2017.5.08 A fate amplifier: The Super elongation complex drives neural stem cell commitment

2019-07-11 14:16:14 10




题 目: A fate amplifier: The Super elongation complex drives neural stem cell commitment

报告人: 宋艳 研究员


时 间: 2017-5-8 (周一), 13:00-14:00

地 点: 北京大学老化学楼东配楼一层101报告厅

主持人: 刘峰 研究员


Asymmetric stem cell division establishes an initial difference between a stem cell and its differentiating sibling, critical for maintaining homeostasis and preventing carcinogenesis. Yet the mechanisms that consolidate and lock in such initial fate bias remain obscure. Our laboratory uses fast-cycling Drosophila neural stem cells as a model system to tackle this question. Combining live imaging with genetic, molecular and biochemical approaches, we recently made an unexpected discovery that the super elongation complex (SEC), best known for transcription elongation checkpoint control, acts as an intrinsic amplifier to drive stem cell fate commitment. SEC is highly expressed in fly neural stem cells, where it promotes self-renewal by physically associating with Notch transcription activation complex and enhancing HES gene transcription. HES in turn upregulates SEC activity, forming a self-reinforcing positive feedback loop with SEC. SEC inactivation leads to neural stem cell loss, whereas its forced activation results in neural progenitor dedifferentiation and tumorigenesis. Our studies unveil an SEC-mediated intracellular amplifier mechanism in ensuring robustness and precision in stem cell fate commitment and provide mechanistic explanation for the highly frequent association of SEC overactivation with human cancers.


宋艳研究员于1996年至2000年在北京大学生命科学学院接受本科教育, 2001-2006年,在美国杜克大学攻读博士学位,期间获HHMI博士生奖学金。 2006年获得分子遗传博士学位后,她进入美国斯坦福大学从事博士后研究工作,开始有关神经干细胞不对称分裂及干细胞衍生癌症方向的研究。 2012年底,她回到北京大学生命科学学院担任研究员,开始独立的研究工作。宋艳研究组主要致力于揭示干细胞谱系内细胞命运、身份或状态的决策机制,进而阐明由相关决策事件出现错误引起发育缺陷或疾病的分子机理。宋艳实验室网址:http://bio.pku.edu.cn/teacher_dis_oa.php?cid=146&&teaid=61