Evidence map›Paper›PMID 26630413›Full record

ArticlePLoS genetics2015

Top2 and Sgs1-Top3 Act Redundantly to Ensure rDNA Replication Termination.

Kamilla Mundbjerg, Signe W Jørgensen, Jacob Fredsøe, Ida Nielsen, Jakob Madsen Pedersen, Iben Bach Bentsen, Michael Lisby, Lotte Bjergbaek, Anni H Andersen

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Role and Regulation of Pif1 Family Helicases at the Replication Fork.International journal of molecular sciences · 2022
    Review
  3. The Role of Topoisomerase II in DNA Repair and Recombination inInternational journal of molecular sciences · 2021
    Article
  4. Review
  5. The many lives of type IA topoisomerases.The Journal of biological chemistry · 2020
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
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

9 authors at 2 institutions in 1 country.

Kamilla MundbjergLaboratory of Genome Research, Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark.
Signe W JørgensenLaboratory of Genome Research, Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark.
Jacob FredsøeLaboratory of Genome Research, Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark.
Ida NielsenLaboratory of Genome Research, Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark.
Jakob Madsen PedersenLaboratory of Genome Research, Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark.
Iben Bach BentsenLaboratory of Genome Research, Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark.
Michael LisbyDepartment of Biology, University of Copenhagen, Copenhagen N, Denmark.
Lotte BjergbaekLaboratory of Genome Research, Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark.
Anni H AndersenLaboratory of Genome Research, Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark.
Aarhus University · DKUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Faithful DNA replication with correct termination is essential for genome stability and transmission of genetic information. Here we have investigated the potential roles of Topoisomerase II (Top2) and the RecQ helicase Sgs1 during late stages of replication. We find that cells lacking Top2 and Sgs1 (or Top3) display two different characteristics during late S/G2 phase, checkpoint activation and accumulation of asymmetric X-structures, which are both independent of homologous recombination. Our data demonstrate that checkpoint activation is caused by a DNA structure formed at the strongest rDNA replication fork barrier (RFB) during replication termination, and consistently, checkpoint activation is dependent on the RFB binding protein, Fob1. In contrast, asymmetric X-structures are formed independent of Fob1 at less strong rDNA replication fork barriers. However, both checkpoint activation and formation of asymmetric X-structures are sensitive to conditions, which facilitate fork merging and progression of replication forks through replication fork barriers. Our data are consistent with a redundant role of Top2 and Sgs1 together with Top3 (Sgs1-Top3) in replication fork merging at rDNA barriers. At RFB either Top2 or Sgs1-Top3 is essential to prevent formation of a checkpoint activating DNA structure during termination, but at less strong rDNA barriers absence of the enzymes merely delays replication fork merging, causing an accumulation of asymmetric termination structures, which are solved over time.

Indexed as

Chromosomes, FungalDNA-Binding ProteinsDNA DamageDNA ReplicationDNA, RibosomalDNA Topoisomerases, Type IGenomic InstabilityRecombination, GeneticRecQ HelicasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscription, GeneticDNA-Binding ProteinsDNA, RibosomalDNA Topoisomerases, Type IRecQ HelicasesSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiae

Identifiers

PMID26630413
PMCPMC4668019
OpenAlexW2189357904

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.