ArticlePloS one2014
Telomere recombination preferentially occurs at short telomeres in telomerase-null type II survivors.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Highly mutagenic copying of telomeric circles promotes ALT establishment.Nature communications · 2026Article
- Review
- KEOPS complex promotes homologous recombination via DNA resection.Nucleic acids research · 2019Article
- A subtelomeric region affects telomerase-negative replicative senescence in Saccharomyces cerevisiae.Scientific reports · 2019Article
- 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
- Rad59-facilitated acquisition of Y' elements by short telomeres delays the onset of senescence.PLoS genetics · 2014Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In telomerase negative yeast cells, Rad52-dependent recombination is activated to maintain telomeres. This recombination-mediated telomere elongation usually involves two independent pathways, type I and type II, and leads to generation of type I and type II survivors. It remains elusive whether the recombination-mediated telomere elongation prefers to take place on shorter or longer telomeres. In this study, we exploited the de novo telomere addition system to examine the telomere recombination event in telomerase negative cells. We show that recombination preferentially occurs on shorter rather than longer telomeres in both pre-survivors and established type II survivors. In type II survivors, the short VII-L telomeres could invade either terminal TG1-3 sequence or short tracts of TG1-3 sequence in subtelomeric Y'-X and Y'-Y' junction to initiate recombination. Unexpectedly, short VII-L telomere recombination still takes place in type II survivors lacking either Rad50 or Rad59, which are required for type II survivor generation in senescing telomerase-null cells. Our results support the notion that Rad50 and Rad59 are not essential for the maintenance of type II survivors once established.
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Registered trials
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