English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Mammalian Ino80 mediates double-strand break repair through its role in DNA end strand resection

MPS-Authors
/persons/resource/persons219341

Krastev,  Dragomir
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

Locator
There are no locators available
Fulltext (public)
There are no public fulltexts available
Supplementary Material (public)
There is no public supplementary material available
Citation

Gospodinov, A., Vaissiere, T., Krastev, D., Legube, G., Anachkova, B., & Herceg, Z. (2011). Mammalian Ino80 mediates double-strand break repair through its role in DNA end strand resection. Molecular and Cellular Biology, 31(23), 4735-4745.


Cite as: http://hdl.handle.net/21.11116/0000-0001-0A52-8
Abstract
Chromatin modifications/remodeling are important mechanisms by which cells regulate various functions through providing accessibility to chromatin DNA. Recent studies implicated INO80, a conserved chromatin-remodeling complex, in the process of DNA repair. However, the precise underlying mechanism by which this complex mediates repair in mammalian cells remains enigmatic. Here, we studied the effect of silencing of the Ino80 subunit of the complex on double-strand break repair in mammalian cells. Comet assay and homologous recombination repair reporter system analyses indicated that Ino80 is required for efficient double-strand break repair. Ino80 association with chromatin surrounding double-strand breaks suggested the direct involvement of INO80 in the repair process. Ino80 depletion impaired focal recruitment of 53BP1 but did not impede Rad51 focus formation, suggesting that Ino80 is required for the early steps of repair. Further analysis by using bromodeoxyuridine (BrdU)-labeled single-stranded DNA and replication protein A (RPA) immunofluorescent staining showed that INO80 mediates 5'-3' resection of double-strand break ends.