Evidence map›Paper›PMID 31831741›Full record

ArticleNature communications2019

Evolution of imprinting via lineage-specific insertion of retroviral promoters.

Aaron B Bogutz, Julie Brind'Amour, Hisato Kobayashi, Kristoffer N Jensen, Kazuhiko Nakabayashi, Hiroo Imai, Matthew C Lorincz, Louis Lefebvre

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  18. Roles of retrovirus-derivedFrontiers in cell and developmental biology · 2023
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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

8 authors at 4 institutions in 2 countries.

Aaron B BogutzDepartment of Medical Genetics, Molecular Epigenetics Group, Life Sciences Institute, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada.
Julie Brind'AmourDepartment of Medical Genetics, Molecular Epigenetics Group, Life Sciences Institute, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada.ORCID http://orcid.org/0000-0002-9522-8571
Hisato KobayashiDepartment of Embryology, Nara Medical University, Kashihara, Nara, 634-8521, Japan.ORCID http://orcid.org/0000-0003-3800-4691
Kristoffer N JensenDepartment of Medical Genetics, Molecular Epigenetics Group, Life Sciences Institute, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada.
Kazuhiko NakabayashiDivision of Developmental Genomics, Research Institute, National Center for Child Health and Development, Setagaya, Tokyo, 157-8535, Japan.
Hiroo ImaiMolecular Biology Section, Department of Cellular and Molecular Biology, Primate Research Institute, Kyoto University, Inuyama, Aichi, 484-8506, Japan.
Matthew C LorinczDepartment of Medical Genetics, Molecular Epigenetics Group, Life Sciences Institute, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada. matthew.lorincz@ubc.ca.ORCID http://orcid.org/0000-0003-0885-0467
Louis LefebvreDepartment of Medical Genetics, Molecular Epigenetics Group, Life Sciences Institute, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada. louis.lefebvre@ubc.ca.ORCID http://orcid.org/0000-0001-5664-9480
University of British Columbia · CAKyoto University · JPNara Medical University · JPNational Center For Child Health and Development · JP

Funding

CIHR MOP-119357
6 · The paper itself

Abstract

Imprinted genes are expressed from a single parental allele, with the other allele often silenced by DNA methylation (DNAme) established in the germline. While species-specific imprinted orthologues have been documented, the molecular mechanisms underlying the evolutionary switch from biallelic to imprinted expression are unknown. During mouse oogenesis, gametic differentially methylated regions (gDMRs) acquire DNAme in a transcription-guided manner. Here we show that oocyte transcription initiating in lineage-specific endogenous retroviruses (ERVs) is likely responsible for DNAme establishment at 4/6 mouse-specific and 17/110 human-specific imprinted gDMRs. The latter are divided into Catarrhini- or Hominoidea-specific gDMRs embedded within transcripts initiating in ERVs specific to these primate lineages. Strikingly, imprinting of the maternally methylated genes Impact and Slc38a4 was lost in the offspring of female mice harboring deletions of the relevant murine-specific ERVs upstream of these genes. Our work reveals an evolutionary mechanism whereby maternally silenced genes arise from biallelically expressed progenitors.

Indexed as

DNA MethylationEvolution, MolecularGenomic ImprintingAnimalsEpigenomicsFemaleGerm CellsHaplorhiniHumansMacacaMaleMiceOocytesPan troglodytesPrimatesPromoter Regions, Genetic

Identifiers

PMID31831741
PMCPMC6908575
OpenAlexW2994862706

What OpenQuestion holds

Textmetadata
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.