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Status |
Public on Mar 01, 2013 |
Title |
Rif1 Prevents Resection of DNA Breaks and Promotes Immunoglobulin Class Switching |
Organism |
Mus musculus |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
DNA double-strand breaks (DSBs) represent a threat to the genome because they can lead to 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 it does so directly is not known. Here we identify Rapl-interacting factor 1 (Rif1) as an Ataxia-Telangiectasia Mutated (ATM) 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 G1 and S phases of the cell cycle, interferes with class switch recombination (CSR) in B lymphocytes, and leads to accumulation of chromosome DSBs.
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Overall design |
Study of Rif1 DNA-end protection activity against resection via analysis of single-stranded DNA binding protein RPA and Rad51 accumulation at sites of AID-induced DNA damage by ChIP-seq. All samples shown in Fig. 4 are included (controls and test samples, 7 samples in total).
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Contributor(s) |
Di Virgilio M, Callen E, Yamane A, Zhang W, Jankovic M, Gitlin AD, Feldhahn N, Resch W, Oliveira TY, Chait BT, Nussenzweig A, Casellas R, Robbiani DF, Nussenzweig MC |
Citation(s) |
23306439 |
Submission date |
Nov 14, 2012 |
Last update date |
May 15, 2019 |
Contact name |
Thiago Y Oliveira |
E-mail(s) |
toliveira@rockefeller.edu
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Organization name |
The Rockefeller University
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Department |
Immunology, Virology and Microbiology
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Lab |
Laboratory of Molecular Immunology
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Street address |
1230 YORK AVE
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City |
NEW YORK |
State/province |
New York |
ZIP/Postal code |
10065 |
Country |
USA |
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Platforms (1) |
GPL13112 |
Illumina HiSeq 2000 (Mus musculus) |
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Samples (7)
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Relations |
BioProject |
PRJNA181019 |
SRA |
SRP017184 |