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Article

Nascent DNA processing by RecJ favors lesion repair over translesion synthesis at arrested replication forks in Escherichia coli.

Proceedings of the National Academy of Sciences of the United States of America - 13 Jun 2006

Courcelle Charmain T, Chow Kin-Hoe, Casey Andrew, Courcelle Justin

Abstract excerpt

DNA lesions that arrest replication can lead to rearrangements, mutations, or lethality when not processed accurately. After UV-induced DNA damage in Escherichia coli, RecA and several recF pathway proteins are thought to process arrested replication forks and ensure that replication resumes accurately. Here, we show that the RecJ nuclease and RecQ helicase, which partially degrade the nascent DNA at blocked...

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Source

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Identifiers

PMID: 16754873
DOI: 10.1073/pnas.0600785103
PMCID: PMC1482582

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Nascent DNA processing by RecJ favors lesion repair over translesion synthesis at arrested replication forks in Escherichia coli.PMID 16754873Read ↗

RecO acts with RecF and RecR to protect and maintain replication forks blocked by UV-induced DNA damage in Escherichia coli.Semantic proximity Read ↗

UV-induced DNA damage disrupts the coordination between replication initiation, elongation and completion.Semantic proximity Read ↗

Replication restart in UV-irradiated Escherichia coli involving pols II, III, V, PriA, RecA and RecFOR proteins.Semantic proximity Read ↗

RecFOR proteins are essential for Pol V-mediated translesion synthesis and mutagenesis.Semantic proximity Read ↗

RecQ helicase and RecJ nuclease provide complementary functions to resect DNA for homologous recombination.Semantic proximity Read ↗

RecQ helicases and cellular responses to DNA damage.Semantic proximity Read ↗

A defect in homologous recombination leads to increased translesion synthesis in E. coli.Semantic proximity Read ↗

RecQ helicases: lessons from model organisms.Semantic proximity Read ↗

RecO and RecR are necessary for RecA loading in response to DNA damage and replication fork stress.Semantic proximity Read ↗

Replication fork collapse at a protein-DNA roadblock leads to fork reversal, promoted by the RecQ helicaseSemantic proximity Read ↗

RECQ1 is required for cellular resistance to replication stress and catalyzes strand exchange on stalled replication fork structuresSemantic proximity Read ↗

RecQ helicases: guardian angels of the DNA replication fork.Semantic proximity Read ↗

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