Evidence map›Paper›PMID 34140676›Full record

ArticleNature structural & molecular biology2021

Dnmt1 has de novo activity targeted to transposable elements.

Chuck Haggerty, Helene Kretzmer, Christina Riemenschneider, Abhishek Sampath Kumar, Alexandra L Mattei, Nina Bailly, Judith Gottfreund, Pay Giesselmann, Raha Weigert, Björn Brändl and 14 more

Open access · hybridAbstract read
In one paragraph

Article in Nature structural & molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
11.9field-weighted citation impact, top 1% 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

92 citing papers in PubMed, 178 citations in OpenAlex.

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  19. Insulin-Like Growth Factor 2 Reverses Synaptic and Cognitive Deficits in Fetal Growth Restriction Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  20. Article

32 more citing papers are in PubMed but not listed here.

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

24 authors at 8 institutions in 3 countries.

Chuck Haggerty *Department of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Helene Kretzmer *Department of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Christina RiemenschneiderDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Abhishek Sampath KumarDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Alexandra L MatteiDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID http://orcid.org/0000-0003-1450-8924
Nina BaillyDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Judith GottfreundDepartment of Genetics and Epigenetics, Saarland University, Saarbrücken, Germany.ORCID http://orcid.org/0000-0002-1395-3703
Pay GiesselmannDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID http://orcid.org/0000-0002-1227-897X
Raha WeigertDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Björn BrändlDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Pascal GiehrInstitute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland.
René BuschowMicroscopy and Cryo-electron Microscopy Service Group, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID http://orcid.org/0000-0002-9800-2578
Christina GalonskaDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Ferdinand von MeyennInstitute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland.ORCID http://orcid.org/0000-0001-9920-3075
Melissa B PappalardiEpigenetics Research Unit, Oncology R&D, GlaxoSmithKline, Collegeville, PA, USA.
Michael T McCabeEpigenetics Research Unit, Oncology R&D, GlaxoSmithKline, Collegeville, PA, USA.
Lars WittlerDepartment of Developmental Genetics, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Claudia Giesecke-ThielFlow Cytometry Joint Facilities Scientific Service, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Thorsten MielkeMicroscopy and Cryo-electron Microscopy Service Group, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID http://orcid.org/0000-0001-9275-3146
David MeierhoferMass Spectrometry Joint Facilities Scientific Service, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID http://orcid.org/0000-0002-0170-868X
Bernd TimmermannSequencing Core Facility, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Franz-Josef MüllerDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID http://orcid.org/0000-0001-9478-8430
Jörn WalterDepartment of Genetics and Epigenetics, Saarland University, Saarbrücken, Germany.ORCID http://orcid.org/0000-0003-0563-7417
Alexander MeissnerDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany. meissner@molgen.mpg.de.ORCID http://orcid.org/0000-0001-8646-7469
Max Planck Institute for Molecular Genetics · DEChristian-Albrechts-Universität zu Kiel · DEETH Zurich · CHGlaxoSmithKline (United States) · USSaarland University · DEBroad Institute · USHarvard University · USID Genomics (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA methylation plays a critical role during development, particularly in repressing retrotransposons. The mammalian methylation landscape is dependent on the combined activities of the canonical maintenance enzyme Dnmt1 and the de novo Dnmts, 3a and 3b. Here, we demonstrate that Dnmt1 displays de novo methylation activity in vitro and in vivo with specific retrotransposon targeting. We used whole-genome bisulfite and long-read Nanopore sequencing in genetically engineered methylation-depleted mouse embryonic stem cells to provide an in-depth assessment and quantification of this activity. Utilizing additional knockout lines and molecular characterization, we show that the de novo methylation activity of Dnmt1 depends on Uhrf1, and its genomic recruitment overlaps with regions that enrich for Uhrf1, Trim28 and H3K9 trimethylation. Our data demonstrate that Dnmt1 can catalyze DNA methylation in both a de novo and maintenance context, especially at retrotransposons, where this mechanism may provide additional stability for long-term repression and epigenetic propagation throughout development.

Indexed as

AnimalsCCAAT-Enhancer-Binding ProteinsCells, CulturedChromatinDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3ADNA Methyltransferase 3BDNA Transposable ElementsEmbryonic DevelopmentGene Knockout TechniquesGenomeHistonesMiceMouse Embryonic Stem CellsCCAAT-Enhancer-Binding ProteinsChromatinDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNA Methyltransferase 3BDNA Transposable ElementsDnmt1 protein, mouseHistonesTrim28 protein, mouseTripartite Motif-Containing Protein 28Ubiquitin-Protein LigasesUhrf1 protein, mouse

Identifiers

PMID34140676
PMCPMC8279952
OpenAlexW3171704295

What OpenQuestion holds

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LicenceCC BY
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.