Evidence map›Paper›PMID 30591710›Full record

ArticleScientific reports2018

Quantifying site-specific chromatin mechanics and DNA damage response.

Daniel B Whitefield, Stephen T Spagnol, Travis J Armiger, Li Lan, Kris Noel Dahl

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Mechanical Forces in Nuclear Organization.Cold Spring Harbor perspectives in biology · 2022
    Review
  6. Review
  7. Article
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

5 authors at 2 institutions in 1 country.

Daniel B WhitefieldDepartment of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, PA, 15213, USA.
Stephen T SpagnolDepartment of Chemical Engineering, Carnegie Mellon University, Pittsburgh, PA, 15213, USA.
Travis J ArmigerDepartment of Chemical Engineering, Carnegie Mellon University, Pittsburgh, PA, 15213, USA.
Li LanHillman Cancer Center, University of Pittsburgh Medical Center, Pittsburgh, PA, 15232, USA.
Kris Noel DahlDepartment of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, PA, 15213, USA. krisdahl@cmu.edu.
Carnegie Mellon University · USUniversity of Pittsburgh Medical Center · US

Funding

Training in Biomechanics in Regenerative MedicineT32EB003392 · NIBIB · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WOO, SAVIO L-Y. · 2005 to 2020
$4.0M
Transcription-Coupled Homologous Recombination upon DNA DamageR01GM118833 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LAN, LI · 2016 to 2020
$1.6M
National Science Foundation (NSF) CMMI-1300476NIBIB NIH HHS T32 EB003392NIGMS NIH HHS R01 GM118833U.S. Department of Health & Human Services | National Institutes of Health (NIH) EB003392U.S. Department of Health & Human Services | National Institutes of Health (NIH) GM118833
6 · The paper itself

Abstract

DNA double-strand breaks pose a direct threat to genomic stability. Studies of DNA damage and chromatin dynamics have yielded opposing results that support either increased or decreased chromatin motion after damage. In this study, we independently measure the dynamics of transcriptionally active or repressed chromatin regions using particle tracking microrheology. We find that the baseline motion of transcriptionally repressed regions of chromatin are significantly less mobile than transcriptionally active chromatin, which is statistically similar to the bulk motion of chromatin within the nucleus. Site specific DNA damage using KillerRed tags induced in loci within repressed chromatin causes an increased motion, while loci within transcriptionally active regions remains unchanged at similar time scales. We also observe a time-dependent response associated with a further increase in chromatin decondensation. Global induction of damage with bleocin displays similar trends of chromatin decondensation and increased mobility only at 53BP1-labeled damage sites but not at non-damaged sites, indicating that chromatin dynamics are tightly regulated locally after damage. These results shed light on the evolution of the local and global DNA damage response associated with chromatin remodeling and dynamics, with direct implications for their role in repair.

Indexed as

DNA DamageCell Line, TumorCell NucleusChromatinChromatin Assembly and DisassemblyDNA Breaks, Double-StrandedGenes, ReporterHumansTranscriptional ActivationChromatin

Identifiers

PMID30591710
PMCPMC6308236
OpenAlexW2906141231

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.