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Mouse In Vivo Placental Targeted CRISPR Manipulation
Published on: April 14, 2023
R-spondin3 is required for mouse placental development
Motoko Aoki1, Michihiro Mieda, Toshio Ikeda
1Laboratory for Developmental Gene Regulation, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako, Saitama, Japan.
Developmental Biology
|September 12, 2006
Summary
Mouse R-spondin3 (Rspo3) is crucial for placental development. Mutant mice lacking Rspo3 exhibited embryonic lethality due to impaired labyrinth formation and reduced fetal blood vessel penetration, highlighting Rspo3
Area of Science:
- Developmental Biology
- Genetics
- Reproductive Biology
Background:
- R-spondin3 (Rspo3) is a member of the R-spondin protein family, known for its role in Wnt/beta-catenin signaling.
- Rspo3's specific function in embryonic development, particularly in placental formation, remains incompletely understood.
Purpose of the Study:
- To investigate the role of Rspo3 in mouse embryonic development and placental labyrinthine layer formation.
- To elucidate the molecular mechanisms underlying Rspo3's function in placental vascularization and development.
Main Methods:
- Generation of mice with a targeted mutation in the Rspo3 gene using a lacZ reporter.
- Analysis of homozygous Rspo3 mutant embryos for developmental defects, focusing on placental morphology and gene expression.
- Histological examination of placental tissue to assess vascularization and cellular composition.
Main Results:
- Homozygous Rspo3 mutant mice displayed embryonic lethality around embryonic day 10, primarily due to defective labyrinthine layer formation.
- Mutant placentas showed impaired fetal blood vessel penetration into the chorion.
- Expression of Glial cells missing-1 (Gcm1) was significantly reduced in chorionic trophoblast cells of mutant placentas.
Conclusions:
- Rspo3 plays a critical role in the development of the placental labyrinthine layer.
- Rspo3 is essential for the interaction between the chorion and allantois, facilitating proper vascular development.
- The findings suggest Rspo3 is vital for maintaining Gcm1 expression, which is critical for placental function.

