Evidence map›Paper›PMID 27427477›Full record

ArticleStructure (London, England : 1993)2016

Active Control of Repetitive Structural Transitions between Replication Forks and Holliday Junctions by Werner Syndrome Helicase.

Soochul Shin, Jinwoo Lee, Sangwoon Yoo, Tomasz Kulikowicz, Vilhelm A Bohr, Byungchan Ahn, Sungchul Hohng

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Structure (London, England : 1993), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

7 authors at 4 institutions in 2 countries.

Soochul ShinDepartment of Physics and Astronomy, Seoul National University, Seoul 08826, Republic of Korea; Institute of Applied Physics, Seoul National University, Seoul 08826, Republic of Korea; National Center for Creative Research Initiatives, Seoul National University, Seoul 08826, Republic of Korea.
Jinwoo LeeDepartment of Physics and Astronomy, Seoul National University, Seoul 08826, Republic of Korea; Institute of Applied Physics, Seoul National University, Seoul 08826, Republic of Korea; National Center for Creative Research Initiatives, Seoul National University, Seoul 08826, Republic of Korea.
Sangwoon YooDepartment of Physics and Astronomy, Seoul National University, Seoul 08826, Republic of Korea; Institute of Applied Physics, Seoul National University, Seoul 08826, Republic of Korea; National Center for Creative Research Initiatives, Seoul National University, Seoul 08826, Republic of Korea.
Tomasz KulikowiczLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Byungchan AhnDepartment of Life Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea. Electronic address: bbccahn@mail.ulsan.ac.kr.
Sungchul HohngDepartment of Physics and Astronomy, Seoul National University, Seoul 08826, Republic of Korea; Institute of Applied Physics, Seoul National University, Seoul 08826, Republic of Korea; National Center for Creative Research Initiatives, Seoul National University, Seoul 08826, Republic of Korea; Department of Biophysics and Chemical Biology, Seoul National University, Seoul 08826, Republic of Korea. Electronic address: shohng@snu.ac.kr.
Seoul National University · KRNational Institute on Aging · USNational Institutes of Health · USUniversity of Ulsan · KR

Funding

The Function of Werner Syndrome ProteinZIAAG000721 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$7.7M
Intramural NIH HHS ZIA AG000721
6 · The paper itself

Abstract

The reactivation of stalled DNA replication via fork regression invokes Holliday junction formation, branch migration, and the recovery of the replication fork after DNA repair or error-free DNA synthesis. The coordination mechanism for these DNA structural transitions by molecular motors, however, remains unclear. Here we perform single-molecule fluorescence experiments with Werner syndrome protein (WRN) and model replication forks. The Holliday junction is readily formed once the lagging arm is unwound, and migrated unidirectionally with 3.2 ± 0.03 bases/s velocity. The recovery of the replication fork was controlled by branch migration reversal of WRN, resulting in repetitive fork regression. The Holliday junction formation, branch migration, and migration direction reversal are all ATP dependent, revealing that WRN uses the energy of ATP hydrolysis to actively coordinate the structural transitions of DNA.

Indexed as

DNA ReplicationAdenosine TriphosphateAnimalsBase PairingCarbocyaninesDNA, CruciformFluorescence Resonance Energy TransferFluorescent DyesGene ExpressionHumansRecombinant Fusion ProteinsSf9 CellsSingle Molecule ImagingSpodopteraWerner Syndrome HelicaseAdenosine TriphosphateCarbocyaninescyanine dye 3cyanine dye 5DNA, CruciformFluorescent DyesRecombinant Fusion ProteinsWerner Syndrome HelicaseWRN protein, humanreplication fork regressionsingle-molecule FRETwerner syndrome helicase

Identifiers

PMID27427477
PMCPMC5167498
OpenAlexW2473270061

What OpenQuestion holds

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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.