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Single-molecule imaging reveals multiple pathways for the recruitment of translesion polymerases after DNA damage

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  • Elizabeth S. Thrall

    (Harvard Medical School)

  • James E. Kath

    (Harvard Medical School
    Discovery Chemistry and Technology, AbbVie Inc.)

  • Seungwoo Chang

    (Harvard Medical School)

  • Joseph J. Loparo

    (Harvard Medical School)

Abstract

Unrepaired DNA lesions are a potent block to replication, leading to replication fork collapse, double-strand DNA breaks, and cell death. Error-prone polymerases overcome this blockade by synthesizing past DNA lesions in a process called translesion synthesis (TLS), but how TLS polymerases gain access to the DNA template remains poorly understood. In this study, we use particle-tracking PALM to image live Escherichia coli cells containing a functional fusion of the endogenous copy of Pol IV to the photoactivatable fluorescent protein PAmCherry. We find that Pol IV is strongly enriched near sites of replication only upon DNA damage. Surprisingly, we find that the mechanism of Pol IV recruitment is dependent on the type of DNA lesion, and that interactions with proteins other than the processivity factor β play a role under certain conditions. Collectively, these results suggest that multiple interactions, influenced by lesion identity, recruit Pol IV to sites of DNA damage.

Suggested Citation

  • Elizabeth S. Thrall & James E. Kath & Seungwoo Chang & Joseph J. Loparo, 2017. "Single-molecule imaging reveals multiple pathways for the recruitment of translesion polymerases after DNA damage," Nature Communications, Nature, vol. 8(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-02333-2
    DOI: 10.1038/s41467-017-02333-2
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