Evidence map›Paper›PMID 25049225›Full record

ArticleGenome research2014

The PML-associated protein DEK regulates the balance of H3.3 loading on chromatin and is important for telomere integrity.

Kristina Ivanauskiene, Erwan Delbarre, James D McGhie, Thomas Küntziger, Lee H Wong, Philippe Collas

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed, 85 citations in OpenAlex.

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  11. p53 in the Molecular Circuitry of Bone Marrow Failure Syndromes.International journal of molecular sciences · 2023
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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

6 authors at 2 institutions in 3 countries.

Kristina IvanauskieneStem Cell Epigenetics Laboratory, Institute of Basic Medical Sciences, Faculty of Medicine, and Norwegian Center for Stem Cell Research, University of Oslo, 0317 Oslo, Norway;
Erwan DelbarreStem Cell Epigenetics Laboratory, Institute of Basic Medical Sciences, Faculty of Medicine, and Norwegian Center for Stem Cell Research, University of Oslo, 0317 Oslo, Norway;
James D McGhieEpigenetics and Chromatin (EpiC) Research, Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia.
Thomas KüntzigerStem Cell Epigenetics Laboratory, Institute of Basic Medical Sciences, Faculty of Medicine, and Norwegian Center for Stem Cell Research, University of Oslo, 0317 Oslo, Norway;
Lee H WongEpigenetics and Chromatin (EpiC) Research, Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia philippe.collas@medisin.uio.no lee.wong@monash.edu.
Philippe CollasStem Cell Epigenetics Laboratory, Institute of Basic Medical Sciences, Faculty of Medicine, and Norwegian Center for Stem Cell Research, University of Oslo, 0317 Oslo, Norway; philippe.collas@medisin.uio.no lee.wong@monash.edu.
University of Oslo · NOMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone variant H3.3 is deposited in chromatin at active sites, telomeres, and pericentric heterochromatin by distinct chaperones, but the mechanisms of regulation and coordination of chaperone-mediated H3.3 loading remain largely unknown. We show here that the chromatin-associated oncoprotein DEK regulates differential HIRA- and DAAX/ATRX-dependent distribution of H3.3 on chromosomes in somatic cells and embryonic stem cells. Live cell imaging studies show that nonnucleosomal H3.3 normally destined to PML nuclear bodies is re-routed to chromatin after depletion of DEK. This results in HIRA-dependent widespread chromatin deposition of H3.3 and H3.3 incorporation in the foci of heterochromatin in a process requiring the DAXX/ATRX complex. In embryonic stem cells, loss of DEK leads to displacement of PML bodies and ATRX from telomeres, redistribution of H3.3 from telomeres to chromosome arms and pericentric heterochromatin, induction of a fragile telomere phenotype, and telomere dysfunction. Our results indicate that DEK is required for proper loading of ATRX and H3.3 on telomeres and for telomeric chromatin architecture. We propose that DEK acts as a "gatekeeper" of chromatin, controlling chromatin integrity by restricting broad access to H3.3 by dedicated chaperones. Our results also suggest that telomere stability relies on mechanisms ensuring proper histone supply and routing.

Indexed as

AnimalsCell LineChromatinChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneDNA-Binding ProteinsEmbryonic Stem CellsHistonesHumansMiceOncogene ProteinsPoly-ADP-Ribose Binding ProteinsTelomereChromatinChromosomal Proteins, Non-HistoneDEK protein, humanDEK protein, mouseDNA-Binding ProteinsHistonesOncogene ProteinsPoly-ADP-Ribose Binding Proteins

Identifiers

PMID25049225
PMCPMC4199371
OpenAlexW2163355622

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.