 binds with the IRF-3 homodimer via a Q-rich domain and that an intact histone acetyltransferase (HAT) domain is indispensable for the DNA binding of the holocomplex along with a CH3 domain, which connects the HAT and Q-rich domains. These results highlight a novel function of CBP/p300: direct involvement in sequence-specific DNA binding. Furthermore, the critical function of these domains in virus-induced gene activation was demonstrated in vivo by using p300 mutants.

* This work was supported by grants from the Research for the Future Program; the Japan Society for the Promotion of Science; the Ministry of Education, Science, Sports and Culture of Japan; Nippon Boehringer Ingelheim Co., Ltd.; and Toray Industries Inc.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. Tel./Fax: 81-3-3823-6723; E-mail: fujita@rinshoken.or.jp.

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


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