ArticleMolecular and cellular biology2013
Fission yeast RecQ helicase Rqh1 is required for the maintenance of circular chromosomes.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 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
8 citing papers in PubMed, 11 citations in OpenAlex.
- Homologous recombination mutants cause differing lethality between h- and h+ Schizosaccharomyces pombe strains due to mat1 heterochromatin.The FEBS journal · 2026Article
- Exploring Genetic Interactions with Telomere Protection GeneBiomolecules · 2023Review
- RecQ DNA Helicase Rqh1 Promotes Rad3Molecular and cellular biology · 2020Article
- Homologous recombination repair intermediates promote efficient de novo telomere addition at DNA double-strand breaks.Nucleic acids research · 2020Article
- Review
- Article
- Fission Yeast Exo1 and Rqh1-Dna2 Redundantly Contribute to Resection of Uncapped Telomeres.PloS one · 2015Article
- Rad51-dependent aberrant chromosome structures at telomeres and ribosomal DNA activate the spindle assembly checkpoint.Molecular and cellular biology · 2014Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Protection of telomeres protein 1 (Pot1) binds to single-stranded telomere overhangs and protects chromosome ends. RecQ helicases regulate homologous recombination at multiple stages, including resection, strand displacement, and resolution. Fission yeast pot1 and RecQ helicase rqh1 double mutants are synthetically lethal, but the mechanism is not fully understood. Here, we show that the synthetic lethality of pot1Δ rqh1Δ double mutants is due to inappropriate homologous recombination, as it is suppressed by the deletion of rad51(+). The expression of Rad51 in the pot1Δ rqh1Δ rad51Δ triple mutant, which has circular chromosomes, is lethal. Reduction of the expression of Rqh1 in a pot1 disruptant with circular chromosomes caused chromosome missegregation, and this defect was partially suppressed by the deletion of rad51(+). Taken together, our results suggest that Rqh1 is required for the maintenance of circular chromosomes when homologous recombination is active. Crossovers between circular monomeric chromosomes generate dimers that cannot segregate properly in Escherichia coli. We propose that Rqh1 inhibits crossovers between circular monomeric chromosomes to suppress the generation of circular dimers.
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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.