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Recombination-restarted replication makes inverted chromosome fusions at inverted repeats

Author

Listed:
  • Ken’Ichi Mizuno

    (Genome Damage and Stability Centre, University of Sussex, Brighton, East Sussex BN1 9RQ, UK)

  • Izumi Miyabe

    (Genome Damage and Stability Centre, University of Sussex, Brighton, East Sussex BN1 9RQ, UK)

  • Stephanie A. Schalbetter

    (Genome Damage and Stability Centre, University of Sussex, Brighton, East Sussex BN1 9RQ, UK)

  • Antony M. Carr

    (Genome Damage and Stability Centre, University of Sussex, Brighton, East Sussex BN1 9RQ, UK)

  • Johanne M. Murray

    (Genome Damage and Stability Centre, University of Sussex, Brighton, East Sussex BN1 9RQ, UK)

Abstract

A new mechanism of chromosomal rearrangement is identified through the observation that broken or collapsed DNA replication forks restarted by homologous recombination have a high propensity for U-turns at short inverted repeats; the error-prone nature of this mechanism is suggested to contribute to gross chromosomal rearrangements and copy-number variations present in cancer and other genomic disorders.

Suggested Citation

  • Ken’Ichi Mizuno & Izumi Miyabe & Stephanie A. Schalbetter & Antony M. Carr & Johanne M. Murray, 2013. "Recombination-restarted replication makes inverted chromosome fusions at inverted repeats," Nature, Nature, vol. 493(7431), pages 246-249, January.
    • Handle: RePEc:nat:nature:v:493:y:2013:i:7431:d:10.1038_nature11676
    DOI: 10.1038/nature11676
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    Cited by:

    1. Chinnu Rose Joseph & Sabrina Dusi & Michele Giannattasio & Dana Branzei, 2022. "Rad51-mediated replication of damaged templates relies on monoSUMOylated DDK kinase," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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