Evidence map›Paper›PMID 30177760›Full record

ArticleNature structural & molecular biology2018

Reconstitution of anaphase DNA bridge recognition and disjunction.

Kata Sarlós, Andreas S Biebricher, Anna H Bizard, Julia A M Bakx, Anna G Ferreté-Bonastre, Mauro Modesti, Manikandan Paramasivam, Qi Yao, Erwin J G Peterman, Gijs J L Wuite and 1 more

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In one paragraph

Article in Nature structural & molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

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  6. Mechanistic basis for relaxation of DNA supercoils by human topoisomerase IIIα-RMI1-RMI2.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

11 authors at 3 institutions in 3 countries.

Kata SarlósCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.
Andreas S BiebricherDepartment of Physics and Astronomy and LaserLaB, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Anna H BizardCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-1858-3999
Julia A M BakxDepartment of Physics and Astronomy and LaserLaB, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Anna G Ferreté-BonastreCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.
Mauro ModestiCancer Research Center of Marseille, CNRS UMR7258, INSERM U1068, Institut Paoli-Calmettes, Aix-Marseille Université UM105, Marseille, France.ORCID http://orcid.org/0000-0002-4964-331X
Manikandan ParamasivamCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.
Qi YaoCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.
Erwin J G PetermanDepartment of Physics and Astronomy and LaserLaB, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0003-1058-249X
Gijs J L WuiteDepartment of Physics and Astronomy and LaserLaB, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. g.j.l.wuite@vu.nl.
Ian D HicksonCenter for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark. iandh@sund.ku.dk.ORCID http://orcid.org/0000-0002-0583-566X
University of Copenhagen · DKVrije Universiteit Amsterdam · NLCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Faithful chromosome segregation requires that the sister chromatids be disjoined completely. Defective disjunction can lead to the persistence of histone-free threads of DNA known as ultra-fine bridges (UFBs) that connect the separating sister DNA molecules during anaphase. UFBs arise at specific genomic loci and can only be visualized by detection of associated proteins such as PICH, BLM, topoisomerase IIIα, and RPA. However, it remains unknown how these proteins work together to promote UFB processing. We used a combination of ensemble biochemistry and new single-molecule assays to reconstitute key steps of UFB recognition and processing by these human proteins in vitro. We discovered characteristic patterns of hierarchical recruitment and coordinated biochemical activities that were specific for DNA structures modeling UFBs arising at either centromeres or common fragile sites. Our results describe a mechanistic model for how unresolved DNA replication structures are processed by DNA-structure-specific binding factors in mitosis to prevent pathological chromosome nondisjunction.

Indexed as

AnaphaseCell DivisionCentromereChromosome SegregationDNAGenomic InstabilityHumansDNA

Identifiers

PMID30177760
OpenAlexW2888774667

What OpenQuestion holds

Textmetadata
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.