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Template switching during break-induced replication

Author

Listed:
  • Catherine E. Smith

    (Columbia University Medical Center, 701 West 168th Street, New York, New York 10032, USA
    Columbia University, 1212 Amsterdam Avenue, New York, New York 10027, USA)

  • Bertrand Llorente

    (Unité de Génétique Moléculaire des Levures (URA2171 CNRS and UFR927 Université Pierre et Marie Curie), Institut Pasteur, 25 rue du docteur Roux, F-75724 Paris, Cedex 15, France)

  • Lorraine S. Symington

    (Columbia University Medical Center, 701 West 168th Street, New York, New York 10032, USA)

Abstract

One way of repairing a DNA break is through invasion of an end into a homologous, intact duplex, which can set up a replication fork. However, this work shows that the initial invasion events are unstable in the vicinity of the break, so that multiple rounds of invasion and dissociation can take place.

Suggested Citation

  • Catherine E. Smith & Bertrand Llorente & Lorraine S. Symington, 2007. "Template switching during break-induced replication," Nature, Nature, vol. 447(7140), pages 102-105, May.
    • Handle: RePEc:nat:nature:v:447:y:2007:i:7140:d:10.1038_nature05723
    DOI: 10.1038/nature05723
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    Cited by:

    1. Sameer Bikram Shah & Youhang Li & Shibo Li & Qing Hu & Tong Wu & Yanmeng Shi & Tran Nguyen & Isaac Ive & Linda Shi & Hailong Wang & Xiaohua Wu, 2024. "53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR)," Nature Communications, Nature, vol. 15(1), pages 1-20, December.
    2. Anastasiya Kishkevich & Sanjeeta Tamang & Michael O. Nguyen & Judith Oehler & Elena Bulmaga & Christos Andreadis & Carl A. Morrow & Manisha Jalan & Fekret Osman & Matthew C. Whitby, 2022. "Rad52’s DNA annealing activity drives template switching associated with restarted DNA replication," Nature Communications, Nature, vol. 13(1), pages 1-13, December.
    3. Yi-Li Feng & Qian Liu & Ruo-Dan Chen & Si-Cheng Liu & Zhi-Cheng Huang & Kun-Ming Liu & Xiao-Ying Yang & An-Yong Xie, 2022. "DNA nicks induce mutational signatures associated with BRCA1 deficiency," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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