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Updated: Apr 28, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
Published on: February 28, 2017
Notchless is required for axial skeleton formation in mice
Sarah Beck-Cormier1, Marie Escande2, Céline Souilhol2
1Mouse Functional Genetics, Department of Developmental & Stem Cell Biology, Institut Pasteur, Paris, France; Centre National de la Recherche Scientifique, URA 2578, Institut Pasteur, Paris, France.
Notchless homolog 1 (Nle1) is crucial for embryonic development. Deleting Nle1 in epiblast cells causes severe defects and lethality, highlighting its role in organogenesis and axial skeletal formation.
Area of Science:
- Developmental Biology
- Genetics
- Cell Biology
Background:
- Cell survival is vital for embryonic development.
- Notchless homolog 1 (Drosophila) (Nle1) is important for inner cell mass survival post-implantation in mice.
Purpose of the Study:
- To investigate the function of Nle1 in mouse epiblast cells after implantation.
- To analyze the effects of mosaic Nle1 deletion during organogenesis using a Cre-lox system.
Main Methods:
- Utilized the Meox2(tm1(cre)Sor) mouse model for epiblast-specific Cre recombinase expression.
- Induced mosaic deletion of Nle1 in developing embryos.
- Examined developmental anomalies and cell death in mutant embryos.
Main Results:
- Nle1-deficient epiblast cells were rapidly eliminated, confirming Nle1's requirement for cell survival.
- Mosaic Nle1 deletion led to severe developmental abnormalities and lethality at birth.
- Mutant embryos exhibited defects in axial skeletal formation, linked to increased apoptotic cell death in somites.
Conclusions:
- Nle1 plays an essential role in post-implantation epiblast cell survival.
- Nle1 is critical for proper organogenesis, particularly axial skeletal development.
- Loss of Nle1 function results in increased apoptosis during embryonic development.
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