RIF1 is essential for 53BP1-dependent nonhomologous end joining and suppression of DNA double-strand break resection.

Journal article

The appropriate execution of DNA double-strand break (DSB) repair is critical for genome stability and tumor avoidance. 53BP1 and BRCA1 directly influence DSB repair pathway choice by regulating 5' end resection, but how this is achieved remains uncertain. Here we report that Rif1(-/-) mice are severely compromised for 53BP1-dependent class switch recombination (CSR) and fusion of dysfunctional telomeres. The inappropriate accumulation of RIF1 at DSBs in S phase is antagonized by BRCA1, and d...

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Authors: Chapman, R; Barral, P; Vannier, J; Borel, V; Steger, M

• Journal: Molecular cell
• Volume: 49
• Issue: 5
• Pages: 858-871
• Publication date: 2013-03-01
• DOI: 10.1016/j.molcel.2013.01.002
• EISSN: 1097-4164
• ISSN: 1097-2765
• Language: English
• Keywords: DNA; DNA Breaks, Double-Stranded; Chromosomal Proteins, Non-Histone; Recombination, Genetic; DNA-Binding Proteins; Telomere-Binding Proteins; Humans; Hela Cells; Transfection; DNA End-Joining Repair; Telomere; Mice; Animals