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The DNA Replication Fork01:02

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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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Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
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Transcription-replication collisions trigger high-fidelity replication reset.

Matthew B Cooke1, Kobie T Welch1, Laura Deus Ramirez1

  • 1Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, United States.

Nucleic Acids Research
|November 26, 2025
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Summary
This summary is machine-generated.

Translation-transcription decoupling causes DNA breaks via transcription-replication collisions (TRCs). A novel "replication reset" mechanism resolves these DNA ends, preserving genome stability without triggering damage responses.

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Double-stranded DNA ends pose a threat to genome stability.
  • Transcription-replication collisions (TRCs) are a known source of DNA damage.

Purpose of the Study:

  • To identify factors involved in DNA end formation in Escherichia coli.
  • To elucidate the mechanism by which TRCs lead to DNA end formation and resolution.

Main Methods:

  • Genomic CRISPRi screens were employed to identify DNA end formation factors.
  • Investigated the roles of RecBCD and recombination pathways in DNA end processing.

Main Results:

  • Translation-transcription decoupling was found to cause DNA end formation through a TRC-dependent pathway.
  • TRCs lead to replisome stalling and subsequent DNA end generation, not strand breaks.
  • A novel process termed "replication reset" resolves these DNA ends via replicore degradation, avoiding recombination, DNA damage response, or mutagenesis.

Conclusions:

  • A novel DNA safeguard mechanism, "replication reset," preserves genome stability during replication stress.
  • Challenges the assumption that TRCs invariably lead to genome instability in bacteria.