Mll2 Controls Cardiac Lineage Differentiation of Mouse Embryonic Stem Cells by Promoting H3K4me3 Deposition at Cardiac-Specific Genes

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• 作者：Xiaoling Wan (1) (2)
  Lulu Liu (1) (2)
  Xiaodan Ding (2) (3)
  Peipei Zhou (2)
  Xiujie Yuan (2)
  Zhongwen Zhou (4)
  Ping Hu (5)
  Hong Zhou (3)
  Qiang Li (6)
  Shenghai Zhang (7)
  Sidong Xiong (1)
  Yan Zhang (2)
  
• 关键词：Histone methylation ; Cardiac differentiation ; Embryonic stem cells
• 刊名：Stem Cell Reviews and Reports
• 出版年：2014
• 出版时间：October 2014
• 年：2014
• 卷：10
• 期：5
• 页码：643-652
• 全文大小：1,257 KB
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• 作者单位：Xiaoling Wan (1) (2)
  Lulu Liu (1) (2)
  Xiaodan Ding (2) (3)
  Peipei Zhou (2)
  Xiujie Yuan (2)
  Zhongwen Zhou (4)
  Ping Hu (5)
  Hong Zhou (3)
  Qiang Li (6)
  Shenghai Zhang (7)
  Sidong Xiong (1)
  Yan Zhang (2)
  
  1. Institute of Biology and Medical Sciences, Soochow University, 199 Renai Road, Nanjing, Jiangsu, 215123, China
  2. Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, 320 Yue-yang road, Shanghai, 200031, China
  3. Department of Microbiology & Immunology, Nanjing Medical University, Nanjing, Jiangsu, 210029, China
  4. Department of pathology, Huanshan Hospital of Fudan University, Shanghai, 200040, China
  5. Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, 200031, China
  6. Children鈥檚 Hospital of Fudan University, Shanghai, 201102, China
  7. Institute of Ophthalmology, Eye and ENT Hospital of Fudan University, Shanghai, 200031, China
  
• ISSN：1558-6804

文摘

Trithorax group (TrxG) proteins play critical roles in transcriptional activation by promoting methylation of histone H3 Lysine 4 (H3K4), but the precise functions of the individual TrxG members during embryonic differentiation are not fully understood. Here we show that Mll2, a TrxG member, is required for proliferation but is dispensable for maintaining the pluripotency of mouse embryonic stem cells (ESCs). In addition, differentiation of ESCs toward mesodermal and endodermal lineages is severely altered and, in particular, the cardiac lineage differentiation of ESCs is completely abolished in the absence of Mll2. Moreover, the expression of core cardiac transcription factors and the levels of H3K4 tri-methylation of these cardiac-specific promoters are significantly decreased by the loss of Mll2. Taken together, our results reveal a critical role for Mll2 in proliferation and cardiac lineage differentiation of mouse ESCs, and provide novel molecular insight into the mechanisms of cardiac development and disease.