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Originally published In Press as doi:10.1074/jbc.M100482200 on February 23, 2001

J. Biol. Chem., Vol. 276, Issue 19, 15650-15658, May 11, 2001
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p53 Latency
C-TERMINAL DOMAIN PREVENTS BINDING OF p53 CORE TO TARGET BUT NOT TO NONSPECIFIC DNA SEQUENCES*

Tatiana YakovlevaDagger , Aladdin Pramanik§, Takashi Kawasaki, Koichi Tan-NoDagger , Irina GilevaDagger ||, Heléne LindegrenDagger , Ülo Langel**Dagger Dagger , Tomas J. EkströmDagger , Rudolf Rigler§, Lars TereniusDagger , and Georgy BakalkinDagger §§

From the Dagger  Experimental Alcohol and Drug Addiction Research Section, Department of Clinical Neuroscience, the § Department of Medical Biochemistry and Biophysics, and the  Microbiology and Tumor Biology Center, Karolinska Institute and the ** Department of Neurochemistry and Neurotoxicology, Stockholm University, Stockholm, Sweden

The p53 transcription factor is either latent or activated through multi-site phosphorylation and acetylation of the negative regulatory region in its C-terminal domain (CTD). How CTD modifications activate p53 binding to target DNA sequences via its core domain is still unknown. It has been proposed that nonmodified CTD interacts either with the core domain or with DNA preventing binding of the core domain to DNA and that the fragments of the CTD regulatory region activate p53 by interfering with these interactions. We here characterized the sequence and target specificity of p53 activation by CTD fragments, interaction of activating peptides with p53 and target DNA, and interactions of "latent" p53 with DNA by a band shift assay and by fluorescence correlation spectroscopy. In addition to CTD fragments, several long basic peptides activated p53 and also transcription factor YY1. These peptides and CTD aggregated target DNA but apparently did not interact with p53. The potency to aggregate DNA correlated with the ability to activate p53, suggesting that p53 binds to target sequences upon interactions with tightly packed DNA in aggregates. Latent full-length p53 dissociated DNA aggregates via its core and CTD, and this effect was potentiated by GTP. Latent p53 also formed complexes via both its core and CTD with long nontarget DNA molecules. Such p53-DNA interactions may occur if latent p53 binding to DNA via CTD prevents the interaction of the core domain with target DNA sites but not with nonspecific DNA sequences.

* This work was supported by Swedish Cancer Society Grants 3935 and 5281 (to G. B. and T. J. E.), by Swedish Medical Research Council Grants 12190 (to G. B.) and 3166 (to L. T.), and by a fellowship from the Royal Swedish Academy of Sciences (to I. G.).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.

|| Permanent address: State Research Center of Virology and Biotechnology Vector, Inst. of Molecular Biology, 633159 Koltsovo, Novosibirsk region, Russian Federation.

Dagger Dagger Present address: Harold L. Dorris Neurological Research Center, Dept. of Neuropharmacology, Scripps Research Inst., 10550 North Torrey Pines Rd., Mail SR-307, La Jolla, CA 92037.

§§ To whom correspondence should be addressed: Experimental Alcohol and Drug Addiction Research Section, Dept. of Clinical Neuroscience, Karolinska Inst., S 171 76 Stockholm, Sweden. Tel.: 46-8-5177-5751; Fax: 46-8-5177-6180; E-mail: Georgy.Bakalkin@cmm.ki.se.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.