The ontogeny of the neural crest in avian embryo chimaeras

Douarin, Nicole M. Le

doi:10.1038/286663a0

Cited by 294 publications

(93 citation statements)

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“…Both in vivo and in vitro studies (1,2) have shown that the neurotransmitter choice is labile during a prolonged period of life. Tyrosine hydroxylase [TyrOHase; tyrosine 3-monooxygenase; L-tyrosine,tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.…”

mentioning

confidence: 99%

“…16.2] is a specific marker for adrenergic neurons and has been widely used to study their ontogeny. The regulation of the expression of TyrOHase has been shown to be influenced by the target tissue (1,2), by neural activity (3,4) and by chemical or hormonal factors such as glucocorticoids (5-7) and nerve growth factor (7,8). A full understanding of the regulation of this enzyme requires an analysis of the DNA encoding its gene and of its RNA transcripts.…”

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confidence: 99%

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Identification of cDNA clones coding for rat tyrosine hydroxylase antigen.

Lamouroux¹,

Biguet²,

Samolyk³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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Five recombinant DNA plasmids have been constructed that contain structural gene sequences for rat tyrosine hydroxylase [TyrOHase; tyrosine 3-monooxygenase; L-tyrosine,tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14. The peripheral autonomic nervous system provides a useful model of neuronal development because the neurons in the sympathetic ganglia, which arise from the neural crest, become either cholinergic or adrenergic. Both in vivo and in vitro studies (1, 2) have shown that the neurotransmitter choice is labile during a prolonged period of life. Tyrosine hydroxylase [TyrOHase; tyrosine 3-monooxygenase; L-tyrosine,tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] is a specific marker for adrenergic neurons and has been widely used to study their ontogeny. The regulation of the expression of TyrOHase has been shown to be influenced by the target tissue (1, 2), by neural activity (3, 4) and by chemical or hormonal factors such as glucocorticoids (5-7) and nerve growth factor (7,8). A full understanding of the regulation of this enzyme requires an analysis of the DNA encoding its gene and of its RNA transcripts.As a first step we report here the isolation of recombinant plasmids carrying DNA sequences complementary to a mRNA coding for rat TyrOHase antigen. To carry out this work we have taken advantage of a cloned cell line of rat pheochromocytoma characterized by relatively high levels of catecholamine-synthesizing enzyme and transmitter (9). TyrOHase cDNA clones were selected by the combined use of differential colony hybridization and immunoprecipitation ofthe products ofplasmidselected mRNA translation. The TyrOHase cDNA probes allowed the characterization of TyrOHase mRNA from PC 12 cells and human pheochromocytoma. MATERIALS AND METHODSGrowth of Cells and Tissues and RNA Isolation. Rat pheochromocytoma PC 12 cells, originally obtained through the generosity of L. A. Greene, were grown and harvested after treatment with dexamethasone as described (10). In addition, PC 12 cells (= 107) were used to subcutaneously inoculate nude mice. Tumor nodules could be palpated at the site ofinoculation after 5-7 weeks. Four days before the turnors were collected, the animals were daily subjected to dexamethasone treatment (100 ug/kg). The final dose of dexamethasone (300 ,ug/kg) was given 6 hr before harvesting. Human pheochromocytoma were obtained from J. P. Luton (Hopital Cochin, Paris) 15-30 min after surgery and were stored frozen (-70°C) until RNA extraction. Rat livers were dissected from adult Sprague-Dawley rats killed without anesthesia.RNAs were extracted from tumors as described by Lomedico and Saunders (11) and from PC 12 cells and liver by the method of Auffray and Rougeon (12).Poly(A)-RNA Separation, in Vitro Protein Synthesis, and Immunoprecipitations. Polyadenylylated mRNAs were obtained from total RNA preparations by two cycles of oligo(dT)-cellulose chromatography (13). mRNA coding for TyrOHase antigen was further enriched by centrifugation in a...

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confidence: 99%

mentioning

confidence: 99%

Identification of cDNA clones coding for rat tyrosine hydroxylase antigen.

Lamouroux¹,

Biguet²,

Samolyk³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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“…The molecular mechanisms by which different levels of BMP activate a diversity of pathways of differentiation are yet to be defined, and our in vitro model may offer a path for such a study. Molecular mechanisms and genetic pathways involved in melanocyte development were originally described in chicken models using chimeras (26,27). These pioneer studies demonstrated that melanocytes initially derive from a group of migratory embryonic cells referred to as the neural crest, which secondarily mature under the control of BMPs, Wnt/β-catenin, and FGFs into pigmented progenitors (28).…”

Section: Discussionmentioning

confidence: 99%

Functional melanocytes derived from human pluripotent stem cells engraft into pluristratified epidermis

Nissan

Larribère

Saidani

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Melanocytes are essential for skin homeostasis and protection, and their defects in humans lead to a wide array of diseases that are potentially extremely severe. To date, the analysis of molecular mechanisms and the function of human melanocytes have been limited because of the difficulties in accessing large numbers of cells with the specific phenotypes. This issue can now be addressed via a differentiation protocol that allows melanocytes to be obtained from pluripotent stem cell lines, either induced or of embryonic origin, based on the use of moderate concentrations of a single cytokine, bone morphogenic protein 4. Human melanocytes derived from pluripotent stem cells exhibit all the characteristic features of their adult counterparts. This includes the enzymatic machinery required for the production and functional delivery of melanin to keratinocytes. Melanocytes also integrate appropriately into organotypic epidermis reconstructed in vitro. The availability of human cells committed to the melanocytic lineage in vitro will enable the investigation of those mechanisms that guide the developmental processes and will facilitate analysis of the molecular mechanisms responsible for genetic diseases. Access to an unlimited resource may also prove a vital tool for the treatment of hypopigmentation disorders when donors with matching haplotypes become available in clinically relevant banks of pluripotent stem cell lines.

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“…Interestingly, the 10 d grafted quail wings were seen to contain some cells of chick origin. These were always located in close association with nerve bundles and were presumably Schwann cells, which are known to be of neural crest origin (LeDouarin, 1980).…”

Section: Generalmentioning

confidence: 99%

Survival of motoneurons in the brachial lateral motor column of limbless mutant chick embryos depends on the periphery

Jl¹,

Fallon²

1986

J. Neurosci.

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Motoneuron survival in the embryonic spinal cord is influenced by the presence or absence of the developing limb bud. We have recently begun a reexamination of the relationship between limb absence and motoneuron survival in a nonsurgical limb deletion model, the limbless mutant chick embryo. As in surgically limbdeleted normal embryos, only 10% of the motoneurons that are intially produced in the limbless mutant lateral motor column (LMC) survive the embryonic period (Lanser and Fallon, 1984). We now report' that, when supplied with a normal periphery (i.e., a normal limb bud), more than 40% of the motoneurons initially produced in the limbless LMC survive the embryonic period. Motoneuron cell counts in one-winged limbless embryos reveal that over 3.5 times as many motoneurons survive the cell death period in the LMC on the side with the limb than on the opposite, limbless side. This demonstrates the dependence of embryonic LMC motoneurons on the developing limb for survival and indicates that the limbless mutant is an appropriate model for studying the death and survival of LMC motoneurons during development. Using the limbless mutant to study LMC motoneuron survival eliminates the complication of possible direct surgical effects on motoneuron death. In addition, we found that a substantial effect of the wing on rescuing LMC motoneurons was exerted prior to the 6th day of embryonic development. Normally, little cell loss occurs in the brachial LMC during this time. Accordingly, motoneuron death in the limb-deprived brachial LMC, whether in surgically limb-deleted normal embryos or in genetically limbless embryos, is accelerated with respect to cell death in the normal brachial LMC.Since cell death was first established as an integral part of the development of specific nerve centers (Hamburger and LeviMontalcini, 1949), the phenomenon of naturally occurring neuronal death has been widely documented but incompletely understood (for a historical review, see Oppenheim, 198 1). One neuronal population where cell death has been extensively studied is the lateral motor column (LMC) of the spinal cord (see Lamb, 1984, for review). The LMC contains the motoneurons that innervate the muscles of the vertebrate limb. It has been

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The ontogeny of the neural crest in avian embryo chimaeras

Cited by 294 publications

References 44 publications

Identification of cDNA clones coding for rat tyrosine hydroxylase antigen.

Identification of cDNA clones coding for rat tyrosine hydroxylase antigen.

Functional melanocytes derived from human pluripotent stem cells engraft into pluristratified epidermis

Survival of motoneurons in the brachial lateral motor column of limbless mutant chick embryos depends on the periphery

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