53BP1 Regulates DSB Repair Using Rif1 to Control 5′ End Resection | Zendy

Michal Zimmermann | Zendy; Francisca Lottersberger | Zendy; Sara B.C. Buonomo | Zendy; Agnel Sfeir | Zendy; Titia de Lange | Zendy

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

Author(s) -

Michal Zimmermann,

Francisca Lottersberger,

Sara B.C. Buonomo,

Agnel Sfeir,

Titia de Lange

Publication year - 2013

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.1231573

Subject(s) - telomere , dna repair , dna , dna damage , immunoglobulin class switching , genome instability , microbiology and biotechnology , biology , chemistry , antibody , genetics , b cell

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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