Evidence map›Paper›PMID 33893291›Full record

ArticleNature communications2021

Imaging the response to DNA damage in heterochromatin domains reveals core principles of heterochromatin maintenance.

Anna Fortuny, Audrey Chansard, Pierre Caron, Odile Chevallier, Olivier Leroy, Olivier Renaud, Sophie E Polo

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 59 citations in OpenAlex.

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  18. Mitotic chromatin marking governs asymmetric segregation of DNA damage.bioRxiv : the preprint server for biology · 2024
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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

7 authors at 2 institutions in 1 country.

Anna FortunyEpigenetics and Cell Fate Centre, UMR7216 CNRS, Université de Paris, Paris, France.
Audrey ChansardEpigenetics and Cell Fate Centre, UMR7216 CNRS, Université de Paris, Paris, France.
Pierre CaronEpigenetics and Cell Fate Centre, UMR7216 CNRS, Université de Paris, Paris, France.
Odile ChevallierEpigenetics and Cell Fate Centre, UMR7216 CNRS, Université de Paris, Paris, France.
Olivier LeroyCell and Tissue Imaging Facility, UMR3215 PICT-IBiSA, Institut Curie, Paris, France.ORCID http://orcid.org/0000-0002-6307-8644
Olivier RenaudCell and Tissue Imaging Facility, UMR3215 PICT-IBiSA, Institut Curie, Paris, France.ORCID http://orcid.org/0000-0003-0187-6680
Sophie E PoloEpigenetics and Cell Fate Centre, UMR7216 CNRS, Université de Paris, Paris, France. sophie.polo@univ-paris-diderot.fr.ORCID http://orcid.org/0000-0003-4821-9354
Centre National de la Recherche Scientifique · FRGénétique et biologie du développement · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heterochromatin is a critical chromatin compartment, whose integrity governs genome stability and cell fate transitions. How heterochromatin features, including higher-order chromatin folding and histone modifications associated with transcriptional silencing, are maintained following a genotoxic stress challenge is unknown. Here, we establish a system for targeting UV damage to pericentric heterochromatin in mammalian cells and for tracking the heterochromatin response to UV in real time. We uncover profound heterochromatin compaction changes during repair, orchestrated by the UV damage sensor DDB2, which stimulates linker histone displacement from chromatin. Despite massive heterochromatin unfolding, heterochromatin-specific histone modifications and transcriptional silencing are maintained. We unveil a central role for the methyltransferase SETDB1 in the maintenance of heterochromatic histone marks after UV. SETDB1 coordinates histone methylation with new histone deposition in damaged heterochromatin, thus protecting cells from genome instability. Our data shed light on fundamental molecular mechanisms safeguarding higher-order chromatin integrity following DNA damage.

Indexed as

DNA DamageDNA RepairAnimalsCell Line, TumorChromatin Assembly and DisassemblyDNADNA-Binding ProteinsHeterochromatinHistone-Lysine N-MethyltransferaseHistonesHumansMCF-7 CellsMethylationMiceNIH 3T3 CellsUltraviolet RaysDDB2 protein, humanDNADNA-Binding ProteinsHeterochromatinHistone-Lysine N-MethyltransferaseHistonesSETDB1 protein, human

Identifiers

PMID33893291
PMCPMC8065061
OpenAlexW3155975039

What OpenQuestion holds

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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.