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Title: dBRWD3 Regulates Tissue Overgrowth and Ectopic Gene Expression Caused by Polycomb Group Mutations
Authors: Hsueh-Tzu Shih;Wei-Yu Chen;Kwei-Yan Liu;Zong-Siou Shih;Yi-Jyun Chen;Paul-Chen Hsieh;Kuan-Lin Kuo;Kuo-How Huang;Pang-Hung Hsu;Ya-Wen Liu;Shih-Peng Chan;Hsiu-Hsiang Lee;Yu-Chen Tsai;June-Tai Wu
Contributors: 國立臺灣海洋大學:生命科學系
Date: 2016-09-02
Issue Date: 2017-09-21T08:21:58Z
Publisher: PLoS Genetics
Abstract: 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: 12(9), e1006262
Appears in Collections:[Department of Life Science] Periodical Articles

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