ArticleCell reports2022
Loss of Slc38a4 imprinting is a major cause of mouse placenta hyperplasia in somatic cell nuclear transferred embryos at late gestation.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Dysregulated differentiation kinetics underlie the essential role of DNA damage repair in placental development.Nature communications · 2026Article
- Metabolic imprinting in trophoblast barrier dysfunction: the role of glucolipotoxicity, endoplasmic reticulum stress, and amino acid transport imbalance.Journal of assisted reproduction and genetics · 2026Review
- Overexpression of placenta-specific noncanonical imprinted genes causes placental enlargement in intersubspecific hybrid mice†.Biology of reproduction · 2026Article
- Folic acid ameliorates placental structure and function in fetal growth restriction via epigenetic modifications.Clinical epigenetics · 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
- Emerging Insights into the Relationship Between Amino Acid Metabolism and Diabetic Cardiomyopathy.Biomolecules · 2025Review
- Non-disruptive 3D profiling of combinations of epigenetic marks in single cells.bioRxiv : the preprint server for biology · 2025Article
- Generation of live mice from haploid ESCs with germline-DMR deletions or switch.Cell discovery · 2025Article
- Determining expression changes of ANO7 and SLC38A4 membrane transporters in colorectal cancer.Heliyon · 2024Article
- Safety of embryo cryopreservation: insights from mid-term placental transcriptional changes.Reproductive biology and endocrinology : RB&E · 2024Article
- Article
- Roles of endogenous retroviral elements in the establishment and maintenance of imprinted gene expression.Frontiers in cell and developmental biology · 2024Review
- Deciphering the placental abnormalities associated with somatic cell nuclear transfer at single-nucleus resolution.Protein & cell · 2023Article
- Inhibition of Wnt activity improves peri-implantation development of somatic cell nuclear transfer embryos.National science review · 2023Article
- Mouse somatic cell nuclear transfer: What has changed and remained unchanged in 25 years.The Journal of reproduction and development · 2023Article
- Farrerol directly activates the deubiqutinase UCHL3 to promote DNA repair and reprogramming when mediated by somatic cell nuclear transfer.Nature communications · 2023Article
- Cloning by SCNT: Integrating Technical and Biology-Driven Advances.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Transient Polycomb activity represses developmental genes in growing oocytes.Clinical epigenetics · 2022Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Placenta hyperplasia is commonly observed in cloned animals and is believed to impede the proper development of cloned embryos. However, the mechanism underlying this phenomenon is largely unknown. Here, we show that placenta hyperplasia of cloned mouse embryos occurs in both middle and late gestation. Interestingly, restoring paternal-specific expression of an amino acid transporter Slc38a4, which loses maternal H3K27me3-dependent imprinting and becomes biallelically expressed in cloned placentae, rescues the overgrowth of cloned placentae at late gestation. Molecular analyses reveal that loss of Slc38a4 imprinting leads to over-activation of the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway in cloned placentae, which is likely due to the increased amino acids transport by SLC38A4. Collectively, our study not only reveals loss of Slc38a4 imprinting is responsible for overgrowth of cloned placentae at late gestation but also suggests the underlying mechanism involves increased amino acid transport and over-activation of mTORC1.
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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.