ArticleJournal of molecular biology2010
Response of the bacteriophage T4 replisome to noncoding lesions and regression of a stalled replication fork.
Article in Journal of molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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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
22 citing papers in PubMed, 31 citations in OpenAlex.
- Pathological R-loops in bacteria from engineered expression of endogenous antisense RNAs whose synthesis is ordinarily terminated by Rho.Nucleic acids research · 2024Article
- Embracing Heterogeneity: Challenging the Paradigm of Replisomes as Deterministic Machines.Chemical reviews · 2023Review
- Resolving Toxic DNA repair intermediates in every E. coli replication cycle: critical roles for RecG, Uup and RadD.Nucleic acids research · 2020Article
- Dynamic structural insights into the molecular mechanism of DNA unwinding by the bacteriophage T7 helicase.Nucleic acids research · 2020Article
- Transcription-mediated replication hindrance: a major driver of genome instability.Genes & development · 2019Review
- Rescuing Replication from Barriers: Mechanistic Insights from Single-Molecule Studies.Molecular and cellular biology · 2019Review
- RNase H1 promotes replication fork progression through oppositely transcribed regions ofThe Journal of biological chemistry · 2019Article
- Helicase promotes replication re-initiation from an RNA transcript.Nature communications · 2018Article
- Genome-wide relationship between R-loop formation and antisense transcription in Escherichia coli.Nucleic acids research · 2018Article
- T7 replisome directly overcomes DNA damage.Nature communications · 2015Article
- Replication fork reversal in eukaryotes: from dead end to dynamic response.Nature reviews. Molecular cell biology · 2015Review
- Dynamics of leading-strand lesion skipping by the replisome.Molecular cell · 2013Article
- Interaction of T4 UvsW helicase and single-stranded DNA binding protein gp32 through its carboxy-terminal acidic tail.Journal of molecular biology · 2013Article
- Bacterial replication, transcription and translation: mechanistic insights from single-molecule biochemical studies.Nature reviews. Microbiology · 2013Review
- Rescuing stalled or damaged replication forks.Cold Spring Harbor perspectives in biology · 2013Review
- Rho-dependent transcription termination is essential to prevent excessive genome-wide R-loops in Escherichia coli.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- A proposal: Source of single strand DNA that elicits the SOS response.Frontiers in bioscience (Landmark edition) · 2013Review
- Direct observation of stalled fork restart via fork regression in the T4 replication system.Science (New York, N.Y.) · 2012Article
- Bypass of a nick by the replisome of bacteriophage T7.The Journal of biological chemistry · 2011Article
- Presynaptic filament dynamics in homologous recombination and DNA repair.Critical reviews in biochemistry and molecular biology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
DNA is constantly damaged by endogenous and exogenous agents. The resulting DNA lesions have the potential to halt the progression of the replisome, possibly leading to replication fork collapse. Here, we examine the effect of a noncoding DNA lesion in either leading strand template or lagging strand template on the bacteriophage T4 replisome. A damaged base in the lagging strand template does not affect the progression of the replication fork. Instead, the stalled lagging strand polymerase recycles from the lesion and initiates the synthesis of a new Okazaki fragment upstream of the damaged base. In contrast, when the replisome encounters a blocking lesion in the leading strand template, the replication fork only travels approximately 1 kb beyond the point of the DNA lesion before complete replication fork collapse. The primosome and the lagging strand polymerase remain active during this period, and an Okazaki fragment is synthesized beyond the point of the leading strand lesion. There is no evidence for a new priming event on the leading strand template. Instead, the DNA structure that is produced by the stalled replication fork is a substrate for the DNA repair helicase UvsW. UvsW catalyzes the regression of a stalled replication fork into a "chicken-foot" structure that has been postulated to be an intermediate in an error-free lesion bypass pathway.
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What OpenQuestion holds
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.