Retinoic acid synthesis and hindbrain patterning in the mouse embryo
K Niederreither1, J Vermot, B Schuhbaur
1Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP/Collège de France, CU de Strasbourg.
Development (Cambridge, England)
|February 2, 2000
Summary
Embryonic retinoic acid (RA) deficiency disrupts hindbrain development in mice. Lack of RA impairs posterior cell fate generation, leading to abnormal hindbrain development and neural crest cell migration.
Area of Science:
- Developmental biology
- Genetics
- Neuroscience
Background:
- Retinoic acid (RA) is crucial for embryonic development.
- Targeted disruption of the Raldh2 gene eliminates embryonic RA synthesis.
- Raldh2 knockout mice exhibit midgestational lethality.
Purpose of the Study:
- To investigate the effects of RA deficiency on hindbrain and neural crest development.
- To understand the role of embryonic RA in establishing posterior hindbrain cell fates.
Main Methods:
- Analysis of Raldh2-/- mouse embryos.
- Gene expression analysis (Krox20, Meis2, Hoxb1, Wnt8A, kreisler, Eph receptors).
- Assessment of apoptosis and neural crest cell migration.
Main Results:
- Impaired hindbrain segmentation and caudal reduction in Raldh2-/- embryos.
- Abnormal expression of hindbrain patterning genes (Krox20, Meis2, Hoxb1, Wnt8A, kreisler).
- Increased apoptosis and altered neural crest migration impacting branchial arch development.
Conclusions:
- Embryonic RA is essential for posterior hindbrain cell fate determination.
- RA deficiency results in an abnormal r3 and r4 identity in the caudal hindbrain.
- RA is critical for normal hindbrain and neural crest development.
