Evidence map›Paper›PMID 26158780›Full record

ArticleNature communications2015

Two routes to senescence revealed by real-time analysis of telomerase-negative single lineages.

Zhou Xu, Emilie Fallet, Camille Paoletti, Steffen Fehrmann, Gilles Charvin, Maria Teresa Teixeira

Abstract 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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

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  14. Telomere Replication: Solving Multiple End Replication Problems.Frontiers in cell and developmental biology · 2021
    Review
  15. Article
  16. Article
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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.

Zhou Xu1] Centre National de la Recherche Scientifique, UMR8226, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Institut de Biologie Physico-Chimique, 75005 Paris, France [2] Sorbonne Universités, UPMC University Paris 06, UMR8226, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Institut de Biologie Physico-Chimique, 75005 Paris, France.
Emilie Fallet1] Centre National de la Recherche Scientifique, UMR8226, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Institut de Biologie Physico-Chimique, 75005 Paris, France [2] Sorbonne Universités, UPMC University Paris 06, UMR8226, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Institut de Biologie Physico-Chimique, 75005 Paris, France.
Camille PaolettiInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, Illkirch, 67400, France.
Steffen FehrmannInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, Illkirch, 67400, France.
Gilles CharvinInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, Illkirch, 67400, France.
Maria Teresa Teixeira1] Centre National de la Recherche Scientifique, UMR8226, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Institut de Biologie Physico-Chimique, 75005 Paris, France [2] Sorbonne Universités, UPMC University Paris 06, UMR8226, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Institut de Biologie Physico-Chimique, 75005 Paris, France.

Funding

European Research Council 260906
6 · The paper itself

Abstract

In eukaryotes, telomeres cap chromosome ends to maintain genomic stability. Failure to maintain telomeres leads to their progressive erosion and eventually triggers replicative senescence, a pathway that protects against unrestricted cell proliferation. However, the mechanisms underlying the variability and dynamics of this pathway are still elusive. Here we use a microfluidics-based live-cell imaging assay to investigate replicative senescence in individual Saccharomyces cerevisiae cell lineages following telomerase inactivation. We characterize two mechanistically distinct routes to senescence. Most lineages undergo an abrupt and irreversible switch from a replicative to an arrested state, consistent with telomeres reaching a critically short length. In contrast, other lineages experience frequent and stochastic reversible arrests, consistent with the repair of accidental telomere damage by Pol32, a subunit of polymerase δ required for break-induced replication and for post-senescence survival. Thus, at the single-cell level, replicative senescence comprises both deterministic cell fates and chaotic cell division dynamics.

Indexed as

Cell Cycle CheckpointsTelomere ShorteningBlotting, SouthernCell DivisionCell LineageDNA BreaksDNA-Directed DNA PolymeraseDNA RepairLab-On-A-Chip DevicesMicroscopy, FluorescenceMicroscopy, Phase-ContrastSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTelomeraseTelomereTime-Lapse ImagingDNA-Directed DNA PolymerasePol32 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTelomerase

Identifiers

PMID26158780
PMCPMC4503340

What OpenQuestion holds

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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.