The quail-chick chimera system (see Box 1) has been used over the years to establish a fate map of the NC along the neural axis. These studies have shown that melanocytes arise from the entire length of the NC in higher vertebrates, whereas mesectodermal derivatives originate only from the cephalic NC region. NC-derived cells that contribute to the PNS and ENS arise only from some areas of the neural axis (Fig. 1).Using the quail-chick system, well-defined areas of the NC have been exchanged to assess NCC plasticity (see Fig. 1). For example, in one study, the vagal region of the NC (which is located between somites 1 and 7, and gives rise to the enteric ganglia) was exchanged with NC from between somites 18 and 24 (which gives rise to the adrenal medulla and sympathetic ganglia) (Le Douarin and Teillet, 1974). This swap resulted Review 4638 in the normal colonisation of the suprarenal gland and sympathetic ganglia by NCCs fated to colonise the gut. However, although the adrenomedullary trunk NCCs invaded the pre-umbilical gut wall and differentiated into normal enteric plexuses, they failed to reach the post-umbilical bowel .This experimental system has since been used together with various molecular markers, such as the Schwann cell myelin protein (SMP), which is present on Schwann cells but not on other PNS and ENS glial cells, to allow a more refined analysis of NCC plasticity. These studies have shown that NCC differentiation into a specific type of glia depends upon the environment in which they develop (Dulac et al., 1988;Dulac and Le Douarin, 1991; Cameron-Curry et al., 1993). Similarly, the differentiation of the various types of autonomic neurons varies according to the milieu in which they differentiate (for reviews, see Le Douarin, 1982;Le Douarin and Kalcheim, 1999).The conclusion of these heterotopic grafting experiments was that the fate of the NCCs that form the PNS and ENS is not fully determined before these cells migrate, but instead remains plastic until they receive differentiation signals at the end of, and possibly during, their migration. This finding raised the issue of whether all the precursors of PNS ganglion cells became fully differentiated and/or committed soon after reaching their sites of arrest, or whether some remained as quiescent undifferentiated cells. This was explored in the experiments discussed in the following section. Undifferentiated precursors in PNS gangliaTo investigate the developmental potentials of PNS ganglion cells, fragments of sensory and autonomic ganglia from quail embryos, taken from embryonic day (E) 4 up to the end of the incubation period, were implanted into NCC migration pathways of E2 chick hosts when their own NCCs were migrating. The grafted neurons themselves died (probably because the necessary survival factors are not present in the younger host). However, the non-neuronal cells of implanted ganglia migrated and homed to host sensory and autonomic ganglia, where they differentiated into the types of neurons and glia corresponding to their novel...
Fgf8 exerts a strong effect on the mesenchymal cells of neural crest (NC) origin that are fated to form the facial skeleton. Surgical extirpation of facial skeletogenic NC domain (including mid-diencephalon down through rhombomere 2), which does not express Hox genes, results in the failure of facial skeleton development and inhibition of the closure of the forebrain neural tube, while Fgf8 expression in the telencephalon and in the branchial arch (BA) ectoderm is abolished. We demonstrate here that (i) exogenous FGF8 is able to rescue facial skeleton development by promoting the proliferation of NC cells from a single rhombomere, r3, which in normal development contributes only marginally to mesenchyme of BA1, and (ii) expression of Fgf8 in forebrain and in BA ectoderm is subjected to signal(s) arising from NC cells, thus showing that the development of cephalic NC-derived structures depends on FGF8 signaling, which is itself triggered by the NC cells.cephalic neural crest ͉ facial skeleton ͉ forebrain ͉ regeneration ͉ quail-chick chimeras I n vertebrates, the skeleton and connective components of the face are derived from the cephalic neural crest (NC), which can be divided into two domains. The first, a rostral domain, in which no Hox genes are expressed, extends from the presumptive level of the epiphysis down through the second rhombomere (r2); it yields the cartilages and membrane bones of the face (Fig. 1 A). It is referred to here as the facial skeletogenic NC (FSNC). The second, posterior domain (from r4 through r8) generates part of the hyoid cartilages and does not form any membrane bone. In this posterior domain of the NC, Hox genes of the four first paralogous groups are expressed both in neural tube and NC (1-3). A few NC cells (NCC) from r3 contribute to both domains. However, this contribution to branchial arches (BAs) is very small because most r3-derived NCC are undergoing apoptosis (4, 5).When the entire Hox-negative domain of the NC is removed, no facial structures develop, meaning that Hox-expressing NCC do not substitute for the Hox-negative ones (6, 7). In contrast, any fragment of the Hox-negative crest, grafted in the anterior cephalic region following the ablation of the FSNC, can regenerate a normal face (6). Thus, the Hox-negative crest behaves as an equivalence group showing that, at the early stages, the crest cells themselves do not possess the information to construct the specific bones and cartilages that constitute the facial skeleton. The ventrolateral endoderm of the foregut is able to provide the NCC with the information necessary for patterning the facial skeleton and also the hyoid cartilage (6,8). Later in development of the facial structures, the ectoderm of the facial process also participates in the final patterning of the beak (9, 10).The investigations reported here were prompted by the observation that removal of the FSNC resulted in a dramatic decrease of Fgf8 expression in the forebrain anlage, as well as in the BA ectoderm ( Fig. 1 B-E). This was followed by the t...
Studies carried out in the avian embryo and based on the construction of quail-chick chimeras have shown that most of the skull and all the facial and visceral skeleton are derived from the cephalic neural crest (NC). Contribution of the mesoderm is limited to its occipital and (partly) to its otic domains. NC cells (NCCs) participating in membrane bones and cartilages of the vertebrate head arise from the diencephalon (posterior half only), the mesencephalon and the rhombencephalon. They can be divided into an anterior domain (extending down to r2 included) in which genes of the Hox clusters are not expressed (Hox-negative skeletogenic NC) and a posterior domain including r4 to r8 in which Hox genes of the four first paraloguous groups are expressed. The NCCs that form the facial skeleton belong exclusively to the anterior Hox-negative domain and develop from the first branchial arch (BA1). This rostral domain of the crest is designated as FSNC for facial skeletogenic neural crest.Rhombomere 3 (r3) participates modestly to both BA1 and BA2. Forced expression of Hox genes (Hoxa2, Hoxa3 and Hoxb4) in the neural fold of the anterior domain inhibits facial skeleton development. Similarly, surgical excision of these anterior Hox-negative NCCs results in the absence of facial skeleton, showing that Hox-positive NCCs cannot replace the Hox-negative domain for facial skeletogenesis. We also show that excision of the FSNC results in dramatic down-regulation of Fgf8 expression in the head, namely in ventral forebrain and in BA1 ectoderm. We have further demonstrated that exogenous FGF8 applied to the presumptive BA1 territory at the 5-6-somite stage (5-6ss) restores to a large extent facial skeleton development. The source of the cells responsible for this regeneration was shown to be r3, which is at the limit between the Hox-positive and Hox-negative domain. NCCs that respond to FGF8 by survival and proliferation are in turn necessary for the expression/maintenance of Fgf8 expression in the ectoderm. These results strongly support the emerging picture according to which the processes underlying morphogenesis of the craniofacial skeleton are regulated by epithelial-mesenchymal bidirectional crosstalk.
In vertebrates, the eye is an ectodermal compound structure associating neurectodermal and placodal anlagen. In addition, it benefits early on from a mesenchymal ectoderm-derived component, the neural crest. In this respect, the construction of chimeras between quail and chick has been a turning point, instrumental in appraising the contribution of the cephalic neural crest to the development of ocular and periocular structures. Given the variety of crest derivatives underscored in the developing eye, this study illustrates the fascinating ability of this unique structure to finely adapt its differentiation to microenvironmental cues. This analysis of neural crest cell contribution to ocular development emphasizes their paramount role to design the anterior segment of the eye, supply refracting media and contribute to the homeostasy of the anterior optic chamber.
Hyoid bone is a part of the visceral skeleton which arises from both Hox-expressing (Hox؉) and Hox-nonexpressing (Hox-) cephalic neural crest cells. In a previous work, we have demonstrated that the Hox-neural crest domain behaves as a naïve entity to which the ventral foregut endoderm confers patterning cues to specify the shape and orientation of the nasal and mandibular skeleton. By using ablation and grafting approaches, we have extended our study to the formation of the hyoid bone and tested the patterning ability of more caudal levels of the lateroventral foregut endoderm in the chick embryo at the early neurula stage. In this study, endodermal stripes have first been delineated according to the projection of mid-and posterior rhombencephalic structures. The extirpation of endodermal transverse stripes along the anteroposterior axis selectively hampers the formation of the ceratobranchials and epibranchials. Thus defined, the patterning ability of the endodermal stripes was further explored in their medial and lateral parts. When homotopically engrafted on the migration pathway of cephalic neural crest cells, ventromedial zones of endoderm lead to the formation of supernumerary basihyal and basibranchial, while lateral zones generate additional cartilaginous pieces recognizable as ceratobranchial and epibranchial. Taken together, our data demonstrate that, early in development, the ventral foregut endoderm exerts a regionalized patterning activity on the cephalic neural crest to build up the primary facial and visceral skeleton in jaws and neck and enable a map of the endodermal skeletogenic areas to be drawn. This map reveals that a cryptic metamerization of the anterior foregut endoderm precedes the formation of the branchial arches. Developmental Dynamics 228: 239 -246, 2003.
Since the time of Ramon y Cajal, very significant progress has been accomplished in our knowledge of the fate of the early neural primordium. The origin of the peripheral nervous system from the transient and pluripotent embryonic structure, the neural crest has been fully deciphered using appropriate cell marking techniques. Most of the pioneer work in this field was carried out in lower vertebrates up to 1950 and later on in the avian embryo. New techniques which allow the genetic labelling of embryonic cells by transgenesis are now applied in mammals and fish. One of the highlights of neural crest studies was its paramount role in head and face morphogenesis. Work pursued in our laboratory for the last fifteen years or so has analysed at both cellular and molecular levels the contribution of the NCCs to the construction of the facial and cranial structures. Recently, we have found that the cephalic neural crest plays also a key role in the formation of the fore- and mid-brain.
Encephalisation is the most important characteristic in the evolutionary transition leading from protochordates to vertebrates. This event has coincided with the emergence of a transient and pluripotent structure, the neural crest (NC), which is absent in protochordates. In vertebrates, NC provides the rostral cephalic vesicles with skeletal protection and functional vascularization. The surgical extirpation of the cephalic NC, which is responsible for building up the craniofacial skeleton, results in the absence of facial skeleton together with severe defects of preotic brain development, leading to exencephaly. Here, we have analyzed the role of the NC in forebrain and midbrain development. We show that (i) NC cells (NCC) control Fgf8 expression in the anterior neural ridge, which is considered the prosencephalic organizer; (ii) the cephalic NCC are necessary for the closure of the neural tube; and (iii) NCC contribute to the proper patterning of genes that are expressed in the prosencephalic and mesencephalic alar plate. Along with the development of the roof plate, NCC also concur to the patterning of the pallial and subpallial structures. We show that the NC-dependent production of FGF8 in anterior neural ridge is able to restrict Shh expression to the ventral prosencephalon. All together, these findings support the notion that the cephalic NC controls the formation of craniofacial structures and the development of preotic brain.Fgf8 ͉ exencephaly ͉ preotic vesicles ͉ prosencephalic organizer ͉ quail-chick chimeras F ate mapping experiments conducted in the avian embryo and based on the construction of quail chick chimeras have led to the notion that the facial and hypobranchial skeletons are derived from neural crest (NC) cells (NCC) migrating from the mid-diencephalon down to rhombomere (r)8 (1, 2). This domain is divided into two parts. The rostral part yields the entire facial skeleton, designated facial skeletogenic NC (FSNC), in which no genes of Hox clusters are expressed, and the posterior part yields the middle and posterior parts of the hyoid bone, in which Hox genes of the four first paralogue groups are expressed (Fig. 3, which is published as supporting information on the PNAS web site). The limit between these two domains corresponds to r3, the NCC of which play a pivotal role between the rostral Hoxnegative and the caudal Hox-positive NCC populations (3-6). Some r3 NCC migrate to branchial arch (BA)1, whereas others diverge to participate in BA2. The former lose their Hoxa2 expression during the migration, whereas the latter maintain it within the BA2 environment.Experiments in which the Hox-negative neural fold (NF) was removed before NCC emigration (Fig. 1 A-C) resulted in the complete absence of facial skeleton, whereas only a third of the anterior, Hox-negative territory left in situ (or grafted from quail to chick) was sufficient to generate a complete face. These and other data (7-9) led us to consider that Hox-positive cephalic NCC cannot substitute for their Hox-negative counterpart i...
As a transitory structure providing adult tissues of the vertebrates with very diverse cell types, the neural crest (NC) has attracted for long the interest of developmental biologists and is still the subject of ongoing research in a variety of animal models. Here we review a number of data from in vivo cell tracing and in vitro single cell culture experiments, which gained new insights on the mechanisms of cell migration, proliferation and differentiation during NC ontogeny. We put emphasis on the role of Hox genes, morphogens and interactions with neighbouring tissues in specifying and patterning the skeletogenic NC cells in the head. We also include advances made towards characterizing multipotent stem cells in the early NC as well as in various NC derivatives in embryos and even in adult.
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