ArticleThe EMBO journal2007
Replication blocking lesions present a unique substrate for homologous recombination.
Article in The EMBO journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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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Who cites it
49 citing papers in PubMed, 78 citations in OpenAlex.
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- NuRD chromatin remodeling is required to repair exogenous DSBs in thebioRxiv : the preprint server for biology · 2025Article
- PLK1 depletion alters homologous recombination and synaptonemal complex disassembly events during mammalian spermatogenesis.Molecular biology of the cell · 2022Article
- DNA repair, recombination, and damage signaling.Genetics · 2022Review
- ZSWIM7 Is Associated With Human Female Meiosis and Familial Primary Ovarian Insufficiency.The Journal of clinical endocrinology and metabolism · 2022Article
- Mechanism of mitotic recombination: insights from C. elegans.Current opinion in genetics & development · 2021Review
- Analysis of representative mutants for key DNA repair pathways on healthspan in Caenorhabditis elegans.Mechanisms of ageing and development · 2021Article
- Nucleotide proofreading functions by nematode RAD51 paralogs facilitate optimal RAD51 filament function.Nature communications · 2021Article
- DNA topoisomerase 3 is required for efficient germ cell quality control.The Journal of cell biology · 2021Article
- Single-molecule analysis reveals cooperative stimulation of Rad51 filament nucleation and growth by mediator proteins.Molecular cell · 2021Article
- Zuo1 supports G4 structure formation and directs repair toward nucleotide excision repair.Nature communications · 2020Article
- Article
- Synthetic Lethality between DNA Polymerase Epsilon and RTEL1 in Metazoan DNA Replication.Cell reports · 2020Article
- Centrobin plays a role in the cellular response to DNA damage.Cell cycle (Georgetown, Tex.) · 2019Article
- Reduction of mRNA export unmasks different tissue sensitivities to low mRNA levels during Caenorhabditis elegans development.PLoS genetics · 2019Article
- Shu complex SWS1-SWSAP1 promotes early steps in mouse meiotic recombination.Nature communications · 2018Article
- Stalled replication forks generate a distinct mutational signature in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- CX-5461 is a DNA G-quadruplex stabilizer with selective lethality in BRCA1/2 deficient tumours.Nature communications · 2017Article
- JMJD-5/KDM8 regulates H3K36me2 and is required for late steps of homologous recombination and genome integrity.PLoS genetics · 2017Article
- LINC complexes promote homologous recombination in part through inhibition of nonhomologous end joining.The Journal of cell biology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homologous recombination (HR) plays a critical role in the restart of blocked replication forks, but how this is achieved remains poorly understood. We show that mutants in the single Rad51 paralog in Caenorhabditis elegans, rfs-1, permit discrimination between HR substrates generated at DNA double-strand breaks (DSBs), or following replication fork collapse from HR substrates assembled at replication fork barriers (RFBs). Unexpectedly, RFS-1 is dispensable for RAD-51 recruitment to meiotic and ionizing radiation (IR)-induced DSBs and following replication fork collapse, yet, is essential for RAD-51 recruitment to RFBs formed by DNA crosslinking agents and other replication blocking lesions. Deletion of rfs-1 also suppresses the accumulation of toxic HR intermediates in him-6; top-3 mutants and accelerates deletion formation at presumed endogenous RFBs formed by poly G/C tracts in the absence of DOG-1. These data suggest that RFS-1 is not a general mediator of HR-dependent DSB repair, but acts specifically to promote HR at RFBs. HR substrates generated at conventional DSBs or following replication fork collapse are therefore intrinsically different from those produced during normal repair of blocked replication forks.
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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.