Induction of the epibranchial placodes

Development ◽  
1999 ◽  
Vol 126 (5) ◽  
pp. 895-902 ◽  
Author(s):  
J. Begbie ◽  
J.F. Brunet ◽  
J.L. Rubenstein ◽  
A. Graham
Keyword(s):  
Neural Crest ◽  
Neuronal Cells ◽  
Signalling Molecule ◽  
Pharyngeal Endoderm ◽  
Inductive Interaction ◽  
Embryonic Origin ◽  
The Central Nervous System ◽  
Cranial Sensory Ganglia ◽  
Inductive Signal ◽  
Epibranchial Placodes

The cranial sensory ganglia, in contrast to those of the trunk, have a dual embryonic origin arising from both neurogenic placodes and neural crest. Neurogenic placodes are focal thickenings of ectoderm, found exclusively in the head of vertebrate embryos. These structures can be split into two groups based on the positions that they occupy within the embryo, dorsolateral and epibranchial. The dorsolateral placodes develop alongside the central nervous system, while the epibranchial placodes are located close to the top of the clefts between the branchial arches. Importantly, previous studies have shown that the neurogenic placodes form under the influence of the surrounding cranial tissues. In this paper, we have analysed the nature of the inductive signal underlying the formation of the epibranchial placodes. We find that epibranchial placodes do not require neural crest for their induction, but rather that it is the pharyngeal endoderm that is the source of the inductive signal. We also find that, while cranial ectoderm is competent to respond to this inductive signal, trunk ectoderm is not. We have further identified the signalling molecule Bmp7 as the mediator of this inductive interaction. This molecule is expressed in a manner consistent with it playing such a role and, when added to ectoderm explants, it will promote the formation of epibranchial neuronal cells. Moreover, the Bmp7 antagonist follstatin will block the ability of pharyngeal endoderm to induce placodal neuronal cells, demonstrating that Bmp7 is required for this inductive interaction. This work answers the long standing question regarding the induction of the epibranchial placodes, and represents the first elucidation of an inductive mechanism, and a molecular effector, underlying the formation of any primary sensory neurons in higher vertebrates.

CNS control of a critical period for peripheral induction of central neurons in the leech

Development ◽  
1992 ◽  
Vol 116 (2) ◽  
pp. 427-434 ◽  
Author(s):  
T. Becker ◽  
E.R. Macagno
Keyword(s):  
Central Nervous System ◽  
Male Genitalia ◽  
Critical Period ◽  
Central Neurons ◽  
Inductive Interaction ◽  
The Central Nervous System ◽  
Transplantation Experiments ◽  
Inductive Signal ◽  
Inductive Period ◽  
Cns Control

Most midbody ganglia in the central nervous system (CNS) of the leech Hirudo medicinalis contain about 400 neurons. However, those in the fifth and sixth midbody segments (ganglia M5 and M6) are specialized for reproductive functions, and each contain several hundred additional small neurons. These neurons arise late in embryogenesis as a result of an innervation-dependent inductive interaction between the male genitalia and M5 and M6 and are therefore known as peripherally induced central (PIC) neurons. The results of a series of ablation and transplantation experiments show that the PIC neurons are induced during a 1 to 2 day period about midway in embryogenesis (E15). The male genitalia are not necessary for induction before or after this period, and their presence for only one day may be sufficient for the induction to take place. Heterochronic transplantation of male genitalia shows that the critical period of interaction is independent of the age of the inducing tissues. Since the inductive signal is available from E10 to postembryonic stages, both the beginning and the end of the inductive period are determined by the CNS, not the periphery.

scholarly journals P2X2 receptors differentiate placodal vs. neural crest C-fiber phenotypes innervating guinea pig lungs and esophagus

2008 ◽  
Vol 295 (5) ◽  
pp. L858-L865 ◽  
Author(s):  
Kevin Kwong ◽  
Marian Kollarik ◽  
Christina Nassenstein ◽  
Fei Ru ◽  
Bradley J. Undem
Keyword(s):  
Guinea Pig ◽  
Neural Crest ◽  
Single Cell ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Receptor Activation ◽  
Rt Pcr ◽  
C Fibers ◽  
Embryonic Origin ◽  
Ganglion Neurons

The lungs and esophagus are innervated by sensory neurons with somata in the nodose, jugular, and dorsal root ganglion. These sensory ganglia are derived from embryonic placode (nodose) and neural crest tissues (jugular and dorsal root ganglia; DRG). We addressed the hypothesis that the neuron's embryonic origin (e.g., placode vs. neural crest) plays a greater role in determining particular aspects of its phenotype than the environment in which it innervates (e.g., lungs vs. esophagus). This hypothesis was tested using a combination of extracellular and patch-clamp electrophysiology and single-cell RT-PCR from guinea pig neurons. Nodose, but not jugular C-fibers innervating the lungs and esophagus, responded to α,β-methylene ATP with action potential discharge that was sensitive to the P2X3 (P2X2/3) selective receptor antagonist A-317491. The somata of lung- and esophagus-specific sensory fibers were identified using retrograde tracing with a fluorescent dye. Esophageal- and lung-traced neurons from placodal tissue (nodose neurons) responded similarly to α,β-methylene ATP (30 μM) with a large sustained inward current, whereas in neurons derived from neural crest tissue (jugular and DRG neurons), the same dose of α,β-methylene ATP resulted in only a transient rapidly inactivating current or no detectable current. It has been shown previously that only activation of P2X2/3 heteromeric receptors produce sustained currents, whereas homomeric P2X3 receptor activation produces a rapidly inactivating current. Consistent with this, single-cell RT-PCR analysis revealed that the nodose ganglion neurons innervating the lungs and esophagus expressed mRNA for P2X2 and P2X3 subunits, whereas the vast majority of jugular and dorsal root ganglia innervating these tissues expressed only P2X3 mRNA with little to no P2X2 mRNA expression. We conclude that the responsiveness of C-fibers innervating the lungs and esophagus to ATP and other purinergic agonists is determined more by their embryonic origin than by the environment of the tissue they ultimately innervate.

scholarly journals Migrating into Genomics with the Neural Crest

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Marianne E. Bronner
Keyword(s):  
Neural Crest ◽  
Gene Regulatory Network ◽  
Regulatory Network ◽  
Neural Crest Cells ◽  
Embryonic Cell ◽  
Putative Gene ◽  
Peripheral Neurons ◽  
Neural Plate Border ◽  
The Central Nervous System ◽  
Gene Regulatory

Neural crest cells are a fascinating embryonic cell type, unique to vertebrates, which arise within the central nervous system but emigrate soon after its formation and migrate to numerous and sometimes distant locations in the periphery. Following their migratory phase, they differentiate into diverse derivatives ranging from peripheral neurons and glia to skin melanocytes and craniofacial cartilage and bone. The molecular underpinnings underlying initial induction of prospective neural crest cells at the neural plate border to their migration and differentiation have been modeled in the form of a putative gene regulatory network. This review describes experiments performed in my laboratory in the past few years aimed to test and elaborate this gene regulatory network from both an embryonic and evolutionary perspective. The rapid advances in genomic technology in the last decade have greatly expanded our knowledge of important transcriptional inputs and epigenetic influences on neural crest development. The results reveal new players and new connections in the neural crest gene regulatory network and suggest that it has an ancient origin at the base of the vertebrate tree.

scholarly journals How Neural Crest Transcription Factors Contribute to Melanoma Heterogeneity, Cellular Plasticity, and Treatment Resistance

2021 ◽  
Vol 22 (11) ◽  
pp. 5761
Author(s):  
Anja Wessely ◽  
Theresa Steeb ◽  
Carola Berking ◽  
Markus Vincent Heppt
Keyword(s):  
Drug Resistance ◽  
Neural Crest ◽  
Physiological Function ◽  
Acquired Resistance ◽  
Treatment Resistance ◽  
Transcriptional Regulators ◽  
Disease Stage ◽  
Cellular Plasticity ◽  
Embryonic Origin ◽  
Promote Disease Progression

Cutaneous melanoma represents one of the deadliest types of skin cancer. The prognosis strongly depends on the disease stage, thus early detection is crucial. New therapies, including BRAF and MEK inhibitors and immunotherapies, have significantly improved the survival of patients in the last decade. However, intrinsic and acquired resistance is still a challenge. In this review, we discuss two major aspects that contribute to the aggressiveness of melanoma, namely, the embryonic origin of melanocytes and melanoma cells and cellular plasticity. First, we summarize the physiological function of epidermal melanocytes and their development from precursor cells that originate from the neural crest (NC). Next, we discuss the concepts of intratumoral heterogeneity, cellular plasticity, and phenotype switching that enable melanoma to adapt to changes in the tumor microenvironment and promote disease progression and drug resistance. Finally, we further dissect the connection of these two aspects by focusing on the transcriptional regulators MSX1, MITF, SOX10, PAX3, and FOXD3. These factors play a key role in NC initiation, NC cell migration, and melanocyte formation, and we discuss how they contribute to cellular plasticity and drug resistance in melanoma.

The cephalic neural crest provides pericytes and smooth muscle cells to all blood vessels of the face and forebrain

Development ◽  
2001 ◽  
Vol 128 (7) ◽  
pp. 1059-1068 ◽  
Author(s):  
H.C. Etchevers ◽  
C. Vincent ◽  
N.M. Le Douarin ◽  
G.F. Couly
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Neural Crest ◽  
Muscle Cells ◽  
Embryonic Cell ◽  
Avian Embryo ◽  
Connective Tissues ◽  
The Face ◽  
Mesodermal Origin ◽  
The Central Nervous System

Most connective tissues in the head develop from neural crest cells (NCCs), an embryonic cell population present only in vertebrates. We show that NCC-derived pericytes and smooth muscle cells are distributed in a sharply circumscribed sector of the vasculature of the avian embryo. As NCCs detach from the neural folds that correspond to the future posterior diencephalon, mesencephalon and rhombencephalon, they migrate between the ectoderm and the neuroepithelium into the anterior/ventral head, encountering mesoderm-derived endothelial precursors. Together, these two cell populations build a vascular tree rooted at the departure of the aorta from the heart and ramified into the capillary plexi that irrigate the forebrain meninges, retinal choroids and all facial structures, before returning to the heart. NCCs ensheath each aortic arch-derived vessel, providing every component except the endothelial cells. Within the meninges, capillaries with pericytes of diencephalic and mesencephalic neural fold origin supply the forebrain, while capillaries with pericytes of mesodermal origin supply the rest of the central nervous system, in a mutually exclusive manner. The two types of head vasculature contact at a few defined points, including the anastomotic vessels of the circle of Willis, immediately ventral to the forebrain/midbrain boundary. Over the course of evolution, the vertebrate subphylum may have exploited the exceptionally broad range of developmental potentialities and the plasticity of NCCs in head remodelling that resulted in the growth of the forebrain.

scholarly journals Evolution of the hypoxia-sensitive cells involved in amniote respiratory reflexes

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Dorit Hockman ◽  
Alan J Burns ◽  
Gerhard Schlosser ◽  
Keith P Gates ◽  
Benjamin Jevans ◽  
...  
Keyword(s):  
Neural Crest ◽  
Blood Vessels ◽  
Carotid Body ◽  
Lineage Tracing ◽  
Neuroendocrine Cells ◽  
Genetic Lineage ◽  
Glomus Cells ◽  
Evolutionary Origins ◽  
Embryonic Origin ◽  
Respiratory Reflexes

The evolutionary origins of the hypoxia-sensitive cells that trigger amniote respiratory reflexes – carotid body glomus cells, and ‘pulmonary neuroendocrine cells’ (PNECs) - are obscure. Homology has been proposed between glomus cells, which are neural crest-derived, and the hypoxia-sensitive ‘neuroepithelial cells’ (NECs) of fish gills, whose embryonic origin is unknown. NECs have also been likened to PNECs, which differentiate in situ within lung airway epithelia. Using genetic lineage-tracing and neural crest-deficient mutants in zebrafish, and physical fate-mapping in frog and lamprey, we find that NECs are not neural crest-derived, but endoderm-derived, like PNECs, whose endodermal origin we confirm. We discover neural crest-derived catecholaminergic cells associated with zebrafish pharyngeal arch blood vessels, and propose a new model for amniote hypoxia-sensitive cell evolution: endoderm-derived NECs were retained as PNECs, while the carotid body evolved via the aggregation of neural crest-derived catecholaminergic (chromaffin) cells already associated with blood vessels in anamniote pharyngeal arches.

The signalling molecule BMP4 mediates apoptosis in the rhombencephalic neural crest

Nature ◽  
1994 ◽  
Vol 372 (6507) ◽  
pp. 684-686 ◽  
Author(s):  
Anthony Graham ◽  
Philippa Francis-West ◽  
Paul Brickell ◽  
Andrew Lumsden
Keyword(s):  
Neural Crest ◽  
Signalling Molecule

Interactions between rhombomeres modulate Krox-20 and follistatin expression in the chick embryo hindbrain

Development ◽  
1996 ◽  
Vol 122 (2) ◽  
pp. 473-480 ◽  
Author(s):  
A. Graham ◽  
A. Lumsden
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Cell Lineage ◽  
Signalling Molecule ◽  
Neighbour Interaction

The rhombomeres of the embryonic hindbrain display compartment properties, including cell lineage restriction, genetic definition and modular anatomical phenotype. Consistent with the idea that rhombomeres are autonomous developmental units, previous studies have shown that certain aspects of rhombomere phenotype are determined early, at the time of rhombomere formation. By contrast, the apoptotic depletion of neural crest from rhombomeres 3 and 5 is due to an interaction with their neighbouring rhombomeres, involving the signalling molecule Bmp4. In this paper, we have examined whether inter-rhombomere interactions control further aspects of rhombomere phenotype. We find that the expression of Krox-20 and the repression of follistatin in r3 is dependent upon neighbour interaction, whereas these genes are expressed autonomously in r5. We further demonstrate that modulation of Krox-20 and follistatin expression is not dependent on Bmp4, indicating the existence of multiple pathways of interaction between adjacent rhombomeres. We also show that, although some phenotypic aspects of r3 are controlled by neighbour interactions, the axial identity of the segment is intrinsically determined.

scholarly journals H2S-based therapies for ischaemic stroke: opportunities and challenges

2019 ◽  
Vol 4 (2) ◽  
pp. 63-66 ◽  
Author(s):  
Jia Jia ◽  
Jie Li ◽  
Jian Cheng
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ischaemic Stroke ◽  
Stroke Patients ◽  
Stroke Outcomes ◽  
Mortality And Morbidity ◽  
Functional Roles ◽  
Cellular Models ◽  
Signalling Molecule ◽  
The Central Nervous System

Stroke is a cerebrovascular disease displaying high mortality and morbidity. Despite extensive efforts, only very few therapies are available for stroke patients as yet. Hydrogen sulfide (H2S) is thought to be a signalling molecule that is endogenously produced and plays functional roles in the central nervous system. Currently, numerous studies show that H2S impacts stroke outcomes in animal and cellular models. Here, we review the recent research regarding the effects of endogenously produced H2S as well as exogenous H2S donors on stroke pathology, focusing on the potential of H2S-based therapies in treating ischaemic stroke. We also discuss the several issues that hinder the clinical translation of H2S-based therapies from the bench. Taken together, we think that H2S-based therapies are promising strategies for treating cerebral ischaemia if we successfully address these issues.

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