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The importance of repairing stalled replication forks

Author

Listed:
  • Michael M. Cox

    (University of Wisconsin-Madison)

  • Myron F. Goodman

    (University of Southern California)

  • Kenneth N. Kreuzer

    (Duke University Medical Center)

  • David J. Sherratt

    (University of Oxford)

  • Steven J. Sandler

    (University of Massachusetts)

  • Kenneth J. Marians

    (Molecular Biology Program, Memorial Sloan-Kettering Cancer Center)

Abstract

The bacterial SOS response to unusual levels of DNA damage has been recognized and studied for several decades. Pathways for re-establishing inactivated replication forks under normal growth conditions have received far less attention. In bacteria growing aerobically in the absence of SOS-inducing conditions, many replication forks encounter DNA damage, leading to inactivation. The pathways for fork reactivation involve the homologous recombination systems, are nonmutagenic, and integrate almost every aspect of DNA metabolism. On a frequency-of-use basis, these pathways represent the main function of bacterial DNA recombination systems, as well as the main function of a number of other enzymatic systems that are associated with replication and site-specific recombination.

Suggested Citation

  • Michael M. Cox & Myron F. Goodman & Kenneth N. Kreuzer & David J. Sherratt & Steven J. Sandler & Kenneth J. Marians, 2000. "The importance of repairing stalled replication forks," Nature, Nature, vol. 404(6773), pages 37-41, March.
    • Handle: RePEc:nat:nature:v:404:y:2000:i:6773:d:10.1038_35003501
    DOI: 10.1038/35003501
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    Cited by:

    1. Alexander T. Duckworth & Peter L. Ducos & Sarah D. McMillan & Kenneth A. Satyshur & Katelien H. Blumenthal & Haley R. Deorio & Joseph A. Larson & Steven J. Sandler & Timothy Grant & James L. Keck, 2023. "Replication fork binding triggers structural changes in the PriA helicase that govern DNA replication restart in E. coli," Nature Communications, Nature, vol. 14(1), pages 1-13, December.

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