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Replication fork reactivation downstream of a blocked nascent leading strand

Author

Listed:
  • Ryan C. Heller

    (Weill Graduate School of Medical Sciences of Cornell University)

  • Kenneth J. Marians

    (Weill Graduate School of Medical Sciences of Cornell University
    Memorial Sloan-Kettering Cancer Center)

Abstract

Unrepaired lesions in the DNA template pose a threat to accurate replication. Several pathways exist in Escherichia coli to reactivate a blocked replication fork. The process of recombination-dependent restart of broken forks is well understood, but the consequence of replication through strand-specific lesions is less well known. Here we show that replication can be restarted and leading-strand synthesis re-initiated downstream of an unrepaired block to leading-strand progression, even when the 3′-OH of the nascent leading strand is unavailable. We demonstrate that the loading by a replication restart system of a single hexamer of the replication fork helicase, DnaB, on the lagging-strand template is sufficient to coordinate priming by the DnaG primase of both the leading and lagging strands. These observations provide a mechanism for damage bypass during fork reactivation, demonstrate how daughter-strand gaps are generated opposite leading-strand lesions during the replication of ultraviolet-light-irradiated DNA, and help to explain the remarkable speed at which even a heavily damaged DNA template is replicated.

Suggested Citation

  • Ryan C. Heller & Kenneth J. Marians, 2006. "Replication fork reactivation downstream of a blocked nascent leading strand," Nature, Nature, vol. 439(7076), pages 557-562, February.
    • Handle: RePEc:nat:nature:v:439:y:2006:i:7076:d:10.1038_nature04329
    DOI: 10.1038/nature04329
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    Cited by:

    1. Longfu Xu & Matthew T. J. Halma & Gijs J. L. Wuite, 2024. "Mapping fast DNA polymerase exchange during replication," Nature Communications, Nature, vol. 15(1), pages 1-11, December.

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