TRIM24 links a non-canonical histone signature to breast cancer

Wen-Wei Tsai, Zhanxin Wang, Teresa T. Yiu, Kadir C. Akdemir, Weiya Xia, Stefan Winter, Cheng-Yu Tsai, Xiaobing Shi, Dirk Schwarzer, William Plunkett, Bruce Aronow, Or Gozani, Wolfgang Fischle, Mien-Chie Hung, Dinshaw J. Patel () and Michelle Craig Barton ()
Additional contact information
Wen-Wei Tsai: Program in Genes and Development, Graduate School of Biomedical Sciences, University of Texas M.D. Anderson Cancer Center
Zhanxin Wang: Structural Biology Program, Memorial Sloan-Kettering Cancer Center
Teresa T. Yiu: Program in Genes and Development, Graduate School of Biomedical Sciences, University of Texas M.D. Anderson Cancer Center
Kadir C. Akdemir: Centers for Cancer Epigenetics and Stem Cell and Developmental Biology, University of Texas M.D. Anderson Cancer Center
Weiya Xia: University of Texas M.D. Anderson Cancer Center
Stefan Winter: Laboratory of Chromatin Biochemistry, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Goettingen, Germany
Cheng-Yu Tsai: University of Texas M.D. Anderson Cancer Center
Xiaobing Shi: Program in Genes and Development, Graduate School of Biomedical Sciences, University of Texas M.D. Anderson Cancer Center
Dirk Schwarzer: Leibniz-Institut für Molekulare Pharmakologie (FMP), Robert-Roessle-Strasse 10, 13125 Berlin, Germany
William Plunkett: University of Texas M.D. Anderson Cancer Center
Bruce Aronow: Computational Medicine Center, Cincinnati Children's Hospital Medical Center
Or Gozani: Stanford University
Wolfgang Fischle: Laboratory of Chromatin Biochemistry, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Goettingen, Germany
Mien-Chie Hung: University of Texas M.D. Anderson Cancer Center
Dinshaw J. Patel: Structural Biology Program, Memorial Sloan-Kettering Cancer Center
Michelle Craig Barton: Program in Genes and Development, Graduate School of Biomedical Sciences, University of Texas M.D. Anderson Cancer Center

Nature, 2010, vol. 468, issue 7326, 927-932

Abstract: Abstract Recognition of modified histone species by distinct structural domains within ‘reader’ proteins plays a critical role in the regulation of gene expression. Readers that simultaneously recognize histones with multiple marks allow transduction of complex chromatin modification patterns into specific biological outcomes. Here we report that chromatin regulator tripartite motif-containing 24 (TRIM24) functions in humans as a reader of dual histone marks by means of tandem plant homeodomain (PHD) and bromodomain (Bromo) regions. The three-dimensional structure of the PHD-Bromo region of TRIM24 revealed a single functional unit for combinatorial recognition of unmodified H3K4 (that is, histone H3 unmodified at lysine 4, H3K4me0) and acetylated H3K23 (histone H3 acetylated at lysine 23, H3K23ac) within the same histone tail. TRIM24 binds chromatin and oestrogen receptor to activate oestrogen-dependent genes associated with cellular proliferation and tumour development. Aberrant expression of TRIM24 negatively correlates with survival of breast cancer patients. The PHD-Bromo of TRIM24 provides a structural rationale for chromatin activation through a non-canonical histone signature, establishing a new route by which chromatin readers may influence cancer pathogenesis.

Date: 2010
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DOI: 10.1038/nature09542

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