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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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Updated: Mar 28, 2026

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
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T7 replisome directly overcomes DNA damage.

Bo Sun1,2,3, Manjula Pandey4, James T Inman1,2

  • 1Department of Physics, Laboratory of Atomic and Solid State Physics, Cornell University, Ithaca, New York 14853, USA.

Nature Communications
|December 18, 2015
PubMed
Summary
This summary is machine-generated.

Bacteriophage T7 replisomes can directly replicate through DNA lesions, unlike other pathways that cause delays. This direct replication occurs through specific interactions between DNA polymerase and helicase, avoiding fork stalling.

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Area of Science:

  • Molecular Biology
  • Virology
  • Biochemistry

Background:

  • Cells and viruses utilize DNA replication restart pathways to overcome DNA lesions.
  • Existing bypass pathways often lead to replication fork delays or cell division arrest due to DNA gaps or accessory protein recruitment.

Purpose of the Study:

  • To investigate the mechanism by which the bacteriophage T7 replisome replicates through leading-strand cyclobutane pyrimidine dimer (CPD) lesions.
  • To determine if the T7 replisome can directly bypass DNA lesions without requiring fork adjustment or reassembly.

Main Methods:

  • Utilized single-molecule and ensemble biochemical methods.
  • Analyzed the behavior of the T7 replisome upon encountering a CPD lesion during DNA replication.

Main Results:

  • Demonstrated that the bacteriophage T7 replisome can directly replicate through a leading-strand CPD lesion.
  • Observed that DNA polymerase and helicase remain associated at the lesion, preventing replisome dissociation.
  • Showed that DNA polymerase replicates through the lesion via direct interaction with the helicase.

Conclusions:

  • The T7 replisome possesses a unique, lesion-permissive replication mechanism.
  • This mechanism allows direct lesion bypass without replisome dissociation or fork adjustment.
  • Suggests novel pathways for understanding DNA replication and lesion tolerance in viral systems.