ArticleProceedings of the National Academy of Sciences of the United States of America2013
Protein-DNA complexes are the primary sources of replication fork pausing in Escherichia coli.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 75 citations in OpenAlex.
- Domain dynamics within the PriA DNA helicase regulate DNA replication restart.Nucleic acids research · 2026Article
- The transitional kinetics between open and closed Rep structures can be tuned by salt via two intermediate states.Nucleic acids research · 2026Article
- Transcription-replication collisions trigger high-fidelity replication reset.Nucleic acids research · 2025Article
- Clues to transcription/replication collision-induced DNA damage: it was RNAP, in the chromosome, with the fork.FEBS letters · 2025Review
- Single-molecule characterization of SV40 replisome and novel factors: human FPC and Mcm10.Nucleic acids research · 2024Article
- Genome-wide screen reveals cellular functions that counteract rifampicin lethality inMicrobiology spectrum · 2024Article
- Pif1 Helicase Mediates Remodeling of Protein-Nucleic Acid Complexes by Promoting Dissociation of Sub1 from G-Quadruplex DNA and Cdc13 from G-Rich Single-Stranded DNA.Biochemistry · 2023Article
- Replication fork binding triggers structural changes in the PriA helicase that govern DNA replication restart in E. coli.Nature communications · 2023Article
- The Biochemical Mechanism of Fork Regression in Prokaryotes and Eukaryotes-A Single Molecule Comparison.International journal of molecular sciences · 2022Review
- The RecD2 helicase balances RecA activities.Nucleic acids research · 2022Article
- Single-molecule studies of helicases and translocases in prokaryotic genome-maintenance pathways.DNA repair · 2021Review
- Multiple classes and isoforms of the RNA polymerase recycling motor protein HelD.MicrobiologyOpen · 2021Article
- Bypass of complex co-directional replication-transcription collisions by replisome skipping.Nucleic acids research · 2021Article
- Single-molecule insight into stalled replication fork rescue in Escherichia coli.Nucleic acids research · 2021Review
- Examination of the roles of a conserved motif in the PriA helicase in structure-specific DNA unwinding and processivity.PloS one · 2021Article
- Molecular basis for RNA polymerase-dependent transcription complex recycling by the helicase-like motor protein HelD.Nature communications · 2020Article
- DNA Helicase-SSB Interactions Critical to the Regression and Restart of Stalled DNA Replication forks inGenes · 2020Review
- Review
- Article
- Nuclease dead Cas9 is a programmable roadblock for DNA replication.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Replication fork pausing drives genome instability, because any loss of paused replisome activity creates a requirement for reloading of the replication machinery, a potentially mutagenic process. Despite this importance, the relative contributions to fork pausing of different replicative barriers remain unknown. We show here that Deinococcus radiodurans RecD2 helicase inactivates Escherichia coli replisomes that are paused but still functional in vitro, preventing continued fork movement upon barrier removal or bypass, but does not inactivate elongating forks. Using RecD2 to probe replisome pausing in vivo, we demonstrate that most pausing events do not lead to replisome inactivation, that transcription complexes are the primary sources of this pausing, and that an accessory replicative helicase is critical for minimizing the frequency and/or duration of replisome pauses. These findings reveal the hidden potential for replisome inactivation, and hence genome instability, inside cells. They also demonstrate that efficient chromosome duplication requires mechanisms that aid resumption of replication by paused replisomes, especially those halted by protein-DNA barriers such as transcription complexes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.