Evidence map›Paper›PMID 27779184›Full record

ArticleNature communications2016

Replication intermediates that escape Dna2 activity are processed by Holliday junction resolvase Yen1.

Gizem Ölmezer, Maryna Levikova, Dominique Klein, Benoît Falquet, Gabriele Alessandro Fontana, Petr Cejka, Ulrich Rass

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. DNA Holliday Junction: History, Regulation and Bioactivity.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Gizem ÖlmezerFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, Basel CH-4058, Switzerland.
Maryna LevikovaInstitute of Molecular Cancer Research, University of Zurich, Winterthurerstrasse 190, Zurich CH-8057, Switzerland.
Dominique KleinFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, Basel CH-4058, Switzerland.
Benoît FalquetFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, Basel CH-4058, Switzerland.
Gabriele Alessandro FontanaFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, Basel CH-4058, Switzerland.
Petr CejkaInstitute of Molecular Cancer Research, University of Zurich, Winterthurerstrasse 190, Zurich CH-8057, Switzerland.
Ulrich RassFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, Basel CH-4058, Switzerland.
Friedrich Miescher Institute · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells have evolved mechanisms to protect, restart and repair perturbed replication forks, allowing full genome duplication, even under replication stress. Interrogating the interplay between nuclease-helicase Dna2 and Holliday junction (HJ) resolvase Yen1, we find the Dna2 helicase activity acts parallel to homologous recombination (HR) in promoting DNA replication and chromosome detachment at mitosis after replication fork stalling. Yen1, but not the HJ resolvases Slx1-Slx4 and Mus81-Mms4, safeguards chromosome segregation by removing replication intermediates that escape Dna2. Post-replicative DNA damage checkpoint activation in Dna2 helicase-defective cells causes terminal G2/M arrest by precluding Yen1-dependent repair, whose activation requires progression into anaphase. These findings explain the exquisite replication stress sensitivity of Dna2 helicase-defective cells, and identify a non-canonical role for Yen1 in the processing of replication intermediates that is distinct from HJ resolution. The involvement of Dna2 helicase activity in completing replication may have implications for DNA2-associated pathologies, including cancer and Seckel syndrome.

Indexed as

DNA ReplicationGene Expression Regulation, FungalChromosome SegregationChromosomes, FungalDNA-Binding ProteinsDNA, CruciformDNA HelicasesEndodeoxyribonucleasesEndonucleasesFlap EndonucleasesG2 Phase Cell Cycle CheckpointsHolliday Junction ResolvasesHomologous RecombinationMitosisSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA2 protein, S cerevisiaeDNA-Binding ProteinsDNA, CruciformDNA HelicasesEndodeoxyribonucleasesEndonucleasesFlap EndonucleasesHolliday Junction ResolvasesMMS4 protein, S cerevisiaeMUS81 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSLX1 protein, S cerevisiaeSLX4 protein, S cerevisiaeYen1 protein, S cerevisiae

Identifiers

PMID27779184
PMCPMC5093310
OpenAlexW2534164974

What OpenQuestion holds

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LicenceCC BY
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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.