| First Author | Di Virgilio M | Year | 2013 |
| Journal | Science | Volume | 339 |
| Issue | 6120 | Pages | 711-5 |
| PubMed ID | 23306439 | Mgi Jnum | J:193246 |
| Mgi Id | MGI:5468036 | Doi | 10.1126/science.1230624 |
| Citation | Di Virgilio M, et al. (2013) Rif1 prevents resection of DNA breaks and promotes immunoglobulin class switching. Science 339(6120):711-5 |
| abstractText | DNA double-strand breaks (DSBs) represent a threat to the genome because they can lead to the loss of genetic information and chromosome rearrangements. The DNA repair protein p53 binding protein 1 (53BP1) protects the genome by limiting nucleolytic processing of DSBs by a mechanism that requires its phosphorylation, but whether 53BP1 does so directly is not known. Here, we identify Rap1-interacting factor 1 (Rif1) as an ATM (ataxia-telangiectasia mutated) phosphorylation-dependent interactor of 53BP1 and show that absence of Rif1 results in 5'-3' DNA-end resection in mice. Consistent with enhanced DNA resection, Rif1 deficiency impairs DNA repair in the G(1) and S phases of the cell cycle, interferes with class switch recombination in B lymphocytes, and leads to accumulation of chromosome DSBs. |
