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Migrating bubble during break-induced replication drives conservative DNA synthesis

Author

Listed:
  • Natalie Saini

    (School of Biology and Institute for Bioengineering and Bioscience, Georgia Institute of Technology)

  • Sreejith Ramakrishnan

    (School of Science, IUPUI, Indianapolis, Indiana 46202-5132, USA)

  • Rajula Elango

    (School of Science, IUPUI, Indianapolis, Indiana 46202-5132, USA)

  • Sandeep Ayyar

    (School of Science, IUPUI, Indianapolis, Indiana 46202-5132, USA)

  • Yu Zhang

    (School of Biology and Institute for Bioengineering and Bioscience, Georgia Institute of Technology)

  • Angela Deem

    (School of Science, IUPUI, Indianapolis, Indiana 46202-5132, USA
    Present address: Department of Genomic Medicine, University of Texas MD Anderson Cancer Center, Houston, Texas 77230, USA.)

  • Grzegorz Ira

    (Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA)

  • James E. Haber

    (Department of Biology and Rosenstiel Basic Medical Sciences Research Center)

  • Kirill S. Lobachev

    (School of Biology and Institute for Bioengineering and Bioscience, Georgia Institute of Technology)

  • Anna Malkova

    (School of Science, IUPUI, Indianapolis, Indiana 46202-5132, USA
    College of Liberal Arts and Sciences, University of Iowa)

Abstract

This paper demonstrates that the mechanism of break-induced replication (BIR) is significantly different from S-phase replication, as it proceeds via a migrating bubble driven by Pif1 helicase, results in conservative inheritance of newly synthesized DNA, and is inherently mutagenic.

Suggested Citation

  • Natalie Saini & Sreejith Ramakrishnan & Rajula Elango & Sandeep Ayyar & Yu Zhang & Angela Deem & Grzegorz Ira & James E. Haber & Kirill S. Lobachev & Anna Malkova, 2013. "Migrating bubble during break-induced replication drives conservative DNA synthesis," Nature, Nature, vol. 502(7471), pages 389-392, October.
    • Handle: RePEc:nat:nature:v:502:y:2013:i:7471:d:10.1038_nature12584
    DOI: 10.1038/nature12584
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    Cited by:

    1. Ronan Broderick & Veronica Cherdyntseva & Jadwiga Nieminuszczy & Eleni Dragona & Maria Kyriakaki & Theodora Evmorfopoulou & Sarantis Gagos & Wojciech Niedzwiedz, 2023. "Pathway choice in the alternative telomere lengthening in neoplasia is dictated by replication fork processing mediated by EXD2’s nuclease activity," Nature Communications, Nature, vol. 14(1), pages 1-16, December.
    2. 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.
    3. 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.
    4. Thomas E. Wilson & Samreen Ahmed & Amanda Winningham & Thomas W. Glover, 2024. "Replication stress induces POLQ-mediated structural variant formation throughout common fragile sites after entry into mitosis," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    5. 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.

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