https://scholars.lib.ntu.edu.tw/handle/123456789/568160
標題: | dBRWD3 Regulates Tissue Overgrowth and Ectopic Gene Expression Caused by Polycomb Group Mutations | 作者: | Shih H.-T. Chen W.-Y. Liu K.-Y. Shih Z.-S. Chen Y.-J. PAUL-CHEN HSIEH Kuo K.-L. KUO-HOW HUANG Hsu P.-H. Liu Y.-W. SHIH-PENG CHAN HSIU-HSIANG LEE Tsai Y.-C. Wu J.-T. |
公開日期: | 2016 | 出版社: | Public Library of Science | 卷: | 12 | 期: | 9 | 來源出版物: | PLoS Genetics | 摘要: | 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. © 2016 Shih et al. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84990217438&doi=10.1371%2fjournal.pgen.1006262&partnerID=40&md5=1c4f28e1090c2ae102593cb8df8ea094 https://scholars.lib.ntu.edu.tw/handle/123456789/568160 |
ISSN: | 1553-7390 | DOI: | 10.1371/journal.pgen.1006262 |
顯示於: | 分子醫學研究所 |
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