ArticleNature communications2020
Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas.
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 45 papers.
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.
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.
Who cites it
45 citing papers in PubMed, 88 citations in OpenAlex.
- Epigenetic, environmental, and sex-specific programming of long-term health in Assisted Reproductive Technologies-conceived offspring†.Biology of reproduction · 2026Review
- Dysregulated differentiation kinetics underlie the essential role of DNA damage repair in placental development.Nature communications · 2026Article
- UHRF1 drives hepatocellular carcinoma progression via epigenetic repression of SFMBT2.Scientific reports · 2026Article
- Limitations of serial cloning in mammals.Nature communications · 2026Article
- Overexpression of placenta-specific noncanonical imprinted genes causes placental enlargement in intersubspecific hybrid mice†.Biology of reproduction · 2026Article
- Derivation of embryonic stem cells from cloned blastocysts using improved somatic cell nuclear transfer in common marmosets.Stem cell reports · 2025Article
- mTORC1-dependent suppression of autophagic activity in somatic cell nuclear transfer mouse embryos.Reproduction (Cambridge, England) · 2025Article
- Efficient Somatic Cell Nuclear Transfer by Overcoming Both Pre- and Post-Implantation Epigenetic Barriers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Setd2 overexpression rescues bivalent gene expression during SCNT-mediated ZGA.Protein & cell · 2025Article
- Loss-of-function mutation of NSD2 is associated with abnormal placentation accompanied by fetal growth retardation in mice.PloS one · 2025Article
- Creation of true interspecies hybrids: Rescue of hybrid class with hybrid cytoplasm affecting growth and metabolism.Science advances · 2024Article
- Article
- Article
- Distinct properties of putative trophoblast stem cells established from somatic cell nuclear-transferred pig blastocysts.Biological research · 2024Article
- Deciphering the Epigenetic Landscape: Placental Development and Its Role in Pregnancy Outcomes.Stem cell reviews and reports · 2024Review
- Incomplete activation ofLife science alliance · 2023Article
- Inhibition of Wnt activity improves peri-implantation development of somatic cell nuclear transfer embryos.National science review · 2023Article
- UTX deletion promotes M2 macrophage polarization by epigenetically regulating endothelial cell-macrophage crosstalk after spinal cord injury.Journal of nanobiotechnology · 2023Article
- Mouse somatic cell nuclear transfer: What has changed and remained unchanged in 25 years.The Journal of reproduction and development · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic cell nuclear transfer (SCNT) in mammals is an inefficient process that is frequently associated with abnormal phenotypes, especially in placentas. Recent studies demonstrated that mouse SCNT placentas completely lack histone methylation (H3K27me3)-dependent imprinting, but how it affects placental development remains unclear. Here, we provide evidence that the loss of H3K27me3 imprinting is responsible for abnormal placental enlargement and low birth rates following SCNT, through upregulation of imprinted miRNAs. When we restore the normal paternal expression of H3K27me3-dependent imprinted genes (Sfmbt2, Gab1, and Slc38a4) in SCNT placentas by maternal knockout, the placentas remain enlarged. Intriguingly, correcting the expression of clustered miRNAs within the Sfmbt2 gene ameliorates the placental phenotype. Importantly, their target genes, which are confirmed to cause SCNT-like placental histology, recover their expression level. The birth rates increase about twofold. Thus, we identify loss of H3K27me3 imprinting as an epigenetic error that compromises embryo development following SCNT.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.