ArticlePLoS biology2007
Evidence that a RecQ helicase slows senescence by resolving recombining telomeres.
Article in PLoS biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
- To Fix or Not to Fix: Maintenance of Chromosome Ends Versus Repair of DNA Double-Strand Breaks.Cells · 2022Review
- Telomeric C-circles localize at nuclear pore complexes in Saccharomyces cerevisiae.The EMBO journal · 2022Article
- Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad51- and Rad59-dependent survivors.iScience · 2021Article
- Review
- The nuclear pore complex prevents sister chromatid recombination during replicative senescence.Nature communications · 2020Article
- G-Quadruplex DNA and RNA.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Histone depletion prevents telomere fusions in pre-senescent cells.PLoS genetics · 2018Article
- TERRA and the histone methyltransferase Dot1 cooperate to regulate senescence in budding yeast.PloS one · 2018Article
- Rad6-Bre1-mediated H2B ubiquitination regulates telomere replication by promoting telomere-end resection.Nucleic acids research · 2017Article
- Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae.PLoS genetics · 2016Article
- The many facets of homologous recombination at telomeres.Microbial cell (Graz, Austria) · 2015Review
- Two routes to senescence revealed by real-time analysis of telomerase-negative single lineages.Nature communications · 2015Article
- Article
- Length-dependent processing of telomeres in the absence of telomerase.Nucleic acids research · 2014Article
- Resolution by unassisted Top3 points to template switch recombination intermediates during DNA replication.The Journal of biological chemistry · 2013Article
- DNA repair at telomeres: keeping the ends intact.Cold Spring Harbor perspectives in biology · 2013Review
- Saccharomyces cerevisiae as a Model to Study Replicative Senescence Triggered by Telomere Shortening.Frontiers in oncology · 2013Article
- Yeast hnRNP-related proteins contribute to the maintenance of telomeres.Biochemical and biophysical research communications · 2012Article
- Everything you ever wanted to know about Saccharomyces cerevisiae telomeres: beginning to end.Genetics · 2012Review
- Genomic phenotyping of the essential and non-essential yeast genome detects novel pathways for alkylation resistance.BMC systems 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
5 authors at 1 institution in 1 country.
Funding
Abstract
RecQ helicases, including Saccharomyces cerevisiae Sgs1p and the human Werner syndrome protein, are important for telomere maintenance in cells lacking telomerase activity. How maintenance is accomplished is only partly understood, although there is evidence that RecQ helicases function in telomere replication and recombination. Here we use two-dimensional gel electrophoresis (2DGE) and telomere sequence analysis to explore why cells lacking telomerase and Sgs1p (tlc1 sgs1 mutants) senesce more rapidly than tlc1 mutants with functional Sgs1p. We find that apparent X-shaped structures accumulate at telomeres in senescing tlc1 sgs1 mutants in a RAD52- and RAD53-dependent fashion. The X-structures are neither Holliday junctions nor convergent replication forks, but instead may be recombination intermediates related to hemicatenanes. Direct sequencing of examples of telomere I-L in senescing cells reveals a reduced recombination frequency in tlc1 sgs1 compared with tlc1 mutants, indicating that Sgs1p is needed for tlc1 mutants to complete telomere recombination. The reduction in recombinants is most prominent at longer telomeres, consistent with a requirement for Sgs1p to generate viable progeny following telomere recombination. We therefore suggest that Sgs1p may be required for efficient resolution of telomere recombination intermediates, and that resolution failure contributes to the premature senescence of tlc1 sgs1 mutants.
Indexed as
Identifiers
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.