Evidence map›Paper›PMID 34681628›Full record

ArticleInternational journal of molecular sciences2021

Disruption of Chromatin Dynamics by Hypotonic Stress Suppresses HR and Shifts DSB Processing to Error-Prone SSA.

Lisa Marie Krieger, Emil Mladenov, Aashish Soni, Marilen Demond, Martin Stuschke, George Iliakis

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

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

6 authors at 2 institutions in 1 country.

Lisa Marie KriegerDepartment of Radiation Therapy, Division of Experimental Radiation Biology, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Emil MladenovDepartment of Radiation Therapy, Division of Experimental Radiation Biology, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Aashish SoniDepartment of Radiation Therapy, Division of Experimental Radiation Biology, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.ORCID 0000-0001-9696-1006
Marilen DemondInstitute of Medical Radiation Biology, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Martin StuschkeDepartment of Radiation Therapy, Division of Experimental Radiation Biology, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
George IliakisDepartment of Radiation Therapy, Division of Experimental Radiation Biology, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
University of Duisburg-Essen · DEGerman Cancer Research Center · DE

Funding

Bundesministerium für Bildung und Forschung 02NUK037BBundesministerium für Bildung und Forschung 02NUK043BBundesministerium für Bildung und Forschung 02NUK054BBundesministerium für Wirtschaft und Energie 50WB1836Deutsche Forschungsgemeinschaft GRK1739
6 · The paper itself

Abstract

The processing of DNA double-strand breaks (DSBs) depends on the dynamic characteristics of chromatin. To investigate how abrupt changes in chromatin compaction alter these dynamics and affect DSB processing and repair, we exposed irradiated cells to hypotonic stress (HypoS). Densitometric and chromosome-length analyses show that HypoS transiently decompacts chromatin without inducing histone modifications known from regulated local chromatin decondensation, or changes in Micrococcal Nuclease (MNase) sensitivity. HypoS leaves undisturbed initial stages of DNA-damage-response (DDR), such as radiation-induced ATM activation and H2AX-phosphorylation. However, detection of ATM-pS1981, γ-H2AX and 53BP1 foci is reduced in a protein, cell cycle phase and cell line dependent manner; likely secondary to chromatin decompaction that disrupts the focal organization of DDR proteins. While HypoS only exerts small effects on classical nonhomologous end-joining (c-NHEJ) and alternative end-joining (alt-EJ), it markedly suppresses homologous recombination (HR) without affecting DNA end-resection at DSBs, and clearly enhances single-strand annealing (SSA). These shifts in pathway engagement are accompanied by decreases in HR-dependent chromatid-break repair in the G

Indexed as

Ataxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsCell LineCell ProliferationChromatinDNA Breaks, Double-StrandedDNA End-Joining RepairHistonesHomologous RecombinationHumansHypotonic SolutionsRad52 DNA Repair and Recombination ProteinRadiation, IonizingRNA InterferenceRNA, Small InterferingAtaxia Telangiectasia Mutated ProteinsChromatinH2AX protein, humanHistonesHypotonic SolutionsRad52 DNA Repair and Recombination ProteinRAD52 protein, humanRNA, Small Interferingalternative end-joining (alt-EJ)chromatinchromatin dynamicsDNA-damage-responseDNA double-strand breakshomologous recombination (HR)hypotonic stress (HypoS)ionizing radiation (IR)nonhomologous end-joining (NHEJ)single-strand annealing (SSA)

Identifiers

PMID34681628
PMCPMC8535785
OpenAlexW3206843914

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.