Evidence map›Paper›PMID 24393774›Full record

ArticleNucleic acids research2014

Length-dependent processing of telomeres in the absence of telomerase.

Emilie Fallet, Pascale Jolivet, Julien Soudet, Michael Lisby, Eric Gilson, Maria Teresa Teixeira

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

48 citing papers in PubMed, 78 citations in OpenAlex.

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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

6 authors at 4 institutions in 1 country.

Emilie FalletLaboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Institut de Biologie Physico-Chimique, Centre National de la Recherche Scientifique, Université Pierre et Marie Curie, FRE3354, 75005 Paris, France, Laboratoire de Biologie Moléculaire de la Cellule, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, Université de Lyon 1, UMR5239, 69364 Lyon Cedex 07, France, Department of Biology, University of Copenhagen, Ole Maaløes Vej 5, DK-2200 Copenhagen N, Denmark, Institute for Research on Cancer and Aging, Nice (IRCAN), University of Nice Sophia-Antipolis, CNRS UMR7284/INSERM U1081, Faculty of Medicine, Nice F-06107, France and Department of Medical Genetics, CHU Nice, 06202 Nice cedex 3, France.
Pascale Jolivet
Julien Soudet
Michael Lisby
Eric Gilson
Maria Teresa Teixeira
Laboratoire de Biologie et Modélisation de la Cellule · FRLaboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes · FRÉcole Normale Supérieure de Lyon · FRUniversité Claude Bernard Lyon 1 · FR

Funding

European Research Council 260906
6 · The paper itself

Abstract

In the absence of telomerase, telomeres progressively shorten with every round of DNA replication, leading to replicative senescence. In telomerase-deficient Saccharomyces cerevisiae, the shortest telomere triggers the onset of senescence by activating the DNA damage checkpoint and recruiting homologous recombination (HR) factors. Yet, the molecular structures that trigger this checkpoint and the mechanisms of repair have remained elusive. By tracking individual telomeres, we show that telomeres are subjected to different pathways depending on their length. We first demonstrate a progressive accumulation of subtelomeric single-stranded DNA (ssDNA) through 5'-3' resection as telomeres shorten. Thus, exposure of subtelomeric ssDNA could be the signal for cell cycle arrest in senescence. Strikingly, early after loss of telomerase, HR counteracts subtelomeric ssDNA accumulation rather than elongates telomeres. We then asked whether replication repair pathways contribute to this mechanism. We uncovered that Rad5, a DNA helicase/Ubiquitin ligase of the error-free branch of the DNA damage tolerance (DDT) pathway, associates with native telomeres and cooperates with HR in senescent cells. We propose that DDT acts in a length-independent manner, whereas an HR-based repair using the sister chromatid as a template buffers precocious 5'-3' resection at the shortest telomeres.

Indexed as

Recombinational DNA RepairTelomere ShorteningDNA-Binding ProteinsDNA HelicasesDNA, Single-StrandedEndonucleasesG2 PhaseRecQ HelicasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsS PhaseTelomeraseTelomereTelomere HomeostasisDNA-Binding ProteinsDNA HelicasesDNA, Single-StrandedEndonucleasesMUS81 protein, S cerevisiaeRAD5 protein, S cerevisiaeRecQ HelicasesSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiaeTelomerase

Identifiers

PMID24393774
PMCPMC3973311
OpenAlexW2081948472

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.