Evidence map›Paper›PMID 30982744›Full record

ArticleMolecular cell2019

An Adversarial DNA N

Soo-Mi Kweon, Yibu Chen, Eugene Moon, Kotryna Kvederaviciutė, Saulius Klimasauskas, Douglas E Feldman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

89 citing papers in PubMed, 171 citations in OpenAlex.

  1. Article
  2. A distinct subclade of AlkB family demethylases in ciliates safeguards the positional fidelity of eukaryotic NProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. The Disordered Region of ASXL1 Acts as an Auto-Regulator Through Condensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Targeting NHypertension (Dallas, Tex. : 1979) · 2025
    Article
  9. Article
  10. Article
  11. The Role of Methylation Modification in Neural Injury and Repair.International journal of molecular sciences · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Adenosine Deaminase-Like Gene-Carried Lentivirus Toolkit for Identification of DNA NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article

29 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

6 authors at 2 institutions in 2 countries.

Soo-Mi KweonDepartment of Pathology, Keck School of Medicine of USC, Los Angeles, CA 90033, USA.
Yibu ChenBioinformatics Service, Department of Health Sciences Libraries, Keck School of Medicine of USC, Los Angeles, CA 90033, USA.
Eugene MoonDepartment of Pathology, Keck School of Medicine of USC, Los Angeles, CA 90033, USA.
Kotryna KvederaviciutėInstitute of Biotechnology, Life Sciences Center, Vilnius University, Vilnius LT-10257, Lithuania.
Saulius KlimasauskasInstitute of Biotechnology, Life Sciences Center, Vilnius University, Vilnius LT-10257, Lithuania.
Douglas E FeldmanDepartment of Pathology, Keck School of Medicine of USC, Los Angeles, CA 90033, USA. Electronic address: defeldma@usc.edu.
Keck Hospital of USC · USVilnius University · LT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenine N6 methylation in DNA (6mA) is widespread among bacteria and phage and is detected in mammalian genomes, where its function is largely unexplored. Here we show that 6mA deposition and removal are catalyzed by the Mettl4 methyltransferase and Alkbh4 dioxygenase, respectively, and that 6mA accumulation in genic elements corresponds with transcriptional silencing. Inactivation of murine Mettl4 depletes 6mA and causes sublethality and craniofacial dysmorphism in incross progeny. We identify distinct 6mA sensor domains of prokaryotic origin within the MPND deubiquitinase and ASXL1, a component of the Polycomb repressive deubiquitinase (PR-DUB) complex, both of which act to remove monoubiquitin from histone H2A (H2A-K119Ub), a repressive mark. Deposition of 6mA by Mettl4 triggers the proteolytic destruction of both sensor proteins, preserving genome-wide H2A-K119Ub levels. Expression of the bacterial 6mA methyltransferase Dam, in contrast, fails to destroy either sensor. These findings uncover a native, adversarial 6mA network architecture that preserves Polycomb silencing.

Indexed as

AdenineAlkB Homolog 4, Lysine DemethylaseAnimalsBacterial ProteinsCraniofacial AbnormalitiesDeubiquitinating EnzymesDNADNA MethylationFemaleGene SilencingGenes, LethalHistonesInbreedingMaleMethyltransferasesMice6-methyladenineAdenineALKBH4 protein, mouseAlkB Homolog 4, Lysine DemethylaseAsxl1 protein, mouseBacterial ProteinsDam methyltransferaseDeubiquitinating EnzymesDNAHistonesMethyltransferasesRepressor ProteinsSite-Specific DNA-Methyltransferase (Adenine-Specific)Ubiquitin6mAALKBH1ALKBH4ASXL1DNA methylationMETTL4MPNDTRIP12

Identifiers

PMID30982744
PMCPMC6591016
OpenAlexW2939392127

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.