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Vitamin A-deficient quail embryos have half a hindbrain and other neural defects
M Maden1, E Gale, I Kostetskii
1Developmental Biology Research Centre, King's College, London, UK. udbl124@uk.ac.kcl.cc.bay
Background:
Retinoic acid (RA) is a morphogenetically active signalling molecule thought to be involved in the development of severely embryonic systems (based on its effect when applied in excess and the fact that it can be detected endogenously in embryos). Here, we adopt a novel approach and use the vitamin A-deficient (A-) quail embryo to ask what defects these embryos show when they develop in the absence of RA, with particular reference to the nervous system.
Results:
We have examined the anatomy, the expression domains of a variety of genes and the immunoreactivity to several antibodies in these A- embryos. In addition to the previously documented cardiovascular abnormalities, we find that the somites are smaller in A- embryos, otic vesicle development is abnormal and the somites continue up to and underneath the otic vesicle. In the central nervous system, we find that neural crest cells need RA for normal development and survival, and the neural tube fails to extend any neurites into the periphery. Using general hindbrain morphology and the expression patterns of Hoxa-2, Hoxb-1, Hoxb-4, Krox-20 and FGF-3 as markers, we conclude that segmentation in the myelencephalon (rhombomeres 4-8) is disrupted. In contrast, the dorsoventral axis of the neural tube using Shh, islet-1 and Pax-3 as markers is normal.
Conclusions:
These results demonstrate at least three roles for RA in central nervous system development: neural crest survival, neurite outgrowth and hindbrain patterning.
Insights
Vitamin A deficiency in quail embryos disrupts nervous system development, impacting neural crest cell survival, neurite outgrowth, and hindbrain patterning. These findings highlight crucial roles for retinoic acid in embryonic development.
Area of Science:
- Developmental Biology
- Neuroscience
- Embryology
Background:
- Retinoic acid (RA) is a signaling molecule crucial for embryonic development.
- Previous studies suggested RA's role based on excess application and endogenous detection.
- The function of endogenous RA in normal development remained unclear.
Purpose of the Study:
- To investigate the developmental defects in vitamin A-deficient (A-) quail embryos, focusing on the nervous system.
- To elucidate the specific roles of endogenous retinoic acid in embryonic development.
Main Methods:
- Analysis of anatomy, gene expression, and antibody immunoreactivity in A- quail embryos.
- Examination of central nervous system development, including neural crest cells and hindbrain morphology.
- Utilized molecular markers (Hoxa-2, Hoxb-1, Hoxb-4, Krox-20, FGF-3, Shh, islet-1, Pax-3) to assess neural development.
Main Results:
- A- embryos exhibit smaller somites, abnormal otic vesicle development, and cardiovascular abnormalities.
- Neural crest cell development and survival are impaired in the absence of RA.
- Hindbrain segmentation (myelencephalon) is disrupted, while the neural tube's dorsoventral axis remains normal.
- Neurite outgrowth from the neural tube into the periphery is abolished.
Conclusions:
- Retinoic acid is essential for neural crest cell survival during embryonic development.
- RA plays a critical role in promoting neurite outgrowth.
- RA is indispensable for proper hindbrain patterning in the developing central nervous system.