Evidence map›Paper›PMID 33110091›Full record

ArticleNature communications2020

Maternal DNMT3A-dependent de novo methylation of the paternal genome inhibits gene expression in the early embryo.

Julien Richard Albert, Wan Kin Au Yeung, Keisuke Toriyama, Hisato Kobayashi, Ryutaro Hirasawa, Julie Brind'Amour, Aaron Bogutz, Hiroyuki Sasaki, Matthew Lorincz

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

Julien Richard AlbertDepartment of Medical Genetics, University of British Columbia, Vancouver, Canada.ORCID 0000-0001-9950-9461
Wan Kin Au YeungDivision of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.ORCID 0000-0002-0312-1073
Keisuke ToriyamaDivision of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Hisato KobayashiNODAI Genome Research Center, Tokyo University of Agriculture, Tokyo, Japan.ORCID 0000-0003-3800-4691
Ryutaro HirasawaDivision of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Julie Brind'AmourDepartment of Medical Genetics, University of British Columbia, Vancouver, Canada.ORCID 0000-0002-9522-8571
Aaron BogutzDepartment of Medical Genetics, University of British Columbia, Vancouver, Canada.
Hiroyuki SasakiDivision of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.ORCID 0000-0001-8239-8275
Matthew LorinczDepartment of Medical Genetics, University of British Columbia, Vancouver, Canada. mlorincz@mail.ubc.ca.ORCID 0000-0003-0885-0467
Kyushu University · JPUniversity of British Columbia · CATokyo University of Agriculture · JP

Funding

CIHR PJT-153049
6 · The paper itself

Abstract

De novo DNA methylation (DNAme) during mammalian spermatogenesis yields a densely methylated genome, with the exception of CpG islands (CGIs), which are hypomethylated in sperm. While the paternal genome undergoes widespread DNAme loss before the first S-phase following fertilization, recent mass spectrometry analysis revealed that the zygotic paternal genome is paradoxically also subject to a low level of de novo DNAme. However, the loci involved, and impact on transcription were not addressed. Here, we employ allele-specific analysis of whole-genome bisulphite sequencing data and show that a number of genomic regions, including several dozen CGI promoters, are de novo methylated on the paternal genome by the 2-cell stage. A subset of these promoters maintains DNAme through development to the blastocyst stage. Consistent with paternal DNAme acquisition, many of these loci are hypermethylated in androgenetic blastocysts but hypomethylated in parthenogenetic blastocysts. Paternal DNAme acquisition is lost following maternal deletion of Dnmt3a, with a subset of promoters, which are normally transcribed from the paternal allele in blastocysts, being prematurely transcribed at the 4-cell stage in maternal Dnmt3a knockout embryos. These observations uncover a role for maternal DNMT3A activity in post-fertilization epigenetic reprogramming and transcriptional silencing of the paternal genome.

Indexed as

GenomeMaternal InheritancePaternal InheritanceAllelesAnimalsBlastocystCpG IslandsDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3AEpigenomicsFemaleGene Expression Regulation, DevelopmentalMaleMice, Inbred DBAOocytesDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADnmt3a protein, mouse

Identifiers

PMID33110091
PMCPMC7591512
OpenAlexW3097439951

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.