ArticleDisease models & mechanisms2011
Fetal overgrowth in the Cdkn1c mouse model of Beckwith-Wiedemann syndrome.
Article in Disease models & mechanisms, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Translational toxicoepigenetic Meta-Analyses identify homologous gene DNA methylation reprogramming following developmental phthalate and lead exposure in mouse and human offspring.Environment international · 2024Pooled it
- Single-cell transcriptome analysis reveals abnormal angiogenesis and placentation by loss of imprinted glutaminyl-peptide cyclotransferase.Journal of Zhejiang University. Science. B · 2025Article
- Mom genes and dad genes: genomic imprinting in the regulation of social behaviors.Epigenomics · 2025Review
- Protein restriction during pregnancy alters Cdkn1c silencing, dopamine circuitry and offspring behaviour without changing expression of key neuronal marker genes.Scientific reports · 2024Article
- Dynamic methylation pattern of H19DMR and KvDMR1 in bovine oocytes and preimplantation embryos.Journal of assisted reproduction and genetics · 2024Article
- Imprinted genes and the manipulation of parenting in mammals.Nature reviews. Genetics · 2023Review
- Drug-induced loss of imprinting revealed using bioluminescent reporters of Cdkn1c.Scientific reports · 2023Article
- Single-nuclei RNA sequencing (snRNA-seq) uncovers trophoblast cell types and lineages in the mature bovine placenta.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Assessing the influence of distinct culture media on human pre-implantation development using single-embryo transcriptomics.Frontiers in cell and developmental biology · 2023Article
- In support of the placental programming hypothesis: Placental endocrine insufficiency programs atypical behaviour in mothers and their offspring.Experimental physiology · 2022Review
- The X-linked splicing regulator MBNL3 has been co-opted to restrict placental growth in eutherians.PLoS biology · 2022Article
- Loss of imprinting of the Igf2-H19 ICR1 enhances placental endocrine capacity via sex-specific alterations in signalling pathways in the mouse.Development (Cambridge, England) · 2022Article
- Differentially expressed tRNA-derived fragments in bovine fetuses with assisted reproduction induced congenital overgrowth syndrome.Frontiers in genetics · 2022Article
- Maternal background alters the penetrance of growth phenotypes and sex-specific placental adaptation of offspring sired by alcohol-exposed males.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Derivation and investigation of the first human cell-based model of Beckwith-Wiedemann syndrome.Epigenetics · 2021Article
- Mapping cis-regulatory elements in the midgestation mouse placenta.Scientific reports · 2021Article
- Epigenetic Mechanisms of ART-Related Imprinting Disorders: Lessons From iPSC and Mouse Models.Genes · 2021Review
- Male Factors: the Role of Sperm in Preimplantation Embryo Quality.Reproductive sciences (Thousand Oaks, Calif.) · 2021Review
- Prenatal correction of IGF2 to rescue the growth phenotypes in mouse models of Beckwith-Wiedemann and Silver-Russell syndromes.Cell reports · 2021Article
- The Role of Long Non-coding RNAs in Human Imprinting Disorders: Prospective Therapeutic Targets.Frontiers in cell and developmental biology · 2021Review
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3 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the imprinted CDKN1C gene are associated with the childhood developmental disorder Beckwith-Wiedemann syndrome (BWS). Multiple mouse models with deficiency of Cdkn1c recapitulate some aspects of BWS but do not exhibit overgrowth of the newborn, a cardinal feature of patients with BWS. In this study, we found that Cdkn1c mutants attained a 20% increase in weight during gestation but experienced a rapid reversal of this positive growth trajectory very late in gestation. We observed a marked effect on placental development concurrently with this loss of growth potential, with the appearance of large thrombotic lesions in the labyrinth zone. The trilaminar trophoblast layer that separates the maternal blood sinusoids from fetal capillaries was disordered with a loss of sinusoidal giant cells, suggesting a role for Cdkn1c in maintaining the integrity of the maternal-fetal interface. Furthermore, the overgrowth of mutant pups decreased in the face of increasing intrauterine competition, identifying a role for Cdkn1c in the allocation of the maternal resources via the placenta. This work explains one difficulty in precisely replicating BWS in this animal model: the differences in reproductive strategies between the multiparous mouse, in which intrauterine competition is high, and humans, in which singleton pregnancies are more common.
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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.