53BP1 Regulates DSB Repair Using Rif1 to Control 5 ' End Resection

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Authors	ZIMMERMANN Michal LOTTERSBERGER Francisca BUONOMO Sara B. SFEIR Agnel DE LANGE Titia
Year of publication	2013
Type	Article in Periodical
Magazine / Source	Science
MU Faculty or unit	Central European Institute of Technology
Citation
Doi	http://dx.doi.org/10.1126/science.1231573
Field	Genetics and molecular biology
Keywords	PROTEIN 53BP1; DNA; RECOMBINATION; TELOMERES; DOMAINS; CELLS; CTIP
Description	The choice between double-strand break (DSB) repair by either homology-directed repair (HDR) or nonhomologous end joining (NHEJ) is tightly regulated. Defects in this regulation can induce genome instability and cancer. 53BP1 is critical for the control of DSB repair, promoting NHEJ, and inhibiting the 5' end resection needed for HDR. Using dysfunctional telomeres and genome-wide DSBs, we identify Rif1 as the main factor used by 53BP1 to impair 5' end resection. Rif1 inhibits resection involving CtIP, BLM, and Exo1; limits accumulation of BRCA1/BARD1 complexes at sites of DNA damage; and defines one of the mechanisms by which 53BP1 causes chromosomal abnormalities in Brca1-deficient cells. These data establish Rif1 as an important contributor to the control of DSB repair by 53BP1.
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