Evidence map›Paper›PMID 26489519›Full record

ArticleNature communications2015

Cell populations can use aneuploidy to survive telomerase insufficiency.

Caroline Millet, Darya Ausiannikava, Thierry Le Bihan, Sander Granneman, Svetlana Makovets

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

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  15. Molecular characterization ofLife science alliance · 2019
    Article
  16. Aneuploidy: Cancer strength or vulnerability?International journal of cancer · 2019
    Review
  17. Article
  18. The diverse consequences of aneuploidy.Nature cell biology · 2019
    Review
  19. Genetic screen identifies adaptive aneuploidy as a key mediator of ER stress resistance in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  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

5 authors at 1 institution in 1 country.

Caroline MilletInstitute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FF, UK.
Darya AusiannikavaInstitute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FF, UK.
Thierry Le BihanCentre for Synthetic and Systems Biology (SynthSys), School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JD, UK.
Sander GrannemanCentre for Synthetic and Systems Biology (SynthSys), School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JD, UK.ORCID http://orcid.org/0000-0003-4387-1271
Svetlana MakovetsInstitute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FF, UK.
University of Edinburgh · GB

Funding

Medical Research Council G0900500Wellcome Trust 091549
6 · The paper itself

Abstract

Telomerase maintains ends of eukaryotic chromosomes, telomeres. Telomerase loss results in replicative senescence and a switch to recombination-dependent telomere maintenance. Telomerase insufficiency in humans leads to telomere syndromes associated with premature ageing and cancer predisposition. Here we use yeast to show that the survival of telomerase insufficiency differs from the survival of telomerase loss and occurs through aneuploidy. In yeast grown at elevated temperatures, telomerase activity becomes limiting: haploid cell populations senesce and generate aneuploid survivors--near diploids monosomic for chromosome VIII. This aneuploidy results in increased levels of the telomerase components TLC1, Est1 and Est3, and is accompanied by decreased abundance of ribosomal proteins. We propose that aneuploidy suppresses telomerase insufficiency through redistribution of cellular resources away from ribosome synthesis towards production of telomerase components and other non-ribosomal proteins. The aneuploidy-induced re-balance of the proteome via modulation of ribosome biogenesis may be a general adaptive response to overcome functional insufficiencies.

Indexed as

AneuploidyCellular SenescenceDiploidyHaploidyRibosomal ProteinsRNASaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTelomeraseTelomere HomeostasisEST1 protein, S cerevisiaeEST3 protein, S cerevisiaeRibosomal ProteinsRNASaccharomyces cerevisiae ProteinsTelomerasetelomerase RNA

Identifiers

PMID26489519
PMCPMC4627575
OpenAlexW2174225329

What OpenQuestion holds

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LicenceCC BY
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.