Evidence map›Paper›PMID 26433224›Full record

ArticleNucleic acids research2016

Acentric chromosome ends are prone to fusion with functional chromosome ends through a homology-directed rearrangement.

Yuko Ohno, Yuki Ogiyama, Yoshino Kubota, Takuya Kubo, Kojiro Ishii

Abstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Mechanisms driving acentric chromosome transmission.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2020
    Review
  14. Article
  15. Article
  16. Telomere Length Dynamics and the Evolution of Cancer Genome Architecture.International journal of molecular sciences · 2018
    Review
  17. Article
  18. 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.

Yuko OhnoGraduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan.
Yuki OgiyamaGraduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan.
Yoshino KubotaGraduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan.
Takuya KuboGraduate School of Environmental Science, Hokkaido University, Sapporo, Hokkaido 060-0810, Japan.
Kojiro IshiiGraduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan Institute for Academic Initiatives, Osaka University, Suita, Osaka 565-0871, Japan ishii@fbs.osaka-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The centromeres of many eukaryotic chromosomes are established epigenetically on potentially variable tandem repeats; hence, these chromosomes are at risk of being acentric. We reported previously that artificially created acentric chromosomes in the fission yeast Schizosaccharomyces pombe can be rescued by end-to-end fusion with functional chromosomes. Here, we show that most acentric/functional chromosome fusion events in S. pombe cells harbouring an acentric chromosome I differed from the non-homologous end-joining-mediated rearrangements that result in deleterious dicentric fusions in normal cells, and were elicited by a previously unidentified homologous recombination (HR) event between chromosome end-associated sequences. The subtelomere repeats associated with the non-fusogenic ends were also destabilized in the surviving cells, suggesting a causal link between general subtelomere destabilization and acentric/functional chromosome fusion. A mutational analysis indicated that a non-canonical HR pathway was involved in the rearrangement. These findings are indicative of a latent mechanism that conditionally induces general subtelomere instability, presumably in the face of accidental centromere loss events, resulting in rescue of the fatal acentric chromosomes by interchromosomal HR.

Indexed as

Chromosomes, FungalGene RearrangementHomologous RecombinationTelomereChromosome MappingDNA Breaks, Double-StrandedDNA End-Joining RepairFungal ProteinsGenomic InstabilityModels, BiologicalRad51 RecombinaseSchizosaccharomycesFungal ProteinsRad51 Recombinase

Identifiers

PMID26433224
PMCPMC4705696

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Registered trials

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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.