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Ubiquitin-dependent DNA damage bypass is separable from genome replication

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  • Yasukazu Daigaku

    (Cancer Research UK London Research Institute, Clare Hall Laboratories, Blanche Lane, South Mimms EN6 3LD, UK
    Present address: Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK.)

  • Adelina A. Davies

    (Cancer Research UK London Research Institute, Clare Hall Laboratories, Blanche Lane, South Mimms EN6 3LD, UK)

  • Helle D. Ulrich

    (Cancer Research UK London Research Institute, Clare Hall Laboratories, Blanche Lane, South Mimms EN6 3LD, UK)

Abstract

Repair at what cost? The PCNA (proliferating cell nuclear antigen) clamp encircles DNA and thus tethers polymerases to DNA during replication. Ubiquitination of PCNA after DNA damage, which is mediated by proteins of the Rad6 pathway of post-replicative repair (PRR), facilitates DNA damage bypass by dictating which polymerase is recruited to the fork. When this occurs has been a topic of much debate. Daigaku et al. now show that PRR can be postponed until much of the undamaged genome is replicated. The experimental system also allows them to conclude that PRR of DNA lesions occurs mainly by an error-prone process, with error-free bypass playing a minor role.

Suggested Citation

  • Yasukazu Daigaku & Adelina A. Davies & Helle D. Ulrich, 2010. "Ubiquitin-dependent DNA damage bypass is separable from genome replication," Nature, Nature, vol. 465(7300), pages 951-955, June.
    • Handle: RePEc:nat:nature:v:465:y:2010:i:7300:d:10.1038_nature09097
    DOI: 10.1038/nature09097
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