首页 | 本学科首页   官方微博 | 高级检索  
     


SQSTM1/p62 mediates crosstalk between autophagy and the UPS in DNA repair
Authors:Graeme Hewitt  Bernadette Carroll  Rezazadeh Sarallah  Clara Correia-Melo  Mikołaj Ogrodnik  Glyn Nelson
Affiliation:1. Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK;2. Department of Biology, University of Rochester, Rochester, NY USA
Abstract:
SQSTM1/p62 (sequestosome 1) selectively targets polyubiquitinated proteins for degradation via macroautophagy and the proteasome. Additionally, SQSTM1 shuttles between the cytoplasmic and nuclear compartments, although its role in the nucleus is relatively unknown. Here, we report that SQSTM1 dynamically associates with DNA damage foci (DDF) and regulates DNA repair. Upon induction of DNA damage SQSTM1 interacts with FLNA (filamin A), which has previously been shown to recruit DNA repair protein RAD51 (RAD51 recombinase) to double-strand breaks and facilitate homologous recombination (HR). SQSTM1 promotes proteasomal degradation of FLNA and RAD51 within the nucleus, resulting in reduced levels of nuclear RAD51 and slower DNA repair. SQSTM1 regulates the ratio between HR and nonhomologous end joining (NHEJ) by promoting the latter at the expense of the former. This SQSTM1-dependent mechanism mediates the effect of macroautophagy on DNA repair. Moreover, nuclear localization of SQSTM1 and its association with DDF increase with aging and are prevented by life-span-extending dietary restriction, suggesting that an imbalance in the mechanism identified here may contribute to aging and age-related diseases.
Keywords:aging  autophagy  DNA damage  homologous recombination  nonhomologous end joining  SQSTM1
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号