ArticleDevelopmental biology2016
Increased dosage of the imprinted Ascl2 gene restrains two key endocrine lineages of the mouse Placenta.
Article in Developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 61 citations in OpenAlex.
- Transcriptomic Analysis ofInternational journal of molecular sciences · 2026Article
- Transcriptomic Analysis ofbioRxiv : the preprint server for biology · 2026Article
- Placental dysfunction reflects endocrine impairment and trophoblast alterations in polycystic ovarian syndrome.Scientific reports · 2026Article
- Maternal α-cypermethrin and permethrin exert differential effects on fetal growth, placental morphology, and fetal neurodevelopment in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Sex differences in placental structure and gene expression in ICR mice during embryonic development.Scientific reports · 2025Article
- Loss-of-function mutation of NSD2 is associated with abnormal placentation accompanied by fetal growth retardation in mice.PloS one · 2025Article
- United by conflict: Convergent signatures of parental conflict in angiosperms and placental mammals.The Journal of heredity · 2024Review
- Article
- Imprinted genes and the manipulation of parenting in mammals.Nature reviews. Genetics · 2023Review
- Regulation of sexually dimorphic placental adaptation in LPS exposure-induced intrauterine growth restriction.Molecular medicine (Cambridge, Mass.) · 2023Article
- Preconception paternal alcohol exposure decreases IVF embryo survival and pregnancy success rates in a mouse model.Molecular human reproduction · 2023Article
- Characterization of placental endocrine function and fetal brain development in a mouse model of small for gestational age.Frontiers in endocrinology · 2023Article
- In support of the placental programming hypothesis: Placental endocrine insufficiency programs atypical behaviour in mothers and their offspring.Experimental physiology · 2022Review
- Paternal alcohol exposures program intergenerational hormetic effects on offspring fetoplacental growth.Frontiers in cell and developmental biology · 2022Article
- Prenatal health behaviours as predictors of human placental lactogen levels.Frontiers in endocrinology · 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
- 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
- ASCL2 reciprocally controls key trophoblast lineage decisions during hemochorial placenta development.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Placental imprinting: Emerging mechanisms and functions.PLoS genetics · 2020Review
- Placental effects on the maternal brain revealed by disrupted placental gene expression in mouse hybrids.Proceedings. Biological sciences · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Imprinted genes are expressed primarily from one parental allele by virtue of a germ line epigenetic process. Achaete-scute complex homolog 2 (Ascl2 aka Mash2) is a maternally expressed imprinted gene that plays a key role in placental and intestinal development. Loss-of-function of Ascl2 results in an expansion of the parietal trophoblast giant cell (P-TGC) lineage, an almost complete loss of Trophoblast specific protein alpha (Tpbpa) positive cells in the ectoplacental cone and embryonic failure by E10.5. Tpbpa expression marks the progenitors of some P-TGCs, two additional trophoblast giant cell lineages (spiral artery and canal), the spongiotrophoblast and the glycogen cell lineage. Using a transgenic model, here we show that elevated expression of Ascl2 reduced the number of P-TGC cells by 40%. Elevated Ascl2 also resulted in a marked loss of the spongiotrophoblast and a substantial mislocalisation of glycogen cells into the labyrinth. In addition, Ascl2-Tg placenta contained considerably more placental glycogen than wild type. Glycogen cells are normally located within the junctional zone in close contact with spongiotrophoblast cells, before migrating through the P-TGC layer into the maternal decidua late in gestation where their stores of glycogen are released. The failure of glycogen cells to release their stores of glycogen may explain both the inappropriate accumulation of glycogen and fetal growth restriction observed late in gestation in this model. In addition, using in a genetic cross we provide evidence that Ascl2 requires the activity of a second maternally expressed imprinted gene, Pleckstrin homology-like domain, family a, member 2 (Phlda2) to limit the expansion of the spongiotrophoblast. This "belts and braces" approach demonstrates the importance of genomic imprinting in regulating the size of the placental endocrine compartment for optimal placental development and fetal growth.
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