Tunghai University Institutional Repository:Item 310901/28717
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    Please use this identifier to cite or link to this item: http://140.128.103.80:8080/handle/310901/28717


    Title: dBRWD3 Regulates Tissue Overgrowth and Ectopic Gene Expression Caused by Polycomb Group Mutations
    Authors: 蔡玉真
    Shih, Hsueh-Tzu
    Chen, Wei-Yu
    Liu, Kwei-Yan
    Shih, Zong-Siou
    Chen, Yi-Jyun
    Hsieh, Paul-Chen
    Kuo, Kuan-Lin
    Huang, Kuo-How
    Hsu, Pang-Hung
    Liu, Ya-Wen
    Chan, Shih- Peng
    Lee, Hsiu-Hsiang
    Tsai, Yu-Chen
    Wu, June-Tai
    Contributors: National Taiwan University
    Far Eastern Memorial Hospital
    National Taiwan Ocean University
    Tunghai University
    Keywords: dBRWD3
    Ectopic Gene Expression
    Polycomb group
    Date: 2016-09
    Issue Date: 2016-10-27
    Publisher: USA:PLOS
    Abstract: To maintain a particular cell fate, a unique set of genes should be expressed while another set is repressed. One way to repress gene expression is through Polycomb group (PcG) proteins that compact chromatin into a silent configuration. In addition to cell fate maintenance, PcG proteins also maintain normal cell physiology, for example cell cycle. In the absence of PcG, ectopic activation of the PcG-repressed genes leads to developmental defects and malignant tumors. Little is known about the molecular nature of ectopic gene expression; especially what differentiates expression of a given gene in the orthotopic tissue (orthotopic expression) and the ectopic expression of the same gene due to PcG mutations. Here we present that ectopic gene expression in PcG mutant cells specifically requires dBRWD3, a negative regulator of HIRA/Yemanuclein (YEM)-mediated histone variant H3.3 deposition. dBRWD3 mutations suppress both the ectopic gene expression and aberrant tissue overgrowth in PcG mutants through a YEM-dependent mechanism. Our findings identified dBRWD3 as a critical regulator that is uniquely required for ectopic gene expression and aberrant tissue overgrowth caused by PcG mutations.
    Relation: PLoS genetics, 12(9), e1006262
    Appears in Collections:[Department of Life Sciences ] Periodical Articles

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