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Please use this identifier to cite or link to this item:
http://140.128.103.80:8080/handle/310901/28717
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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: | [生命科學系所] 期刊論文
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