The triple origin of skull in higher vertebrates: a study in quail-chick chimeras

Development ◽  
1993 ◽  
Vol 117 (2) ◽  
pp. 409-429 ◽  
Author(s):  
G.F. Couly ◽  
P.M. Coltey ◽  
N.M. Le Douarin
Keyword(s):  
Neural Crest ◽  
Sella Turcica ◽  
Parietal Bone ◽  
Paraxial Mesoderm ◽  
Avian Embryo ◽  
Evolutionary Context ◽  
Embryonic Origin ◽  
Neural Crest Origin ◽  
Parietal Bones ◽  
Double Origin

We have used the quail-chick chimera technique to study the origin of the bones of the skull in the avian embryo. Although the contribution of the neural crest to the facial and visceral skeleton had been established previously, the origin of the vault of the skull (i.e. frontal and parietal bones) remained uncertain. Moreover formation of the occipito-otic region from either the somitic or the cephalic paraxial mesoderm had not been experimentally investigated. The data obtained in the present and previous works now allow us to assign a precise embryonic origin from either the mesectoderm, the paraxial cephalic mesoderm or the five first somites, to all the bones forming the avian skull. We distinguish a skull located in front of the extreme tip of the notochord which reaches the sella turcica and a skull located caudally to this boundary. The former ('prechordal skull') is derived entirely from the neural crest, the latter from the mesoderm (cephalic or somitic) in its ventromedial part ('chordal skull') and from the crest for the parietal bone and for part of the otic region. An important point enlighten in this work concerns the double origin of the corpus of the sphenoid in which basipresphenoid is of neural crest origin and the basipostsphenoid is formed by the cephalic mesoderm. Formation of the occipito-otic region of the skeleton is particularly complex and involves the cooperation of the five first somites and the paraxial mesoderm at the hind-brain level. The morphogenetic movements leading to the initial puzzle assembly could be visualized in a reproducible way by means of small grafts of quail mesodermal areas into chick embryos. The data reported here are discussed in the evolutionary context of the ‘New Head’ hypothesis of Gans and Northcutt (1983, Science, 220, 268–274).

The developmental fate of the cephalic mesoderm in quail-chick chimeras

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 1-15 ◽  
Author(s):  
G.F. Couly ◽  
P.M. Coltey ◽  
N.M. Le Douarin
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Avian Embryo ◽  
Facial Skeleton ◽  
Developmental Fate ◽  
Prechordal Mesoderm ◽  
The Face ◽  
Neural Crest Origin ◽  
Neurula Stage

The developmental fate of the cephalic paraxial and prechordal mesoderm at the late neurula stage (3-somite) in the avian embryo has been investigated by using the isotopic, isochronic substitution technique between quail and chick embryos. The territories involved in the operation were especially tiny and the size of the transplants was of about 150 by 50 to 60 microns. At that stage, the neural crest cells have not yet started migrating and the fate of mesodermal cells exclusively was under scrutiny. The prechordal mesoderm was found to give rise to the following ocular muscles: musculus rectus ventralis and medialis and musculus oblicus ventralis. The paraxial mesoderm was separated in two longitudinal bands: one median, lying upon the cephalic vesicles (median paraxial mesoderm—MPM); one lateral, lying upon the foregut (lateral paraxial mesoderm—LPM). The former yields the three other ocular muscles, contributes to mesencephalic meninges and has essentially skeletogenic potencies. It contributes to the corpus sphenoid bone, the orbitosphenoid bone and the otic capsules; the rest of the facial skeleton is of neural crest origin. At 3-somite stage, MPM is represented by a few cells only. The LPM is more abundant at that stage and has essentially myogenic potencies with also some contribution to connective tissue. However, most of the connective cells associated with the facial and hypobranchial muscles are of neural crest origin. The more important result of this work was to show that the cephalic mesoderm does not form dermis. This function is taken over by neural crest cells, which form both the skeleton and dermis of the face. If one draws a parallel between the so-called “somitomeres” of the head and the trunk somites, it appears that skeletogenic potencies are reduced in the former, which in contrast have kept their myogenic capacities, whilst the formation of skeleton and dermis has been essentially taken over by the neural crest in the course of evolution of the vertebrate head.

Abstract 307: Angiotensin II Infusion Does Not Influence the Distribution of Cardiac Neural Crest Derived Smooth Muscle Cells in the Ascending Aorta

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Hisashi Sawada ◽  
Jessica J Moorleghen ◽  
Debra L Rateri ◽  
Alan Daugherty
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Neural Crest ◽  
Ascending Aorta ◽  
Cell Type ◽  
Cardiac Neural Crest ◽  
Adult Mice ◽  
Embryonic Origin ◽  
Neural Crest Origin ◽  
Beta Galactosidase

Objective: Angiotensin II (Ang II) causes vascular pathology including hypertrophy and aneurysms. Smooth muscle cells (SMCs) exert a pivotal role in vascular remodeling. The localization of these vascular pathologies may be associated with distinct embryonic origins of SMCs. While there is evidence that most SMCs derive from the cardiac neural crest in the ascending aorta, other data has inferred a greater complexity of origins for this cell type. The aim of this study was to determine whether heterogeneity of the embryonic origin of SMCs in the ascending aorta is influenced by AngII. Methods and Results: ROSA26 lacZ mice were bred to mice expressing Cre under control of the Wnt1 promoter to track SMCs of cardiac neural crest origin. Gross examination of beta-galactosidase stained aortas from adult mice demonstrated cells of cardiac neural crest present from the sinotubular ascending aorta to just distal to the subclavian branch. For further examination of cell type distribution, both sagittal and cross sections were obtained. These stained sections demonstrated there was a distinct distribution on the anterior aspect of the ascending aorta, with SMCs of cardiac neural crest origin only being present in the inner laminal layers. On the proximal area of this region, there was transmural staining for beta-galactosidase. Much of the aortic arch to the subclavian branch also had transmural beta-galactosidase staining. Previous studies have demonstrated that infusion of AngII promotes pathology that varies along the length of the ascending aorta. Also, the medial pathology is most pronounced on the adventitial aspect. Therefore, we examined whether the distribution of cardiac neural crest-derived SMCs was influenced during AngII infusion. However, after 28 days of pressor infusion rates of AngII, there was no overt change in the distribution of cardiac neural crest-derived SMCs in the ascending aorta. Conclusion: SMCs from the outer aspect of the media are derived from a different embryonic origin. Cardiac neural crest derived-SMCs retain their unique distribution in the inner media of the ascending aorta during AngII infusion in adult mice.

scholarly journals Cranial Neural Crest Cells and Their Role in the Pathogenesis of Craniofacial Anomalies and Coronal Craniosynostosis

2020 ◽  
Vol 8 (3) ◽  
pp. 18 ◽  
Author(s):  
Erica M. Siismets ◽  
Nan E. Hatch
Keyword(s):  
Neural Crest ◽  
Treatment Strategies ◽  
Neural Crest Cells ◽  
Parietal Bone ◽  
Paraxial Mesoderm ◽  
Treacher Collins Syndrome ◽  
Craniofacial Anomalies ◽  
Cranial Neural Crest ◽  
Craniofacial Skeleton ◽  
Cranial Neural Crest Cells

Craniofacial anomalies are among the most common of birth defects. The pathogenesis of craniofacial anomalies frequently involves defects in the migration, proliferation, and fate of neural crest cells destined for the craniofacial skeleton. Genetic mutations causing deficient cranial neural crest migration and proliferation can result in Treacher Collins syndrome, Pierre Robin sequence, and cleft palate. Defects in post-migratory neural crest cells can result in pre- or post-ossification defects in the developing craniofacial skeleton and craniosynostosis (premature fusion of cranial bones/cranial sutures). The coronal suture is the most frequently fused suture in craniosynostosis syndromes. It exists as a biological boundary between the neural crest-derived frontal bone and paraxial mesoderm-derived parietal bone. The objective of this review is to frame our current understanding of neural crest cells in craniofacial development, craniofacial anomalies, and the pathogenesis of coronal craniosynostosis. We will also discuss novel approaches for advancing our knowledge and developing prevention and/or treatment strategies for craniofacial tissue regeneration and craniosynostosis.

scholarly journals Differences in Steady-State Erythropoiesis in Different Mouse Bones and Postnatal Spleen

2021 ◽  
Vol 9 ◽  
Author(s):  
Vamsee D. Myneni ◽  
Ildikó Szalayova ◽  
Eva Mezey
Keyword(s):  
Steady State ◽  
Parietal Bone ◽  
Erythroid Progenitors ◽  
Erythroid Progenitor ◽  
Hematopoietic Stem ◽  
Erythroid Precursors ◽  
Embryonic Origin ◽  
Cortical Regions ◽  
Parietal Bones ◽  
Substantial Heterogeneity

Adult erythropoiesis is a highly controlled sequential differentiation of hematopoietic stem cells (HSCs) to mature red blood cells in the bone marrow (BM). The bones which contain BM are diverse in their structure, embryonic origin, and mode of ossification. This has created substantial heterogeneity in HSCs function in BM of different bones, however, it is not known if this heterogeneity influences erythropoiesis in different bones and different regions of the same bone. In this study, we examined steady state BM erythroid progenitors and precursors from different bones – the femur, tibia, pelvis, sternum, vertebrae, radius, humerus, frontal, parietal bone, and compared all to the femur. Trabecular and cortical regions of the femur were also compared for differences in erythropoiesis. In addition, mouse spleen was studied to determine at which age erythropoietic support by the spleen was lost postnatally. We report that total erythroid cells, and erythroid precursors in the femur are comparable to tibia, pelvis, humerus and sternum, but are significantly reduced in the vertebrae, radius, frontal, and parietal bones. Erythroid progenitors and multipotential progenitor numbers are comparable in all the bones except for reduced number in the parietal bone. In the femur, the epiphysis and metaphysis have significantly reduced number of erythroid precursors and progenitors, multipotential progenitors and myeloid progenitors compared to the diaphysis region. These results show that analysis of erythroid precursors from diaphysis region of the femur is representative of tibia, pelvis, humerus and sternum and have significant implications on the interpretation of the steady-state erythropoiesis finding from adult BM. Postnatal spleen supports erythroid precursors until 6 weeks of age which coincides with reduced number of red pulp macrophages. The residual erythroid progenitor support reaches the adult level by 3 months of age. In conclusion, our findings provide insights to the differences in erythropoiesis between different bones, between trabecular and cortical regions of the femur, and developmental changes in postnatal spleen erythropoiesis.

scholarly journals cKit+ cardiac progenitors of neural crest origin

2015 ◽  
Vol 112 (42) ◽  
pp. 13051-13056 ◽  
Author(s):  
Konstantinos E. Hatzistergos ◽  
Lauro M. Takeuchi ◽  
Dieter Saur ◽  
Barbara Seidler ◽  
Susan M. Dymecki ◽  
...  
Keyword(s):  
Neural Crest ◽  
Pluripotent Stem Cells ◽  
Conduction System ◽  
Cardiac Conduction ◽  
Fate Mapping ◽  
Cardiac Progenitors ◽  
Morphogenetic Protein ◽  
Embryonic Origin ◽  
Neural Crest Origin ◽  
Induced Pluripotent

The degree to which cKit-expressing progenitors generate cardiomyocytes in the heart is controversial. Genetic fate-mapping studies suggest minimal contribution; however, whether or not minimal contribution reflects minimal cardiomyogenic capacity is unclear because the embryonic origin and role in cardiogenesis of these progenitors remain elusive. Using high-resolution genetic fate-mapping approaches with cKitCreERT2/+ and Wnt1::Flpe mouse lines, we show that cKit delineates cardiac neural crest progenitors (CNCkit). CNCkit possess full cardiomyogenic capacity and contribute to all CNC derivatives, including cardiac conduction system cells. Furthermore, by modeling cardiogenesis in cKitCreERT2-induced pluripotent stem cells, we show that, paradoxically, the cardiogenic fate of CNCkit is regulated by bone morphogenetic protein antagonism, a signaling pathway activated transiently during establishment of the cardiac crescent, and extinguished from the heart before CNC invasion. Together, these findings elucidate the origin of cKit+ cardiac progenitors and suggest that a nonpermissive cardiac milieu, rather than minimal cardiomyogenic capacity, controls the degree of CNCkit contribution to myocardium.

Interactions and fates of avian craniofacial mesenchyme

Development ◽  
1988 ◽  
Vol 103 (Supplement) ◽  
pp. 121-140 ◽  
Author(s):  
Drew M. Noden
Keyword(s):  
Connective Tissue ◽  
Neural Crest ◽  
Spatial Information ◽  
Vascular Endothelial Cells ◽  
Paraxial Mesoderm ◽  
Avian Embryo ◽  
Vascular Endothelial ◽  
Connective Tissues ◽  
The Central Nervous System ◽  
Lateral Mesoderm

Craniofacial mesenchyme is composed of three mesodermal populations – prechordal plate, lateral mesoderm and paraxial mesoderm, which includes the segmented occipital somites and the incompletely segmented somitomeres – and the neural crest. This paper outlines the fates of each of these, as determined using quail–chick chimaeras, and presents similarities and differences between these cephalic populations and their counterparts in the trunk. Prechordal and paraxial mesodermal populations are the sources of all voluntary muscles of the head. The latter also provides most of the connective precursors of the calvaria, occipital, otic–parietal and basisphenoid tissues. Lateral mesoderm is the source of peripharyngeal connective tissues; the most rostral skeletal tissues it forms are the laryngeal and tracheal cartilages. When migrating neural crest cells encounter segmented paraxial mesoderm (occipital and trunk somites), most move into the region between the dermamyotome and sclerotome in the cranial half of each somite. In contrast, most cephalic crest cells migrate superficial to somitomeres. There is, however, a small subpopulation of the head crest that invades somitomeric mesoderm. These cells subsequently segregate presumptive myogenic precursors of visceral arch voluntary muscles from underlying mesenchyme. In the neurula-stage avian embryo, all paraxial and lateral mesodermal populations contain precursors of vascular endothelial cells, which can be detected in chimaeric embryos using anti-quail endothelial antibodies. Some of these angioblasts differentiate in situ, contributing directly to pre-existing vessels or forming isolated, nonpatent, cords that subsequently vesiculate and fuse with nearby vessels. Many angioblasts migrate in all directions, invading embryonic mesenchymal and epithelial tissues and participating in new blood vessel formation in distant sites. The interactions leading to proper spatial patterning of craniofacial skeletal, muscular, vascular and peripheral neural tissues has been studied by performing heterotopic transplants of each of these mesodermal and neural crest populations. The results consistently indicate that connective tissue precursors, regardless of their origin, contain spatial information used by the precursors of muscles and blood vessels and by outgrowing peripheral nerves. Some of these connective tissue precursors (e.g. the neural crest, paraxial mesoderm) acquire their spatial programming while in association with the central nervous system or developing sensory epithelia (e.g. otic, optic, nasal epithelia).

The dorsal neural tube organizes the dermamyotome and induces axial myocytes in the avian embryo

Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 231-241 ◽  
Author(s):  
M.S. Spence ◽  
J. Yip ◽  
C.A. Erickson
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Intervertebral Discs ◽  
Paraxial Mesoderm ◽  
Avian Embryo ◽  
Dorsal Neural Tube ◽  
Ventral Neural Tube ◽  
Dorsal Ectoderm

Somites, like all axial structures, display dorsoventral polarity. The dorsal portion of the somite forms the dermamyotome, which gives rise to the dermis and axial musculature, whereas the ventromedial somite disperses to generate the sclerotome, which later comprises the vertebrae and intervertebral discs. Although the neural tube and notochord are known to regulate some aspects of this dorsoventral pattern, the precise tissues that initially specify the dermamyotome, and later the myotome from it, have been controversial. Indeed, dorsal and ventral neural tube, notochord, ectoderm and neural crest cells have all been proposed to influence dermamyotome formation or to regulate myocyte differentiation. In this report we describe a series of experimental manipulations in the chick embryo to show that dermamyotome formation is regulated by interactions with the dorsal neural tube. First, we demonstrate that when a neural tube is rotated 180 degrees around its dorsoventral axis, a secondary dermamyotome is induced from what would normally have developed as sclerotome. Second, if we ablate the dorsal neural tube, dermamyotomes are absent in the majority of embryos. Third, if we graft pieces of dorsal neural tube into a ventral position between the notochord and ventral somite, a dermamyotome develops from the sclerotome that is proximate to the graft, and myocytes differentiate. In addition, we also show that myogenesis can be regulated by the dorsal neural tube because when pieces of dorsal neural tube and unsegmented paraxial mesoderm are combined in tissue culture, myocytes differentiate, whereas mesoderm cultures alone do not produce myocytes autonomously. In all of the experimental perturbations in vivo, the dorsal neural tube induced dorsal structures from the mesoderm in the presence of notochord and floorplate, which have been reported previously to induce sclerotome. Thus, we have demonstrated that in the context of the embryonic environment, a dorsalizing signal from the dorsal neural tube can compete with the diffusible ventralizing signal from the notochord. In contrast to dorsal neural tube, pieces of ventral neural tube, dorsal ectoderm or neural crest cells, all of which have been postulated to control dermamyotome formation or to induce myogenesis, either fail to do so or provoke only minimal inductive responses in any of our assays. However, complicating the issue, we find consistent with previous studies that following ablation of the entire neural tube, dermamyotome formation still proceeds adjacent to the dorsal ectoderm. Together these results suggest that, although dorsal ectoderm may be less potent than the dorsal neural tube in inducing dermamyotome, it does nonetheless possess some dermamyotomal-inducing activity. Based on our data and that of others, we propose a model for somite dorsoventral patterning in which competing diffusible signals from the dorsal neural tube and from the notochord/floorplate specify dermamyotome and sclerotome, respectively. In our model, the positioning of the dermamyotome dorsally is due to the absence or reduced levels of the notochord-derived ventralizing signals, as well as to the presence of dominant dorsalizing signals. These dorsal signals are possibly localized and amplified by binding to the basal lamina of the ectoderm, where they can signal the underlying somite, and may also be produced by the ectoderm as well.

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.

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