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Retention but not recruitment of Crb2 at double-strand breaks requires Rad1 and Rad3 complexes (2003)
| Venue: | Mol. Cell. Biol |
| Citations: | 18 - 7 self |
BibTeX
@ARTICLE{Du03retentionbut,
author = {Li-lin Du and Toru M. Nakamura and Bettina A. Moser and Paul Russell},
title = {Retention but not recruitment of Crb2 at double-strand breaks requires Rad1 and Rad3 complexes},
journal = {Mol. Cell. Biol},
year = {2003},
pages = {6150--6158}
}
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Abstract
The fission yeast checkpoint protein Crb2, related to budding yeast Rad9 and human 53BP1 and BRCA1, has been suggested to act as an adapter protein facilitating the phosphorylation of specific substrates by Rad3-Rad26 kinase. To further understand its role in checkpoint signaling, we examined its localization in live cells by using fluorescence microscopy. In response to DNA damage, Crb2 localizes to distinct nuclear foci, which represent sites of DNA double-strand breaks (DSBs). Crb2 colocalizes with Rad22 at persistent foci, suggesting that Crb2 is retained at sites of DNA damage during repair. Damage-induced Crb2 foci still form in cells defective in Rad1, Rad3, and Rad17 complexes, but these foci do not persist as long as in wild-type cells. Our results suggest that Crb2 functions at the sites of DNA damage, and its regulated persistent localization at damage sites may be involved in facilitating DNA repair and/or maintaining the checkpoint arrest while DNA repair is under way. Eukaryotic cells respond to DNA damage by activating checkpoint signaling pathways conserved from yeast to humans (26, 51). Current models of DNA damage checkpoint signaling envision distinct groups of sensor, adapter, and effector pro-teins acting in a sequential manner to effect checkpoint re-
Keyphrases
dna damage double-strand break rad3 complex dna repair regulated persistent localization rad17 complex checkpoint arrest damage site checkpoint signaling specific substrate eukaryotic cell respond sequential manner yeast rad9 persistent focus adapter protein live cell dna double-strand break fission yeast checkpoint protein crb2 envision distinct group nuclear focus crb2 function dna damage checkpoint wild-type cell damage-induced crb2 focus current model rad3-rad26 kinase effect checkpoint re fluorescence microscopy
