Retinoids and their receptors in vertebrate embryogenesis
S M Smith1, E D Dickman, S C Power
1Department of Nutritional Sciences, University of Wisconsin-Madison 53706, USA.
Abstract:
Vitamin A and its derivatives, the retinoids, participate in formation of diverse embryonic structures, including face, heart, eye, limb and nervous system. Studies of retinoid-deficient and -treated embryos, and of receptor null mutants, provide evidence that this participation involves interactions between retinoids and their receptors. Targeted retinoid application and retinoid deficiency, using in ovo avian embryos, has identified early cardiogenic contributions, including cardiocyte gene expression and differentiation, heart tube fusion and laterality, and segmental identity. Also useful is a mammalian model, which targets retinoid deficiency to distinct gestational windows, circumventing limitations of traditional deficiency studies and current null mutant technologies. Rat embryos made deficient in retinoids during gestational d 11.5-13.5 exhibit specific cardiac, limb, ocular and nervous system deficits. That many of the anomalies previously reported in retinoid receptor null mutants are observed in deficiency confirms that ligand-receptor interactions are essential for embryonic development. Other defects are novel, reemphasizing the functional redundancy of retinoid receptors and that retinoid receptors have multiple and overlapping contributions to morphogenesis.
Insights
Vitamin A (retinoids) are crucial for embryonic development, influencing the formation of the face, heart, and nervous system. Retinoid signaling through receptors is essential for normal embryonic morphogenesis.
Area of Science:
- Developmental Biology
- Molecular Biology
- Embryology
Background:
- Retinoids, vitamin A derivatives, are vital for embryonic development.
- Their role in forming facial, cardiac, ocular, limb, and nervous systems is established.
- Understanding retinoid-receptor interactions is key to developmental processes.
Purpose of the Study:
- To investigate the essential roles of retinoids in embryonic development.
- To elucidate the specific contributions of retinoid-receptor signaling pathways.
- To identify novel developmental defects associated with retinoid signaling disruption.
Main Methods:
- Utilizing in ovo avian embryos for targeted retinoid application and deficiency studies.
- Employing a mammalian model (rat embryos) with targeted retinoid deficiency during specific gestational windows.
- Analyzing cardiac, limb, ocular, and nervous system development in retinoid-altered embryos.
Main Results:
- Retinoid deficiency during gestational days 11.5-13.5 in rats caused specific cardiac, limb, ocular, and nervous system deficits.
- Avian embryo studies revealed early cardiogenic contributions, including gene expression, differentiation, heart tube fusion, and laterality.
- Observed defects in deficiency models mirrored those in retinoid receptor null mutants, confirming ligand-receptor essentiality.
- Novel defects highlighted functional redundancy and overlapping roles of retinoid receptors in morphogenesis.
Conclusions:
- Ligand-receptor interactions involving retinoids are indispensable for embryonic development.
- Retinoid signaling pathways play critical, multifaceted roles in organogenesis and morphogenesis.
- Functional redundancy among retinoid receptors suggests complex regulatory networks in embryonic development.
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