ArticleProceedings of the National Academy of Sciences of the United States of America2008
Regression supports two mechanisms of fork processing in phage T4.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- The telomerase reverse transcriptase elongates reversed replication forks at telomeric repeats.Science advances · 2023Article
- Replication fork uncoupling causes nascent strand degradation and fork reversal.Nature structural & molecular biology · 2023Article
- In vitro reconstitution of DNA replication initiated by genetic recombination: a T4 bacteriophage model for a type of DNA synthesis important for all cells.Molecular biology of the cell · 2019Article
- Replication Fork Reversal during DNA Interstrand Crosslink Repair Requires CMG Unloading.Cell reports · 2018Article
- Differential requirement of Srs2 helicase and Rad51 displacement activities in replication of hairpin-forming CAG/CTG repeats.Nucleic acids research · 2017Article
- Low doses of ultraviolet radiation and oxidative damage induce dramatic accumulation of mitochondrial DNA replication intermediates, fork regression, and replication initiation shift.Molecular biology of the cell · 2015Article
- Replication fork reversal in eukaryotes: from dead end to dynamic response.Nature reviews. Molecular cell biology · 2015Review
- Recombination and replication.Cold Spring Harbor perspectives in biology · 2014Review
- DNA damage responses in prokaryotes: regulating gene expression, modulating growth patterns, and manipulating replication forks.Cold Spring Harbor perspectives in biology · 2013Review
- Replication forks stalled at ultraviolet lesions are rescued via RecA and RuvABC protein-catalyzed disintegration in Escherichia coli.The Journal of biological chemistry · 2012Article
- Mimivirus reveals Mre11/Rad50 fusion proteins with a sporadic distribution in eukaryotes, bacteria, viruses and plasmids.Virology journal · 2011Article
- Initiation of bacteriophage T4 DNA replication and replication fork dynamics: a review in the Virology Journal series on bacteriophage T4 and its relatives.Virology journal · 2010Review
- Fusion of nearby inverted repeats by a replication-based mechanism leads to formation of dicentric and acentric chromosomes that cause genome instability in budding yeast.Genes & development · 2009Article
- Replication fork reversal and the maintenance of genome stability.Nucleic acids research · 2009Review
- Cleavage of a model DNA replication fork by a Type I restriction endonuclease.Nucleic acids research · 2009Article
- Checkpoint responses to unusual structures formed by DNA repeats.Molecular carcinogenesis · 2009Review
- Fork regression is an active helicase-driven pathway in bacteriophage T4.EMBO reports · 2009Article
- SRS2 and SGS1 prevent chromosomal breaks and stabilize triplet repeats by restraining recombination.Nature structural & molecular biology · 2009Article
- Diversity and evolution of chromatin proteins encoded by DNA viruses.Biochimica et biophysica actaReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Replication forks routinely encounter damaged DNA and tightly bound proteins, leading to fork stalling and inactivation. To complete DNA synthesis, it is necessary to remove fork-blocking lesions and reactivate stalled fork structures, which can occur by multiple mechanisms. To study the mechanisms of stalled fork reactivation, we used a model fork intermediate, the origin fork, which is formed during replication from the bacteriophage T4 origin, ori(34). The origin fork accumulates within the T4 chromosome in a site-specific manner without the need for replication inhibitors or DNA damage. We report here that the origin fork is processed in vivo to generate a regressed fork structure. Furthermore, origin fork regression supports two mechanisms of fork resolution that can potentially lead to fork reactivation. Fork regression generates both a site-specific double-stranded end (DSE) and a Holliday junction. Each of these DNA elements serves as a target for processing by the T4 ATPase/exonuclease complex [gene product (gp) 46/47] and Holliday junction-cleaving enzyme (EndoVII), respectively. In the absence of both gp46 and EndoVII, regressed origin forks are stabilized and persist throughout infection. In the presence of EndoVII, but not gp46, there is significantly less regressed origin fork accumulation apparently due to cleavage of the regressed fork Holliday junction. In the presence of gp46, but not EndoVII, regressed origin fork DSEs are processed by degradation of the DSE and a pathway that includes recombination proteins. Although both mechanisms can occur independently, they may normally function together as a single fork reactivation pathway.
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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.