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Placental defects revealed by modelling PWS in mice
Anna E Webberley1, Raquel Boque-Sastre2, Lauren Bailey1
1Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK.
Disease Models & Mechanisms
|July 7, 2026
Summary
Prader-Willi syndrome (PWS) may involve placental dysfunction. PWS gene loss in mice reduced placental cells, suggesting compromised nutrient transfer impacting fetal development.
Area of Science:
- Genetics
- Developmental Biology
- Reproductive Biology
Background:
- Prader-Willi syndrome (PWS) is a neurodevelopmental disorder caused by the loss of paternally expressed genes on chromosome 15q11-q13.
- Abnormal feeding behaviors in PWS may originate from in utero programming via placental dysfunction.
Purpose of the Study:
- To investigate the expression of PWS genes in the mouse placenta.
- To determine the impact of PWS gene deletion on placental development and function in a mouse model.
Main Methods:
- Analysis of PWS gene expression in mouse placenta.
- Utilizing a novel PWS deletion mouse model (Large+/-).
- Quantification of Kdr-positive fetal endothelial cells in the placental labyrinth zone.
Main Results:
- Several PWS genes, including Magel2, Necdin, and Sngh14, are expressed in mouse placental fetal endothelial cells.
- The Large+/- PWS mouse model exhibited reduced placental PWS gene expression and a ~25% decrease in Kdr-positive cells.
- No significant reduction in late-gestation fetal growth was observed despite placental alterations.
Conclusions:
- PWS gene expression is present in the mouse placenta, specifically in cells crucial for nutrient transport.
- PWS gene deletion in mice leads to placental abnormalities, including reduced fetal endothelial cell populations.
- These findings suggest potential placental dysfunction and compromised nutrient transfer in PWS, possibly contributing to postnatal phenotypes.
