Role of the neural crest in face and brain development

Douarin, Nicole M. Le; Brito, José M.; Creuzet, Sophie

doi:10.1016/j.brainresrev.2007.06.023

Cited by 107 publications

(85 citation statements)

References 48 publications

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“…In recent work, we showed that after excision of Shh-expressing anterior foregut endoderm along with the entire forehead at early neurula stages (5-6 ss), the cephalic NCCs which colonize BA1 exiting from the mesencephalon migrated normally but were further on subjected to massive apoptosis, whereas Shh was not expressed in the pharyngeal endoderm. Fgf8 and Bmp4 transcripts were absent in BA1 ectoderm at E3-4 and the embryos were further deprived of Meckel's cartilage and lower jaw (Brito et al, 2006;Le Douarin et al, 2007). These data suggested that the ability of the anterior pharyngeal endoderm to instruct BA1 to form an ectopic lower beak (Couly et al, 2002) might be related to its capacity to produce Shh.…”

Section: Shh Signal Is Pivotal For the Development Of Meckel's Cartilmentioning

confidence: 96%

Induction of mirror-image supernumerary jaws in chicken mandibular mesenchyme by Sonic Hedgehog-producing cells

2008

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Previous studies have shown that Sonic Hedgehog (Shh) signaling is crucial for the development of the first branchial arch (BA1) into a lower-jaw in avian and mammalian embryos. We have already shown that if Shhexpression is precociously inhibited in pharyngeal endoderm, neural crest cells migrate to BA1 but fail to survive, and Meckel's cartilage and associated structures do not develop. This phenotype can be rescued by addition of an exogenous source of Shh. To decipher the role of Shh, we explored the consequences of providing an extra source of Shh to the presumptive BA1 territory. Grafting quail fibroblasts engineered to produce Shh (QT6-Shh), at the 5- to 8-somite stage, resulted in the induction of mirror-image extra lower jaws, caudolateral to the normal one. It turns out that the oral opening epithelium, in which Shh, Fgf8 and Bmp4 are expressed in a definite pattern, functions as an organizing center for lower-jaw development. In our experimental design, the extra source of Shh activates Fgf8, Bmp4 and Shh genes in caudal BA1 ectoderm in a spatial pattern similar to that of the oral epithelium, and regularly leads to the formation of two extra lower-jaw-organizing centers with opposite rostrocaudal polarities. These results emphasize the similarities between the developmental processes of the limb and mandibular buds, and show that in both cases Shh-producing cells create a zone of polarizing activity for the structures deriving from them.

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Section: Shh Signal Is Pivotal For the Development Of Meckel's Cartilmentioning

confidence: 96%

Induction of mirror-image supernumerary jaws in chicken mandibular mesenchyme by Sonic Hedgehog-producing cells

2008

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“…Cranial neural crest cells (CNCCs) emigrate from the caudal forebrain, midbrain and hindbrain to the level of the first somite and give rise to additional cell fates in comparison to trunk NCCs, contributing to cartilage, bone and connective tissue (Le Douarin et al, 2007;Santagati and Rijli, 2003). CNCCs migrate into the branchial arches (BAs), becoming NC-derived mesenchymal progenitor cells (MPCs), which produce cartilage and skeletogenic elements of the craniofacial region.…”

Section: Introductionmentioning

confidence: 99%

“…In particular, cells in BA1 and anterior domains are devoid of Hox gene expression, which allows formation of the chondrogenic and skeletal elements of the facial region (Creuzet et al, 2002;Kanzler et al, 1998;Minoux and Rijli, 2010). In addition to these intrinsic cues, CNCC fates are regulated by environmental signals, such as Tgfβ (Wurdak et al, 2006) and Fgf8 expressed from the facial and BA ectoderm (Le Douarin et al, 2007;Santagati and Rijli, 2003). As a consequence of such signaling, expression of the transcription factor Sox9 is upregulated in MPCs, while expression levels of the NC specifier gene and NC stem cell (NCSC) marker Sox10 decrease (John et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Ezh2 is required for neural crest-derived cartilage and bone formation

et al. 2014

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The emergence of craniofacial skeletal elements, and of the jaw in particular, was a crucial step in the evolution of higher vertebrates. Most facial bones and cartilage are generated during embryonic development by cranial neural crest cells, while an osteochondrogenic fate is suppressed in more posterior neural crest cells. Key players in this process are Hox genes, which suppress osteochondrogenesis in posterior neural crest derivatives. How this specific pattern of osteochondrogenic competence is achieved remains to be elucidated. Here we demonstrate that Hox gene expression and osteochondrogenesis are controlled by epigenetic mechanisms. Ezh2, which is a component of polycomb repressive complex 2 (PRC2), catalyzes trimethylation of lysine 27 in histone 3 (H3K27me3), thereby functioning as transcriptional repressor of target genes. Conditional inactivation of Ezh2 does not interfere with localization of neural crest cells to their target structures, neural development, cell cycle progression or cell survival. However, loss of Ezh2 results in massive derepression of Hox genes in neural crest cells that are usually devoid of Hox gene expression. Accordingly, craniofacial bone and cartilage formation is fully prevented in Ezh2 conditional knockout mice. Our data indicate that craniofacial skeleton formation in higher vertebrates is crucially dependent on epigenetic regulation that keeps in check inhibitors of an osteochondrogenic differentiation program.

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“…These cells follow preferentially a subectodermal route, contact the presumptive olfactory ectoderm at Hamburger Hamilton stage 10 (HH10) and remain in its close proximity up to HH18 (Couly and Le Douarin, 1990;Couly et al, 1993;Le Douarin et al, 2007). Then, neural crest-derived chondrogenic ectomesenchyme accumulates within the nasal prominences.…”

Section: Introductionmentioning

confidence: 99%

Dlx5 and Dlx6 expression in the anterior neural fold is essential for patterning the dorsal nasal capsule

et al. 2011

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SUMMARYMorphogenesis of the vertebrate facial skeleton depends upon inductive interactions between cephalic neural crest cells (CNCCs) and cephalic epithelia. The nasal capsule is a CNCC-derived cartilaginous structure comprising a ventral midline bar (mesethmoid) overlaid by a dorsal capsule (ectethmoid). Although Shh signalling from the anterior-most region of the endoderm (EZ-I) patterns the mesethmoid, the cues involved in ectethmoid induction are still undefined. Here, we show that ectethmoid formation depends upon Dlx5 and Dlx6 expression in a restricted ectodermal territory of the anterior neural folds, which we name NF-ZA. In both chick and mouse neurulas, Dlx5 and Dlx6 expression is mostly restricted to NF-ZA. Simultaneous Dlx5 and Dlx6 inactivation in the mouse precludes ectethmoid formation, while the mesethmoid is still present. Consistently, siRNA-mediated downregulation of Dlx5 and Dlx6 in the cephalic region of the early avian neurula specifically prevents ectethmoid formation, whereas other CNCC-derived structures, including the mesethmoid, are not affected. Similarly, NF-ZA surgical removal in chick neurulas averts ectethmoid development, whereas grafting a supernumerary NF-ZA results in an ectopic ectethmoid. Simultaneous ablation or grafting of both NF-ZA and EZ-I result, respectively, in the absence or duplication of both dorsal and ventral nasal capsule components. The present work shows that early ectodermal and endodermal signals instruct different contingents of CNCCs to form the ectethmoid and the mesethmoid, which then assemble to form a complete nasal capsule. phenotype has not been yet described in detail (Beverdam et al., 2002; Depew et al., 2002;Levi et al., 2003;Robledo et al., 2002). Noticeably, nasal defects in Dlx5/6 -/-heads are not shared with either single or compound mutations of other Dlx family members (Depew et al., 2005). A recent study has demonstrated that the olfactory pit plays a late role in controlling the morphogenesis of skeletal elements of the avian nasal capsule (Szabo-Rogers et al., 2009). These data were obtained from embryos in which CNCCs had already migrated into the developing olfactory territory and do not provide information about the initial interactions directing CNCCs towards ectethmoid formation. As the olfactory pit derives from the Dlx5/Dlx6-positive anterior part of the neural fold, we decided to explore the possibility that this territory could be endowed with early inductive capacities. Using mouse mutants and surgical and molecular analyses of chick embryos, we demonstrate that an anterior region of the neural fold ectoderm (NF-ZA) is the territory responsible for ectethmoid induction through a Dlx5/Dlx6-dependent mechanism.We conclude that the complete nasal capsule results from the juxtaposition of two independent structures formed by CNCCs competent to respond to different endodermal or ectodermal cues. MATERIALS AND METHODS Avian and mouse embryosAll animal procedures were approved by national and institutional ethical committees. Fertil...

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Role of the neural crest in face and brain development

Cited by 107 publications

References 48 publications

Induction of mirror-image supernumerary jaws in chicken mandibular mesenchyme by Sonic Hedgehog-producing cells

Induction of mirror-image supernumerary jaws in chicken mandibular mesenchyme by Sonic Hedgehog-producing cells

Ezh2 is required for neural crest-derived cartilage and bone formation

Dlx5 and Dlx6 expression in the anterior neural fold is essential for patterning the dorsal nasal capsule

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