Evidence map›Paper›PMID 30395604›Full record

ArticlePLoS computational biology2018

Chromatin remodelers couple inchworm motion with twist-defect formation to slide nucleosomal DNA.

Giovanni B Brandani, Shoji Takada

Abstract read
In one paragraph

Article in PLoS computational biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Article
  2. Article
  3. Journal of chemical theory and computation · 2025
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  4. Article
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  6. Article
  7. Review
  8. Journal of chemical theory and computation · 2024
    Article
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  11. Review
  12. Article
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  15. Article
  16. Review
  17. Review
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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

2 authors.

Giovanni B BrandaniDepartment of Biophysics, Graduate School of Science, Kyoto University, Kyoto, Japan.
Shoji TakadaDepartment of Biophysics, Graduate School of Science, Kyoto University, Kyoto, Japan.ORCID 0000-0001-5385-7217

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATP-dependent chromatin remodelers are molecular machines that control genome organization by repositioning, ejecting, or editing nucleosomes, activities that confer them essential regulatory roles on gene expression and DNA replication. Here, we investigate the molecular mechanism of active nucleosome sliding by means of molecular dynamics simulations of the Snf2 remodeler translocase in complex with a nucleosome. During its inchworm motion driven by ATP consumption, the translocase overwrites the original nucleosome energy landscape via steric and electrostatic interactions to induce sliding of nucleosomal DNA unidirectionally. The sliding is initiated at the remodeler binding location via the generation of a pair of twist defects, which then spontaneously propagate to complete sliding throughout the entire nucleosome. We also reveal how remodeler mutations and DNA sequence control active nucleosome repositioning, explaining several past experimental observations. These results offer a detailed mechanistic picture of remodeling important for the complete understanding of these key biological processes.

Indexed as

Chromatin Assembly and DisassemblyAdenosine TriphosphatasesAdenosine TriphosphateDNAMolecular Dynamics SimulationMutationNucleosomesSaccharomyces cerevisiae ProteinsStatic ElectricityTranscription FactorsAdenosine TriphosphatasesAdenosine TriphosphateDNANucleosomesSaccharomyces cerevisiae ProteinsSNF2 protein, S cerevisiaeTranscription Factors

Identifiers

PMID30395604
PMCPMC6237416

What OpenQuestion holds

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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.