Evidence map›Paper›PMID 25394724›Full record

ArticleNature communications2014

The role of maternal-specific H3K9me3 modification in establishing imprinted X-chromosome inactivation and embryogenesis in mice.

Atsushi Fukuda, Junko Tomikawa, Takumi Miura, Kenichiro Hata, Kazuhiko Nakabayashi, Kevin Eggan, Hidenori Akutsu, Akihiro Umezawa

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Paternal impact on the developmental programming of sexual dimorphism.Frontiers in cell and developmental biology · 2024
    Review
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  12. Review
  13. Article
  14. Role of lncRNAs in aging and age-related diseases.Aging medicine (Milton (N.S.W)) · 2018
    Review
  15. Article
  16. Article
  17. What makes the maternal X chromosome resistant to undergoing imprinted X inactivation?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  18. Genomic imprinting ofGenes & development · 2017
    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

8 authors at 1 institution in 1 country.

Atsushi FukudaDepartment of Reproductive Biology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Junko TomikawaDepartment of Maternal-Foetal Biology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Takumi MiuraDepartment of Reproductive Biology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Kenichiro HataDepartment of Maternal-Foetal Biology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Kazuhiko NakabayashiDepartment of Maternal-Foetal Biology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Kevin EgganThe Howard Hughes Medical Institute, Harvard Stem Cell Institute and the Department of Stem Cell and Regenerative Biology, Harvard University, 7 Divinity Avenue, Cambridge, Massachusetts 02138, USA.
Hidenori AkutsuDepartment of Reproductive Biology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Akihiro UmezawaDepartment of Reproductive Biology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
National Center For Child Health and Development · JP

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Maintaining a single active X-chromosome by repressing Xist is crucial for embryonic development in mice. Although the Xist activator RNF12/RLIM is present as a maternal factor, maternal Xist (Xm-Xist) is repressed during preimplantation phases to establish imprinted X-chromosome inactivation (XCI). Here we show, using a highly reproducible chromatin immunoprecipitation method that facilitates chromatin analysis of preimplantation embryos, that H3K9me3 is enriched at the Xist promoter region, preventing Xm-Xist activation by RNF12. The high levels of H3K9me3 at the Xist promoter region are lost in embryonic stem (ES) cells, and ES-cloned embryos show RNF12-dependent Xist expression. Moreover, lack of Xm-XCI in the trophectoderm, rather than loss of paternally expressed imprinted genes, is the primary cause of embryonic lethality in 70-80% of parthenogenotes immediately after implantation. This study reveals that H3K9me3 is involved in the imprinting that silences Xm-Xist. Our findings highlight the role of maternal-specific H3K9me3 modification in embryo development.

Indexed as

AnimalsBlastocystChromatinEmbryonic DevelopmentFemaleHistone DemethylasesJumonji Domain-Containing Histone DemethylasesMaleMicePromoter Regions, GeneticRNA, Long NoncodingUbiquitin-Protein LigasesX Chromosome InactivationChromatinHistone DemethylasesJumonji Domain-Containing Histone DemethylasesKdm3a protein, mouseKdm4b protein, mouseRlim protein, mouseRNA, Long NoncodingUbiquitin-Protein LigasesXIST non-coding RNA

Identifiers

PMID25394724
PMCPMC4243243
OpenAlexW2136355242

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.