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Rad9/53BP1 promotes DNA repair via crossover recombination by limiting the Sgs1 and Mph1 helicases

Author

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  • Matteo Ferrari

    (Università degli Studi di Milano
    Memorial Sloan Kettering Cancer Center)

  • Chetan C. Rawal

    (Università degli Studi di Milano
    University of Southern California)

  • Samuele Lodovichi

    (Università degli Studi di Milano)

  • Maria Y. Vietri

    (Università degli Studi di Milano)

  • Achille Pellicioli

    (Università degli Studi di Milano)

Abstract

The DNA damage checkpoint (DDC) is often robustly activated during the homologous recombination (HR) repair of DNA double strand breaks (DSBs). DDC activation controls several HR repair factors by phosphorylation, preventing premature segregation of entangled chromosomes formed during HR repair. The DDC mediator 53BP1/Rad9 limits the nucleolytic processing (resection) of a DSB, controlling the formation of the 3′ single-stranded DNA (ssDNA) filament needed for recombination, from yeast to human. Here we show that Rad9 promotes stable annealing between the recombinogenic filament and the donor template in yeast, limiting strand rejection by the Sgs1 and Mph1 helicases. This regulation allows repair by long tract gene conversion, crossover recombination and break-induced replication (BIR), only after DDC activation. These findings shed light on how cells couple DDC with the choice and effectiveness of HR sub-pathways, with implications for genome instability and cancer.

Suggested Citation

  • Matteo Ferrari & Chetan C. Rawal & Samuele Lodovichi & Maria Y. Vietri & Achille Pellicioli, 2020. "Rad9/53BP1 promotes DNA repair via crossover recombination by limiting the Sgs1 and Mph1 helicases," Nature Communications, Nature, vol. 11(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-16997-w
    DOI: 10.1038/s41467-020-16997-w
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    Cited by:

    1. Erica J. Polleys & Isabella Priore & James E. Haber & Catherine H. Freudenreich, 2023. "Structure-forming CAG/CTG repeats interfere with gap repair to cause repeat expansions and chromosome breaks," Nature Communications, Nature, vol. 14(1), pages 1-16, December.

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