动物研究所  |  中国科学院  |  联系我们  
 
学会首页 概况介绍 交流动态 国内学术交流 国际学术交流 海峡两岸学术交流 科研论文
当前位置:首页 > 交流合作 > 科研论文
A feed-forward mechanism involving Drosophila fragile X mental retardation proteintriggers a replication stress induced DNA damage response
来源:中国科学院动物研究所 时间:2014-04-22 

作者: 章文信①,Ying Cheng①,#Yu-Jing Li,陈振平,#金鹏*,陈大华*

摘要: Fragile X syndrome, a common form of inherited mental retardation, is caused by loss of the fragile X mental retardation protein (FMRP). As a selective RNA-binding protein, FMRP is localized predominately in cytoplasm, where it regulates translational control. However, there is a small portion of FMRP present in the nucleus, and its function there has been elusive. Here we show that Drosophila dFMR1 in nucleus is required for replication stress-induced H2Av phosphorylation in the DNA damage response (DDR). Replication stress could induce the expression of dFmr1 and promote the nuclear accumulation of dFMR1. We show that, upon the stimulation of replication stress, dFMR1 is associated with chromatin in a domain-specific manner, which is essential for its ability to induce the phosphorylation of H2Av. These results together reveal an unexpected nuclear role of FMRP in DDR and uncover a feed-forward mechanism by which dFmr1 and early DDR induced by replication stress reciprocally regulate each other, thereby synergistically triggering activity of the DDR signaling cascade.

附件下载:
 
【打印本页】【关闭本页】
  中国动物学会 地址:北京市朝阳区北辰西路1号院5号 邮编:100101
Copyright © 2006-2020 中国科学院动物研究所 备案号:京ICP备05064604号 联系方式:czs@ioz.ac.cn,010-64807051