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J. Biol. Chem., Vol. 283, Issue 14, 9113-9126, April 4, 2008

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Isolation and Characterization of a Novel H1.2 Complex That Acts as a Repressor of p53-mediated Transcription^*

Kyunghwan Kim, Jongkyu Choi, Kyu Heo, Hyunjung Kim, David Levens, Kimitoshi Kohno^¶, Edward M. Johnson^||, Hugh W. Brock^**, and Woojin An, A V Foundation scholar¹

From the Department of Biochemistry and Molecular Biology, University of Southern California Keck School of Medicine, Los Angeles, California 90089, Laboratory of Pathology, NCI, National Institutes of Health, Bethesda, Maryland 20892, ^¶Department of Molecular Biology, University of Occupational and Environmental Health, Kitakyushu, Fukuoka 807-8555, Japan, ^||Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia 23501, and ^**Department of Zoology, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada

Linker histone H1 has been generally viewed as a global repressor of transcription by preventing the access of transcription factors to sites in chromatin. However, recent studies suggest that H1 can interact with other regulatory factors for its action as a negative modulator of specific genes. To investigate these aspects, we established a human cell line expressing H1.2, one of the H1 subtypes, for the purification of H1-interacting proteins. Our results showed that H1.2 can stably associate with sets of cofactors and ribosomal proteins that can significantly repress p53-dependent, p300-mediated chromatin transcription. This repressive action of H1.2 complex involves direct interaction of H1.2 with p53, which in turn blocks p300-mediated acetylation of chromatin. YB1 and PUR, two factors present in the H1.2 complex, together with H1.2 can closely recapitulate the repressive action of the entire H1.2 complex in transcription. Chromatin immunoprecipitation and RNA interference analyses further confirmed that the recruitment of YB1, PUR, and H1.2 to the p53 target gene Bax is required for repression of p53-induced transcription. Therefore, these results reveal a previously unrecognized function of H1 as a transcriptional repressor as well as the underlying mechanism involving specific sets of factors in this repression process.

Received for publication, October 3, 2007 , and in revised form, January 16, 2008.

^* This work was supported in part by the Margaret E. Early Medical Research Trust. 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.

¹ To whom correspondence should be addressed. Tel.: 323-442-4398; Fax: 323-442-7844; E-mail: woojinan{at}usc.edu.

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