Evidence map›Paper›PMID 27920088›Full record

ArticleGenes & development2016

SUV4-20 activity in the preimplantation mouse embryo controls timely replication.

André Eid, Diego Rodriguez-Terrones, Adam Burton, Maria-Elena Torres-Padilla

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. The SUV4-20H Histone Methyltransferases in Health and Disease.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Specification of the First Mammalian Cell Lineages In Vivo and In Vitro.Cold Spring Harbor perspectives in biology · 2020
    Review
  16. Article
  17. Review
  18. Article
  19. Review
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

4 authors at 3 institutions in 2 countries.

André EidInstitut de Génétique et de Biologie Moléculaire et Cellulaire, U964, Centre National de la Recherche Scientifique (CNRS)/Institut National de la Santé et de la Recherche Médicale (INSERM), F-67404 Illkirch, CU de Strasbourg, France.
Diego Rodriguez-TerronesInstitute of Epigenetics and Stem Cells, Helmholtz Zentrum München, D-81377 München, Germany.
Adam BurtonInstitut de Génétique et de Biologie Moléculaire et Cellulaire, U964, Centre National de la Recherche Scientifique (CNRS)/Institut National de la Santé et de la Recherche Médicale (INSERM), F-67404 Illkirch, CU de Strasbourg, France.
Maria-Elena Torres-PadillaInstitut de Génétique et de Biologie Moléculaire et Cellulaire, U964, Centre National de la Recherche Scientifique (CNRS)/Institut National de la Santé et de la Recherche Médicale (INSERM), F-67404 Illkirch, CU de Strasbourg, France.
Centre National de la Recherche Scientifique · FRHelmholtz Zentrum München · DEInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extensive chromatin remodeling after fertilization is thought to take place to allow a new developmental program to start. This includes dynamic changes in histone methylation and, in particular, the remodeling of constitutive heterochromatic marks such as histone H4 Lys20 trimethylation (H4K20me3). While the essential function of H4K20me1 in preimplantation mouse embryos is well established, the role of the additional H4K20 methylation states through the action of the SUV4-20 methyltransferases has not been addressed. Here we show that Suv4-20h1/h2 are mostly absent in mouse embryos before implantation, underscoring a rapid decrease of H4K20me3 from the two-cell stage onward. We addressed the functional significance of this remodeling by introducing Suv4-20h1 and Suv4-20h2 in early embryos. Ectopic expression of Suv4-20h2 leads to sustained levels of H4K20me3, developmental arrest, and defects in S-phase progression. The developmental phenotype can be partially overcome through inhibition of the ATR pathway, suggesting that the main function for the remodeling of H4K20me3 after fertilization is to allow the timely and coordinated progression of replication. This is in contrast to the replication program in somatic cells, where H4K20me3 has been shown to promote replication origin licensing, and anticipates a different regulation of replication during this early developmental time window.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsAtaxia Telangiectasia Mutated ProteinsBlastocystEctopic Gene ExpressionEmbryo, MammalianEmbryonic DevelopmentGenomeHistone-Lysine N-MethyltransferaseHistonesMiceMice, Inbred C57BLRNA, MessengerZygoteAtaxia Telangiectasia Mutated ProteinsAtr protein, mouseHistone-Lysine N-MethyltransferaseHistonesRNA, MessengerSuv4-20h protein, mouseheterochromatinmouse embryoreplication stressSuv4-20

Identifiers

PMID27920088
PMCPMC5159666
OpenAlexW2560022374

What OpenQuestion holds

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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.