Evidence map›Paper›PMID 24278026›Full record

ArticlePLoS genetics2013

Loss of DNMT1o disrupts imprinted X chromosome inactivation and accentuates placental defects in females.

Serge McGraw, Christopher C Oakes, Josée Martel, M Cecilia Cirio, Pauline de Zeeuw, Winifred Mak, Christoph Plass, Marisa S Bartolomei, J Richard Chaillet, Jacquetta M Trasler

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 72 citations in OpenAlex.

  1. DNMT Enzymes and Their Impact on Cervical Cancer: A State-of-the-Art Review.International journal of molecular sciences · 2025
    Review
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  7. Mitigating the detrimental developmental impact of early fetal alcohol exposure using a maternal methyl donor-enriched diet.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  8. Article
  9. Genetic Studies on Mammalian DNA Methyltransferases.Advances in experimental medicine and biology · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. eLife · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

10 authors at 5 institutions in 3 countries.

Serge McGrawDepartments of Pharmacology & Therapeutics, Pediatrics and Human Genetics, Research Institute at The Montreal Children's Hospital of the McGill University Health Centre, McGill University, Montreal, Quebec, Canada.
Christopher C Oakes
Josée Martel
M Cecilia Cirio
Pauline de Zeeuw
Winifred Mak
Christoph Plass
Marisa S Bartolomei
J Richard Chaillet
Jacquetta M Trasler
Montreal Children's Hospital · CAUniversity of Pennsylvania · USUniversity of Pittsburgh · USGerman Cancer Research Center · DEHeidelberg University · DE

Funding

Sequences controlling H19 Gene ImprintingR37GM051279 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BARTOLOMEI, MARISA S. · 2011 to 2020
$3.9M
Epigenetic Variation in Mice with Defective ImprintingR01HD044133 · NICHD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAILLET, J. RICHARD · 2004 to 2014
$2.9M
CIHRNICHD NIH HHS R01 HD044133NIGMS NIH HHS R37 GM051279
6 · The paper itself

Abstract

The maintenance of key germline derived DNA methylation patterns during preimplantation development depends on stores of DNA cytosine methyltransferase-1o (DNMT1o) provided by the oocyte. Dnmt1o(mat-/-) mouse embryos born to Dnmt1(Δ1o/Δ1o) female mice lack DNMT1o protein and have disrupted genomic imprinting and associated phenotypic abnormalities. Here, we describe additional female-specific morphological abnormalities and DNA hypomethylation defects outside imprinted loci, restricted to extraembryonic tissue. Compared to male offspring, the placentae of female offspring of Dnmt1(Δ1o/Δ1o) mothers displayed a higher incidence of genic and intergenic hypomethylation and more frequent and extreme placental dysmorphology. The majority of the affected loci were concentrated on the X chromosome and associated with aberrant biallelic expression, indicating that imprinted X-inactivation was perturbed. Hypomethylation of a key regulatory region of Xite within the X-inactivation center was present in female blastocysts shortly after the absence of methylation maintenance by DNMT1o at the 8-cell stage. The female preponderance of placental DNA hypomethylation associated with maternal DNMT1o deficiency provides evidence of additional roles beyond the maintenance of genomic imprints for DNA methylation events in the preimplantation embryo, including a role in imprinted X chromosome inactivation.

Indexed as

Genomic ImprintingAnimalsDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA MethylationEmbryo, MammalianFemaleGene Expression Regulation, DevelopmentalMaleMicePlacentaPregnancyRNA, Long NoncodingX ChromosomeX Chromosome InactivationDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDnmt1 protein, mouseRNA, Long NoncodingXite transcript, mouse

Identifiers

PMID24278026
PMCPMC3836718
OpenAlexW2090170014

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.