Evidence map›Paper›PMID 29346668›Full record

ArticleNucleic acids research2018

RAD51 and RTEL1 compensate telomere loss in the absence of telomerase.

Margaux Olivier, Cyril Charbonnel, Simon Amiard, Charles I White, Maria E Gallego

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  4. Review
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  6. miR-376a Provokes Rectum AdenocarcinomaFrontiers in cell and developmental biology · 2021
    Article
  7. Downregulation of BarleyFrontiers in plant science · 2021
    Article
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  11. Review
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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

5 authors at 1 institution in 1 country.

Margaux OlivierGénétique, Reproduction et Développement, UMR CNRS 6293 - INSERM U1103 - Université Clermont Auvergne, Faculté de Médecine. 28, place Henri Dunant - BP38 63001 Clermont-Ferrand Cedex 1, France.
Cyril CharbonnelGénétique, Reproduction et Développement, UMR CNRS 6293 - INSERM U1103 - Université Clermont Auvergne, Faculté de Médecine. 28, place Henri Dunant - BP38 63001 Clermont-Ferrand Cedex 1, France.
Simon AmiardGénétique, Reproduction et Développement, UMR CNRS 6293 - INSERM U1103 - Université Clermont Auvergne, Faculté de Médecine. 28, place Henri Dunant - BP38 63001 Clermont-Ferrand Cedex 1, France.
Charles I WhiteGénétique, Reproduction et Développement, UMR CNRS 6293 - INSERM U1103 - Université Clermont Auvergne, Faculté de Médecine. 28, place Henri Dunant - BP38 63001 Clermont-Ferrand Cedex 1, France.
Maria E GallegoGénétique, Reproduction et Développement, UMR CNRS 6293 - INSERM U1103 - Université Clermont Auvergne, Faculté de Médecine. 28, place Henri Dunant - BP38 63001 Clermont-Ferrand Cedex 1, France.
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Replicative erosion of telomeres is naturally compensated by telomerase and studies in yeast and vertebrates show that homologous recombination can compensate for the absence of telomerase. We show that RAD51 protein, which catalyzes the key strand-invasion step of homologous recombination, is localized at Arabidopsis telomeres in absence of telomerase. Blocking the strand-transfer activity of the RAD51 in telomerase mutant plants results in a strikingly earlier onset of developmental defects, accompanied by increased numbers of end-to-end chromosome fusions. Imposing replication stress through knockout of RNaseH2 increases numbers of chromosome fusions and reduces the survival of these plants deficient for telomerase and homologous recombination. This finding suggests that RAD51-dependent homologous recombination acts as an essential backup to the telomerase for compensation of replicative telomere loss to ensure genome stability. Furthermore, we show that this positive role of RAD51 in telomere stability is dependent on the RTEL1 helicase. We propose that a RAD51 dependent break-induced replication process is activated in cells lacking telomerase activity, with RTEL1 responsible for D-loop dissolution after telomere replication.

Indexed as

Telomere ShorteningArabidopsisArabidopsis ProteinsDNA HelicasesDNA ReplicationGenomic InstabilityHomologous RecombinationMutationRad51 RecombinaseRepetitive Sequences, Nucleic AcidRibonucleasesStochastic ProcessesTelomeraseTelomereArabidopsis ProteinsATRAD51 protein, ArabidopsisDNA HelicasesRad51 RecombinaseRibonucleasesRTEL1 protein, ArabidopsisTelomerase

Identifiers

PMID29346668
PMCPMC5861403
OpenAlexW2783066352

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.