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Neural Crest Development (neural + crest_development)
Selected AbstractsSox genes regulate type 2 collagen expression in avian neural crest cellsDEVELOPMENT GROWTH & DIFFERENTIATION, Issue 8 2006Takashi Suzuki Neural crest cells give rise to a wide variety of cell types, including cartilage cells in the cranium and neurons and glial cells in the peripheral nervous system. To examine the relationship of cartilage differentiation and neural crest differentiation, we examined the expression of Col2a1, which encodes type 2 collagen often used as a cartilage marker, and compared it with the expression of Sox transcription factor genes, which are involved in neural crest development and chondrogenesis. We found that Col2a1 is expressed in many neural crest-derived cell types along with combinations of Sox9, Sox10 and LSox5. Overexpression studies reveal the activation of Col2a1 expression by Sox9 and Sox10, and cross-regulation of these Sox genes. Luciferase assay indicates a direct activation of the Col2a1 enhancer/promoter both by Sox9 and Sox10, and this activation is further enhanced by cAMP-dependent kinase (PKA) signaling. Our study suggests that the regulatory mechanisms are similar in cartilage and neural crest differentiation. [source] Wnt11r is required for cranial neural crest migrationDEVELOPMENTAL DYNAMICS, Issue 11 2008Helen K. Matthews Abstract wnt11r is a recently identified member of the Wnt family of genes, which has been proposed to be the true Xenopus homologue to the mammalian wnt11 gene. In this study we have examined the role of wnt11r on neural crest development. Expression analysis of wnt11r and comparison with the neural crest marker snail2 and the noncanonical Wnt, wnt11, shows wnt11r is expressed at the medial or neural plate side of the neural crest while wnt11 is expressed at the lateral or epidermal side. Injection of wnt11r morpholino leads to strong inhibition of neural crest migration with no effect on neural crest induction or maintenance. This effect can be rescued by co-injection of Wnt11r but not by Wnt11 mRNA, demonstrating the specificity of the loss of function treatment. Finally, neural crest graft experiments show that wnt11r is required in a non,cell-autonomous manner to control neural crest migration. Developmental Dynamics 237:3404,3409, 2008. © 2008 Wiley-Liss, Inc. [source] Bmp2 is required for migration but not for induction of neural crest cells in the mouseDEVELOPMENTAL DYNAMICS, Issue 9 2007Ana Catarina Correia Abstract Bone morphogenetic protein (BMP) signaling is essential for neural crest development in several vertebrates. Genetic experiments in the mouse have shown that Bmp2 is essential for the genesis of migratory neural crest cells. Using several markers and a transgenic reporter approach, we now show that neural crest cells are induced in Bmp2 null mutant embryos, but that these cells fail to migrate out of the neural tube. The absence of migratory neural crest cells in these mutants is not due to their elimination by cell death. The neuroectoderm of Bmp2,/, embryos fail to close and create abnormal folds both along the anterior,posterior and medio,lateral axes, which are associated with an apparent medio,lateral expansion of the neural tube. Finally, our data suggest that the molecular cascade downstream of BMP signaling in early neural crest development may be different in mouse and avian embryos. Developmental Dynamics 236:2493,2501, 2007. © 2007 Wiley-Liss, Inc. [source] Potential roles for BMP and Pax genes in the development of iris smooth muscleDEVELOPMENTAL DYNAMICS, Issue 2 2005Abbie M. Jensen Abstract The embryonic optic cup generates four types of tissue: neural retina, pigmented epithelium, ciliary epithelium, and iris smooth muscle. Remarkably little attention has focused on the development of the iris smooth muscle since Lewis ([1903] J. Am. Anat. 2:405,416) described its origins from the anterior rim of the optic cup neuroepithelium. As an initial step toward understanding iris smooth muscle development, I first determined the spatial and temporal pattern of the development of the iris smooth muscle in the chick by using the HNK1 antibody, which labels developing iris smooth muscle. HNK1 labeling shows that iris smooth muscle development is correlated in time and space with the development of the ciliary epithelial folds. Second, because neural crest is the only other neural tissue that has been shown to generate smooth muscle (Le Lievre and Le Douarin [1975] J. Embryo. Exp. Morphol. 34:125,154), I sought to determine whether iris smooth muscle development shares similarities with neural crest development. Two members of the BMP superfamily, BMP4 and BMP7, which may regulate neural crest development, are highly expressed by cells at the site of iris smooth muscle generation. Third, because humans and mice that are heterozygous for Pax6 mutations have no irides (Hill et al. [1991] Nature 354:522,525; Hanson et al. [1994] Nat. Genet. 6:168,173), I determined the expression of Pax6. I also examined the expression of Pax3 in the developing anterior optic cup. The developing iris smooth muscle coexpresses Pax6 and Pax3. I suggest that some of the eye defects caused by mutations in Pax6, BMP4, and BMP7 may be due to abnormal iris smooth muscle. Developmental Dynamics 232:385,392, 2005. © 2004 Wiley-Liss, Inc. [source] Cranial neural crest cell migration in the Australian lungfish, Neoceratodus forsteriEVOLUTION AND DEVELOPMENT, Issue 4 2000Pierre Falck SUMMARY A crucial role for the cranial neural crest in head development has been established for both actinopterygian fishes and tetrapods. It has been claimed, however, that the neural crest is unimportant for head development in the Australian lungfish (Neoceratodus forsteri ,), a member of the group (Dipnoi) which is commonly considered to be the living sister group of the tetrapods. In the present study, we used scanning electron microscopy to study cranial neural crest development in the Australian lungfish. Our results, contrary to those of Kemp, show that cranial neural crest cells do emerge and migrate in the Australian lungfish in the same way as in other vertebrates, forming mandibular, hyoid, and branchial streams. The major difference is in the timing of the onset of cranial neural crest migration. It is delayed in the Australian lungfish in comparison with their living sister group the Lissamphibia. Furthermore, the delay in timing between the emergence of the hyoid and branchial crest streams is very long, indicating a steeper anterior-posterior gradient than in amphibians. We are now extending our work on lungfish head development to include experimental studies (ablation of selected streams of neural crest cells) and fate mapping (using fluoresent tracer dyes such as DiI) to document the normal fate as well as the role in head patterning of the cranial neural crest in the Australian lungfish. [source] 2462: Phenotype/genotype in congenital central hypoventilation syndromeACTA OPHTHALMOLOGICA, Issue 2010D BREMOND-GIGNAC Purpose To report and to classify the ocular motility disorders in congenital central hypoventilation syndrome. This rare syndrome, 1 of 200,000 livebirths, is characterized by a lack of ventilation due to defects of autonomic control especially of hypercapnia. Methods We examine in a study 34 children (range 9 days-old to 15 yo) with congenital central hypoventilation syndrome. They underwent a complete ocular and orthoptic consultation. An informed consent was signed to perform a DNA analysis to precise PHOX-2B gene mutations. Results Anisocoria, stabismus, eso and exotropia or phoria, ptosis, craniofacial palsy were found and we evaluated disorders considering intrinsic ocular motility and extrinsic ocular motility. We classified ocular anomalies in minor and major types with a score. The phenotype score was established in correlation with genotype. The score is higher in patients with genotype of equal or more 7 ALA mutations and a precise table correlation was established. Conclusion The high incidence of ocular motility disorders may result of neurologic defects of the oculomotor nerves and muscles involving neural crest development. A precise phenotype contributes to an evaluation of the severity of the disease and can also lead to a better reeducation of oculomotor anomalies. [source] | ||||||||||