Evidence map›Paper›PMID 19380905›Full record

ArticleGenetics2009

Telomere maintenance and survival in saccharomyces cerevisiae in the absence of telomerase and RAD52.

Catherine Lebel, Emanuel Rosonina, David C F Sealey, Fiona Pryde, David Lydall, Laura Maringele, Lea A Harrington

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 17% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Mgm101: A double-duty Rad52-like protein.Cell cycle (Georgetown, Tex.) · 2016
    Article
  7. The many facets of homologous recombination at telomeres.Microbial cell (Graz, Austria) · 2015
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 6 institutions in 3 countries.

Catherine LebelWellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh, Scotland EH9 3JR.
Emanuel Rosonina
David C F Sealey
Fiona Pryde
David Lydall
Laura Maringele
Lea A Harrington
University of Toronto · CACentre for Life · GBColumbia University · USNewcastle University · GBOntario Institute for Cancer Research · CAWellcome Centre for Cell Biology · GB

Funding

AGING, DISEASE, AND DRUGS ON DIGITALIS SENSITIVITYR01AG002398 · NIA · MICHIGAN STATE UNIVERSITY · PI BRODY, THEODORE M. · 1985 to 1988
–
Howard Hughes Medical Institute HHMI 55005945Medical Research Council G0800081Medical Research Council G0800081-85694NIA NIH HHS R01 AG02398Wellcome Trust 075294Wellcome Trust WT 075294Wellcome Trust WT 081164Wellcome Trust WT 084637
6 · The paper itself

Abstract

Telomeres are essential features of linear genomes that are crucial for chromosome stability. Telomeric DNA is usually replenished by telomerase. Deletion of genes encoding telomerase components leads to telomere attrition with each cycle of DNA replication, eventually causing cell senescence or death. In the Saccharomyces cerevisiae strain W303, telomerase-null populations bypass senescence and, unless EXO1 is also deleted, this survival is RAD52 dependent. Unexpectedly, we found that the S. cerevisiae strain S288C could survive the removal of RAD52 and telomerase at a low frequency without additional gene deletions. These RAD52-independent survivors were propagated stably and exhibited a telomere organization typical of recombination between telomeric DNA tracts, and in diploids behaved as a multigenic trait. The polymerase-delta subunit Pol32 was dispensable for the maintenance of RAD52-independent survivors. The incidence of this rare escape was not affected by deletion of other genes necessary for RAD52-dependent survival, but correlated with initial telomere length. If W303 strains lacking telomerase and RAD52 first underwent telomere elongation, rare colonies could then bypass senescence. We suggest that longer telomeres provide a more proficient substrate for a novel telomere maintenance mechanism that does not rely on telomerase, RAD52, or POL32.

Indexed as

Blotting, SouthernCell DivisionDiploidyDNA-Directed DNA PolymeraseDNA, FungalExodeoxyribonucleasesGene DeletionPenetrancePhenotypeRad52 DNA Repair and Recombination ProteinSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionTelomeraseTelomereTime FactorsDNA-Directed DNA PolymeraseDNA, FungalEST2 protein, S cerevisiaeexodeoxyribonuclease IExodeoxyribonucleasesPol32 protein, S cerevisiaeRad52 DNA Repair and Recombination ProteinRAD52 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTelomerase

Identifiers

PMID19380905
PMCPMC2710150
OpenAlexW2016712010

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.