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1.
Mol Cell Neurosci ; 46(2): 452-9, 2011 Feb.
Article in English | MEDLINE | ID: mdl-21112397

ABSTRACT

The generation of the sensory ganglia involves the migration of a precursor population to the site of ganglion formation and the differentiation of sensory neurons. There is, however, a significant difference between the ganglia of the head and trunk in that while all of the sensory neurons of the trunk are derived from the neural crest, the majority of cranial sensory neurons are generated by the neurogenic placodes. In this study, we have detailed the route through which the placodally-derived sensory neurons are generated, and we find a number of important differences between the head and trunk. Although, the neurogenic placodes release neuroblasts that migrate internally to the site of ganglion formation, we find that there are no placodally-derived progenitor cells within the forming ganglia. The cells released by the placodes differentiate during migration and contribute to the cranial ganglia as post-mitotic neurons. In the trunk, it has been shown that progenitor cells persist in the forming Dorsal Root Ganglia and that much of the process of sensory neuronal differentiation occurs within the ganglion. We also find that the period over which neuronal cells delaminate from the placodes is significantly longer than the time frame over which neural crest cells populate the DRGs. We further show that placodal sensory neuronal differentiation can occur in the absence of local cues. Finally, we find that, in contrast to neural crest cells, the different mature neurogenic placodes seem to lack plasticity. Nodose neuroblasts cannot be diverted to form trigeminal neurons and vice versa.


Subject(s)
Ganglia/embryology , Head/embryology , Head/innervation , Neural Stem Cells/cytology , Neurogenesis/physiology , Sensory Receptor Cells/cytology , Animals , Cell Differentiation/physiology , Cell Movement/physiology , Chick Embryo , Ectoderm/cytology , Electroporation , Ganglia/cytology , Immunohistochemistry , Oligonucleotide Array Sequence Analysis
2.
Dev Dyn ; 239(2): 439-45, 2010 Feb.
Article in English | MEDLINE | ID: mdl-20014097

ABSTRACT

The superior and jugular ganglia (S/JG) are the proximal ganglia of the IXth and Xth cranial nerves and the sensory neurons of these ganglia are neural crest derived. However, it has been unclear the extent to which their differentiation resembles that of the Dorsal Root Ganglia (DRGs). In the DRGs, neural crest cells undergo neuronal differentiation just after the onset of migration and there is evidence suggesting that these cells are pre-specified towards a sensory fate. We have analysed sensory neuronal differentiation in the S/JG. We show, in keeping with previous studies, that neuronal differentiation initiates long after the cessation of neural crest migration. We also find no evidence for the existence of migratory neural crest cells pre-specified towards a sensory phenotype prior to ganglion formation. Rather our results suggest that sensory neuronal differentiation in the S/JG is the result of localised spatiotemporal cues.


Subject(s)
Cell Differentiation , Embryonic Development , Ganglia/cytology , Neural Crest/physiology , Sensory Receptor Cells/cytology , Animals , Cell Movement , Chick Embryo , Forkhead Transcription Factors/metabolism , Glossopharyngeal Nerve/embryology , Neural Crest/cytology , SOXE Transcription Factors/metabolism , Sensory Receptor Cells/metabolism , Vagus Nerve/embryology
3.
Dev Dyn ; 237(3): 592-601, 2008 Mar.
Article in English | MEDLINE | ID: mdl-18224711

ABSTRACT

In the head, neural crest cells generate ectomesenchymal derivatives: cartilage, bone, and connective tissue. Indeed, these cells generate much of the cranial skeleton. There have, however, been few studies of how this lineage is established. Here, we show that neural crest cells stop expressing early neural crest markers upon entering the pharyngeal arches and switch to become ectomesenchymal. By contrast, those neural crest cells that do not enter the arches persist in their expression of early neural crest markers. We further show that fibroblast growth factor (FGF) signaling is involved in directing neural crest cells to become ectomesenchymal. If neural crest cells are rendered insensitive to FGFs, they persist in their expression of early neural crest markers, even after entering the pharyngeal arches. However, our results further suggest that, although FGF signaling is required for the realization of the ectomesenchymal lineages, other cues from the pharyngeal epithelia are also likely to be involved.


Subject(s)
Branchial Region/embryology , Embryonic Development , Fibroblast Growth Factors/metabolism , Mesoderm/physiology , Neural Crest/embryology , Animals , Antigens, Surface/metabolism , Branchial Region/cytology , Chick Embryo , Embryo, Nonmammalian , Gene Expression Regulation, Developmental , Neural Crest/cytology , Signal Transduction , Zebrafish/embryology
4.
Development ; 134(23): 4141-5, 2007 Dec.
Article in English | MEDLINE | ID: mdl-17959723

ABSTRACT

Neurogenic placodes are specialized regions of embryonic ectoderm that generate the majority of the neurons of the cranial sensory ganglia. Here we examine in chick the mechanism underlying the delamination of cells from the epibranchial placodal ectoderm. We show that the placodal epithelium has a distinctive morphology, reflecting a change in cell shape, and is associated with a breach in the underlying basal lamina. Placodal cell delamination is distinct from neural crest cell delamination. In particular, exit of neuroblasts from the epithelium is not associated with the expression of Snail/Snail2 or of the Rho family GTPases required for the epithelial-to-mesenchymal transition seen in neural crest cell delamination. Indeed, cells leaving the placodes do not assume a mesenchymal morphology but migrate from the epithelium as neuronal cells. We further show that the placodal epithelium has a pseudostratified appearance. Examination of proliferation shows that the placodal epithelium is mitotically quiescent, with few phosphohistone H3-positive cells being identified. Where division does occur within the epithelium it is restricted to the apical surface. The neurogenic placodes thus represent specialized ectodermal niches that generate neuroblasts over a protracted period.


Subject(s)
Epithelial Cells/cytology , Ganglia, Sensory/embryology , Mesoderm/cytology , Nervous System/cytology , Nervous System/embryology , Neurons/physiology , Ovum/physiology , Animals , Cell Differentiation , Chick Embryo/ultrastructure , DNA-Binding Proteins/genetics , Ectoderm/cytology , Electroporation , Epithelial Cells/physiology , Female , Gene Expression Regulation, Developmental , Genes, Reporter , In Situ Hybridization , Mesoderm/ultrastructure , Microscopy, Electron , Neurons/cytology , Neurons/ultrastructure , Snail Family Transcription Factors , Transcription Factors/genetics , rhoB GTP-Binding Protein/genetics
5.
Int J Dev Biol ; 51(3): 191-200, 2007.
Article in English | MEDLINE | ID: mdl-17486539

ABSTRACT

We have investigated the role of retinoic acid (RA) in eye development using the vitamin A deficient quail model system, which overcomes problems of retinoic acid synthesising enzyme redundancy in the embryo. In the absence of retinoic acid, the ventral optic stalk and ventral retina are missing, whereas the dorsal optic stalk and dorsal retina develop appropriately. Other ocular abnormalities observed were a thinner retina and the lack of differentiation of the lens. In an attempt to explain this, we studied the expression of various dorsally and ventrally expressed genes such as Pax2, Pax6, Tbx6, Vax2, Raldh1 and Raldh3 and noted that they were unchanged in their expression patterns. In contrast, the RA catabolising enzymes Cyp26A1 and Cyp26B1 which are known to be RA-responsive were not expressed at all in the developing eye. At much earlier stages, the expression domain of Shh in the prechordal plate was reduced, as was Nkx2.1 and we suggest a model whereby the eye field is specified according to the concentration of SHH protein that is present. We also describe another organ, Rathke's pouch which fails to develop in the absence of retinoic acid. We attribute this to the down-regulation of Bmp2, Shh and Fgf8 which are known to be involved in the induction of this structure.


Subject(s)
Coturnix/embryology , Coturnix/physiology , Embryonic Structures/embryology , Eye/embryology , Tretinoin/physiology , Animals , Coturnix/genetics , Embryo, Nonmammalian , Embryonic Structures/cytology , Embryonic Structures/growth & development , Eye/cytology , Eye/growth & development , Gene Expression Regulation, Developmental , Models, Biological , Vitamin A Deficiency/embryology , Vitamin A Deficiency/genetics
6.
Dev Biol ; 285(1): 224-37, 2005 Sep 01.
Article in English | MEDLINE | ID: mdl-16054125

ABSTRACT

We consider here how morphogenetic signals involving retinoic acid (RA) are switched on and off in the light of positive and negative feedback controls which operate in other embryonic signalling systems. Switching on the RA signal involves the synthetic retinaldehyde dehydrogenase (RALDH) enzymes and it is currently thought that switching off the RA signal involves the CYP26 enzymes which catabolise RA. We have tested whether these enzymes are regulated by the presence or absence of all-trans-RA using the vitamin A-deficient quail model system and the application of excess retinoids on beads to various locations within the embryo. The Raldhs are unaffected either by the absence or presence of excess RA, whereas the Cyps are strongly affected. In the absence of RA some, but not all domains of Cyp26A1, Cyp26B1 and Cyp26C1 are down-regulated, in particular the spinal cord (Cyp26A1), the heart and developing vasculature (Cyp26B1) and the rhombomeres (Cyp26C1). In the presence of excess RA, the Cyps show a differential regulation-Cyp26A1 and Cyp26B1 are up-regulated whereas Cyp26C1 is down-regulated. We tested whether the Cyp products have a similar influence on these genes and indeed 4-oxo-RA, 4-OH-RA and 5,6-epoxy-RA do. Furthermore, these 3 metabolites are biologically active in that they fully rescue the vitamin A-deficient quail embryo. Finally, by using retinoic acid receptor selective agonists we show that these compounds regulate the Cyps through the RARalpha receptor. These results are discussed with regard to positive and negative feedback controls in developing systems.


Subject(s)
Tretinoin/metabolism , Animals , Base Sequence , Coturnix/embryology , Coturnix/genetics , Coturnix/metabolism , Cytochrome P-450 Enzyme System/genetics , Cytochrome P-450 Enzyme System/metabolism , DNA, Complementary/genetics , Feedback , Gene Expression Regulation, Developmental , Gene Expression Regulation, Enzymologic , Morphogenesis , Receptors, Retinoic Acid/metabolism , Retinoic Acid 4-Hydroxylase , Signal Transduction , Vitamin A Deficiency/embryology , Vitamin A Deficiency/genetics , Vitamin A Deficiency/metabolism
7.
Neuron ; 47(1): 57-69, 2005 Jul 07.
Article in English | MEDLINE | ID: mdl-15996548

ABSTRACT

During development of the retinocollicular projection in mouse, retinal axons initially overshoot their future termination zones (TZs) in the superior colliculus (SC). The formation of TZs is initiated by interstitial branching at topographically appropriate positions. Ephrin-As are expressed in a decreasing posterior-to-anterior gradient in the SC, and they suppress branching posterior to future TZs. Here we investigate the role of an EphA7 gradient in the SC, which has the reverse orientation to the ephrin-A gradient. We find that in EphA7 mutant mice the retinocollicular map is disrupted, with nasal and temporal axons forming additional or extended TZs, respectively. In vitro, retinal axons are repelled from growing on EphA7-containing stripes. Our data support the idea that EphA7 is involved in suppressing branching anterior to future TZs. These findings suggest that opposing ephrin-A and EphA gradients are required for the proper development of the retinocollicular projection.


Subject(s)
Brain Mapping , Ephrins/metabolism , Receptor, EphA7/metabolism , Superior Colliculi/metabolism , Superior Colliculi/physiology , Vision, Ocular/physiology , Visual Pathways/physiology , Animals , Axons/physiology , Histocytochemistry , In Situ Hybridization , Mice , Mice, Knockout , RNA/biosynthesis , RNA/genetics , Retina/cytology
8.
Dev Dyn ; 227(1): 114-27, 2003 May.
Article in English | MEDLINE | ID: mdl-12701104

ABSTRACT

Retinoic acid is an important signalling molecule in the developing embryo, but its precise distribution throughout development is very difficult to determine by available techniques. Examining the distribution of the enzymes by which it is synthesised by using in situ hybridisation is an alternative strategy. Here, we describe the distribution of three retinoic acid synthesising enzymes and one retinoic acid catabolic enzyme during the early stages of chick embryogenesis with the intention of identifying localized retinoic acid signalling regions. The enzymes involved are Raldh1, Raldh2, Raldh3, and Cyp26A1. Although some of these distributions have been described before, here we assemble them all in one species and several novel sites of enzyme expression are identified, including Hensen's node, the cardiac endoderm, the presumptive pancreatic endoderm, and the dorsal lens. This study emphasizes the dynamic pattern of expression of the enzymes that control the availability of retinoic acid as well as the role that retinoic acid plays in the development of many regions of the embryo throughout embryogenesis. This strategy provides a basis for understanding the phenotypes of retinoic acid teratology and retinoic acid-deficiency syndromes.


Subject(s)
Aldehyde Oxidoreductases/metabolism , Chick Embryo/physiology , Cytochrome P-450 Enzyme System/metabolism , Signal Transduction/physiology , Tretinoin/metabolism , Aldehyde Oxidoreductases/genetics , Animals , Chick Embryo/anatomy & histology , Cytochrome P-450 Enzyme System/genetics , Embryonic Structures/anatomy & histology , Embryonic Structures/physiology , Gene Expression Regulation, Developmental , In Situ Hybridization , Mice , Morphogenesis/physiology , Retinal Dehydrogenase , Retinoic Acid 4-Hydroxylase
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