ArticleGenetics2006
Homologous recombination is required for genome stability in the absence of DOG-1 in Caenorhabditis elegans.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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
48 citing papers in PubMed, 72 citations in OpenAlex.
- The critical role of the iron-sulfur cluster and CTC components in DOG-1/BRIP1 function in Caenorhabditis elegans.Nucleic acids research · 2024Article
- The unfolded protein response of the endoplasmic reticulum protects Caenorhabditis elegans against DNA damage caused by stalled replication forks.G3 (Bethesda, Md.) · 2024Article
- Creation and resolution of non-B-DNA structural impediments during replication.Critical reviews in biochemistry and molecular biology · 2022Article
- Article
- Review
- Synthetic Lethality between DNA Polymerase Epsilon and RTEL1 in Metazoan DNA Replication.Cell reports · 2020Article
- GCNA Preserves Genome Integrity and Fertility Across Species.Developmental cell · 2020Article
- Response of Sulfolobus solfataricus Dpo4 polymerase in vitro to a DNA G-quadruplex.Mutagenesis · 2019Article
- A DNA repair protein and histone methyltransferase interact to promote genome stability in the Caenorhabditis elegans germ line.PLoS genetics · 2019Article
- Replication of G Quadruplex DNA.Genes · 2019Review
- Function and Interactions of ERCC1-XPF in DNA Damage Response.Molecules (Basel, Switzerland) · 2018Review
- Natural Genetic Variation in a Multigenerational Phenotype in C. elegans.Current biology : CB · 2018Article
- MinION-based long-read sequencing and assembly extends theGenome research · 2018Article
- Translesion DNA Synthesis in Cancer: Molecular Mechanisms and Therapeutic Opportunities.Chemical research in toxicology · 2017Review
- CX-5461 is a DNA G-quadruplex stabilizer with selective lethality in BRCA1/2 deficient tumours.Nature communications · 2017Article
- Human Translesion Polymerase κ Exhibits Enhanced Activity and Reduced Fidelity Two Nucleotides from G-Quadruplex DNA.Biochemistry · 2016Article
- Review
- Promotion of Homologous Recombination by SWS-1 in Complex with RAD-51 Paralogs in Caenorhabditis elegans.Genetics · 2016Article
- Mutagenic consequences of a single G-quadruplex demonstrate mitotic inheritance of DNA replication fork barriers.Nature communications · 2015Article
- Evidence for the kinetic partitioning of polymerase activity on G-quadruplex DNA.Biochemistry · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In C. elegans, DOG-1 prevents deletions that initiate in polyG/polyC tracts (G/C tracts), most likely by unwinding secondary structures that can form in G/C tracts during lagging-strand DNA synthesis. We have used the dog-1 mutant to assay the in vivo contribution of various repair genes to the maintenance of G/C tracts. Here we show that DOG-1 and the BLM ortholog, HIM-6, act synergistically during replication; simultaneous loss of function of both genes results in replicative stress and an increase in the formation of small deletions that initiate in G/C tracts. Similarly, we demonstrate that the C. elegans orthologs of the homologous recombination repair genes BARD1, RAD51, and XPF and the trans-lesion synthesis polymerases poleta and polkappa contribute to the prevention of deletions in dog-1 mutants. Finally, we provide evidence that the small deletions generated in the dog-1 background are not formed through homologous recombination, nucleotide excision repair, or nonhomologous end-joining mechanisms, but appear to result from a mutagenic repair mechanism acting at G/C tracts. Our data support the hypothesis that absence of DOG-1 leads to replication fork stalling that can be repaired by deletion-free or deletion-prone mechanisms.
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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.