Abstract:We compared apparent origins, cellular diversity and regulation of initial axon growth for differentiating cranial sensory neurons. We assessed the molecular and cellular composition of the developing olfactory and otic placodes, and cranial sensory ganglia to evaluate contributions of ectodermal placode versus neural crest at each site. Special sensory neuron populations—the olfactory and otic placodes—as well as those in vestibulo-acoustic ganglion are entirely populated with cells expressing cranial placode… Show more
“…2 g and g’ ). This result is in agreement with recent findings showing that the SIX1-positive cells in the trigeminal ganglia are sensory neurons, which could belong to those of placodal origin in the mouse and chick embryos [ 44 , 47 ]. At the level of the anterior rhombencephalon, SIX1 transcripts were highly expressed in otic vesicles, pharynx and the periocular and pharyngeal mesenchyme (Fig.…”
Section: Resultssupporting
confidence: 93%
“…5 j, j’ ), while SIX1 appeared to be expressed in the sensory neurons (Fig. 5 j” ), in agreement with previous data [ 17 , 44 , 47 ]. Fig.…”
BackgroundVertebrate head development depends on a series of interactions between many cell populations of distinct embryological origins. Cranial mesenchymal tissues have a dual embryonic source: - the neural crest (NC), which generates most of craniofacial skeleton, dermis, pericytes, fat cells, and tenocytes; and - the mesoderm, which yields muscles, blood vessel endothelia and some posterior cranial bones. The molecular players that orchestrate co-development of cephalic NC and mesodermal cells to properly construct the head of vertebrates remain poorly understood. In this regard, Six1 gene, a vertebrate homolog of Drosophila Sine Oculis, is known to be required for development of ear, nose, tongue and cranial skeleton. However, the embryonic origin and fate of Six1-expressing cells have remained unclear. In this work, we addressed these issues in the avian embryo model by using quail-chick chimeras, cephalic NC cultures and immunostaining for SIX1.ResultsOur data show that, at early NC migration stages, SIX1 is expressed by mesodermal cells but excluded from the NC cells (NCC). Then, SIX1 becomes widely expressed in NCC that colonize the pre-otic mesenchyme. In contrast, in the branchial arches (BAs), SIX1 is present only in mesodermal cells that give rise to jaw muscles. At later developmental stages, the distribution of SIX1-expressing cells in mesoderm-derived tissues is consistent with a possible role of this factor in the myogenic program of all types of head muscles, including pharyngeal, extraocular and tongue muscles. In NC derivatives, SIX1 is notably expressed in perichondrium and chondrocytes of the nasal septum and in the sclera, although other facial cartilages such as Meckel’s were negative at the stages considered. Moreover, in cephalic NC cultures, chondrocytes and myofibroblasts, not the neural and melanocytic cells express SIX1.ConclusionThe present results point to a dynamic tissue-specific expression of SIX1 in a variety of cephalic NC- and mesoderm-derived cell types and tissues, opening the way for further analysis of Six1 function in the coordinated development of these two cellular populations during vertebrate head formation.Electronic supplementary materialThe online version of this article (10.1186/s12861-017-0155-z) contains supplementary material, which is available to authorized users.
“…2 g and g’ ). This result is in agreement with recent findings showing that the SIX1-positive cells in the trigeminal ganglia are sensory neurons, which could belong to those of placodal origin in the mouse and chick embryos [ 44 , 47 ]. At the level of the anterior rhombencephalon, SIX1 transcripts were highly expressed in otic vesicles, pharynx and the periocular and pharyngeal mesenchyme (Fig.…”
Section: Resultssupporting
confidence: 93%
“…5 j, j’ ), while SIX1 appeared to be expressed in the sensory neurons (Fig. 5 j” ), in agreement with previous data [ 17 , 44 , 47 ]. Fig.…”
BackgroundVertebrate head development depends on a series of interactions between many cell populations of distinct embryological origins. Cranial mesenchymal tissues have a dual embryonic source: - the neural crest (NC), which generates most of craniofacial skeleton, dermis, pericytes, fat cells, and tenocytes; and - the mesoderm, which yields muscles, blood vessel endothelia and some posterior cranial bones. The molecular players that orchestrate co-development of cephalic NC and mesodermal cells to properly construct the head of vertebrates remain poorly understood. In this regard, Six1 gene, a vertebrate homolog of Drosophila Sine Oculis, is known to be required for development of ear, nose, tongue and cranial skeleton. However, the embryonic origin and fate of Six1-expressing cells have remained unclear. In this work, we addressed these issues in the avian embryo model by using quail-chick chimeras, cephalic NC cultures and immunostaining for SIX1.ResultsOur data show that, at early NC migration stages, SIX1 is expressed by mesodermal cells but excluded from the NC cells (NCC). Then, SIX1 becomes widely expressed in NCC that colonize the pre-otic mesenchyme. In contrast, in the branchial arches (BAs), SIX1 is present only in mesodermal cells that give rise to jaw muscles. At later developmental stages, the distribution of SIX1-expressing cells in mesoderm-derived tissues is consistent with a possible role of this factor in the myogenic program of all types of head muscles, including pharyngeal, extraocular and tongue muscles. In NC derivatives, SIX1 is notably expressed in perichondrium and chondrocytes of the nasal septum and in the sclera, although other facial cartilages such as Meckel’s were negative at the stages considered. Moreover, in cephalic NC cultures, chondrocytes and myofibroblasts, not the neural and melanocytic cells express SIX1.ConclusionThe present results point to a dynamic tissue-specific expression of SIX1 in a variety of cephalic NC- and mesoderm-derived cell types and tissues, opening the way for further analysis of Six1 function in the coordinated development of these two cellular populations during vertebrate head formation.Electronic supplementary materialThe online version of this article (10.1186/s12861-017-0155-z) contains supplementary material, which is available to authorized users.
“…Rigorous regulation of RA levels is crucial for normal development of multiple tissues and organs. Indeed, disruption of RA levels, or transcription of RA-regulated genes can lead to changes in anterior-posterior identity of hindbrain neurons and cranial nerves [126, 127]. Changes in RA signaling result in phenotypes similar to those in 22q11DS mouse models or patients [128–140].…”
Pediatric dysphagia—feeding and swallowing difficulties that begin at birth, last throughout childhood, and continue into maturity—is one of the most common, least understood complications in children with developmental disorders. We argue that a major cause of pediatric dysphagia is altered hindbrain patterning during pre-natal development. Such changes can compromise craniofacial structures including oropharyngeal muscles and skeletal elements as well as motor and sensory circuits necessary for normal feeding and swallowing. Animal models of developmental disorders that include pediatric dysphagia in their phenotypic spectrum can provide mechanistic insight into pathogenesis of feeding and swallowing difficulties. A fairly common human genetic developmental disorder, DiGeorge/22q11.2 Deletion Syndrome (22q11DS) includes a substantial incidence of pediatric dysphagia in its phenotypic spectrum. Infant mice carrying a parallel deletion to 22q11DS patients have feeding and swallowing difficulties. Altered hindbrain patterning, neural crest migration, craniofacial malformations, and changes in cranial nerve growth prefigure these difficulties. Thus, in addition to craniofacial and pharyngeal anomalies that arise independently of altered neural development, pediatric dysphagia may reflect disrupted hindbrain patterning and its impact on neural circuit development critical for feeding and swallowing. The mechanisms that disrupt hindbrain patterning and circuitry may provide a foundation to develop novel therapeutic approaches for improved clinical management of pediatric dysphagia.
“…Interestingly, some cranial ganglia are entirely derived from placodal cells, while the majority are of mixed placodal and neural crest origin. 47,48 Much like neural crest cell, placodal cells delaminate from the columnar ectodermal epithelium, migrate, and then aggregate to form or contribute to the cranial ganglia. 49 The vagus and glossopharyngeal nerves monitor oxygen, carbon dioxide, and pH in the carotid sinus and aortic arch, information which is then conveyed to visceral motor neurons in the brainstem to trigger appropriate homeostatic responses.…”
Section: Epibranchial Placodes Contribution To the Development Of Vismentioning
Investigations of the cellular and molecular mechanisms that mediate the development of the autonomic nervous system have identified critical genes and signaling pathways that, when disrupted, cause disorders of the autonomic nervous system. This review summarizes our current understanding of how the autonomic nervous system emerges from the organized spatial and temporal patterning of precursor cell migration, proliferation, communication, and differentiation, and discusses potential clinical implications for developmental disorders of the autonomic nervous system, including familial dysautonomia, Hirschsprung disease, Rett syndrome, and congenital central hypoventilation syndrome.
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