Evidence map›Paper›PMID 30463903›Full record

ArticleGenes & development2018

Adaptation to DNA damage checkpoint in senescent telomerase-negative cells promotes genome instability.

Héloïse Coutelier, Zhou Xu, Mony Chenda Morisse, Maoussi Lhuillier-Akakpo, Serge Pelet, Gilles Charvin, Karine Dubrana, Maria Teresa Teixeira

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Genes & development, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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, 61 citations in OpenAlex.

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  17. DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Héloïse Coutelier *Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, UMR8226, Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Physico-Chimique, Paris Sciences et Lettres (PSL) Research University, Sorbonne Université, F-75005 Paris, France.
Zhou Xu *Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, UMR8226, Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Physico-Chimique, Paris Sciences et Lettres (PSL) Research University, Sorbonne Université, F-75005 Paris, France.ORCID 0000-0001-9468-1406
Mony Chenda MorisseLaboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, UMR8226, Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Physico-Chimique, Paris Sciences et Lettres (PSL) Research University, Sorbonne Université, F-75005 Paris, France.
Maoussi Lhuillier-AkakpoInstitute of Molecular and Cellular Radiobiology, Commissiriat à l'Énergie Atomique et aux Énergies Alternatives (CEA)/Direction de la Recherche Fondamentale (DRF), 92260 Fontenay-aux-Roses Cedex, France.
Serge PeletDepartment of Fundamental Microbiology, University of Lausanne, CH-1015 Lausanne, Switzerland.
Gilles CharvinDepartment of Developmental Biology and Stem Cells, Institut de Génétique et de Biologie Moléculaire et Cellulaire, 67400 Illkirch, France.
Karine DubranaInstitute of Molecular and Cellular Radiobiology, Commissiriat à l'Énergie Atomique et aux Énergies Alternatives (CEA)/Direction de la Recherche Fondamentale (DRF), 92260 Fontenay-aux-Roses Cedex, France.
Maria Teresa TeixeiraLaboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, UMR8226, Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Physico-Chimique, Paris Sciences et Lettres (PSL) Research University, Sorbonne Université, F-75005 Paris, France.ORCID 0000-0002-9466-7951
Centre National de la Recherche Scientifique · FRUniversité Paris-Sud · FRUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In cells lacking telomerase, telomeres gradually shorten during each cell division to reach a critically short length, permanently activate the DNA damage checkpoint, and trigger replicative senescence. The increase in genome instability that occurs as a consequence may contribute to the early steps of tumorigenesis. However, because of the low frequency of mutations and the heterogeneity of telomere-induced senescence, the timing and mechanisms of genome instability increase remain elusive. Here, to capture early mutation events during replicative senescence, we used a combined microfluidic-based approach and live-cell imaging in yeast. We analyzed DNA damage checkpoint activation in consecutive cell divisions of individual cell lineages in telomerase-negative yeast cells and observed that prolonged checkpoint arrests occurred frequently in telomerase-negative lineages. Cells relied on the adaptation to the DNA damage pathway to bypass the prolonged checkpoint arrests, allowing further cell divisions despite the presence of unrepaired DNA damage. We demonstrate that the adaptation pathway is a major contributor to the genome instability induced during replicative senescence. Therefore, adaptation plays a critical role in shaping the dynamics of genome instability during replicative senescence.

Indexed as

Adaptation, PhysiologicalCell Cycle CheckpointsDNA DamageDNA RepairGenome, FungalGenomic InstabilityMicrofluidic Analytical TechniquesMutationOptical ImagingSaccharomyces cerevisiaeTelomeraseTelomeraseadaptationCdc5DNA damage checkpointgenomic instabilitysenescencetelomere

Identifiers

PMID30463903
PMCPMC6295172
OpenAlexW2901884480

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.