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Cranial Neural Crest Cells (cranial + neural_crest_cell)
Selected AbstractsGenetic disruption of CYP26B1 severely affects development of neural crest derived head structures, but does not compromise hindbrain patterningDEVELOPMENTAL DYNAMICS, Issue 3 2009Glenn Maclean Abstract Cyp26b1 encodes a cytochrome-P450 enzyme that catabolizes retinoic acid (RA), a vitamin A derived signaling molecule. We have examined Cyp26b1,/, mice and report that mutants exhibit numerous abnormalities in cranial neural crest cell derived tissues. At embryonic day (E) 18.5 Cyp26b1,/, animals exhibit a truncated mandible, abnormal tooth buds, reduced ossification of calvaria, and are missing structures of the maxilla and nasal process. Some of these abnormalities may be due to defects in formation of Meckel's cartilage, which is truncated with an unfused distal region at E14.5 in mutant animals. Despite the severe malformations, we did not detect any abnormalities in rhombomere segmentation, or in patterning and migration of anterior hindbrain derived neural crest cells. Abnormal migration of neural crest cells toward the posterior branchial arches was observed, which may underlie defects in larynx and hyoid development. These data suggest different periods of sensitivity of anterior and posterior hindbrain neural crest derivatives to elevated levels of RA in the absence of CYP26B1. Developmental Dynamics 238:732,745, 2009. © 2009 Wiley-Liss, Inc. [source] Teratogenic effect of bis-diamine on embryonic rat heartCONGENITAL ANOMALIES, Issue 3 2000Masao Nakagawa ABSTRACT, Bis-diamine induces conotruncal anomalies including persistent truncus arteriosus, tetralogy of Fallot, interruption of the aortic arch, and ventricular septal defect in rat embryos when administered to the mother. Bis-diamine also induces extracardiac malformations including thymic hypoplasia, facial dysmorphism, forelimb anomalies and diaphragmatic hernia. However, the teratogenic mechanisms of this chemical in early developing rat hearts have not been fully established. Chimeric studies in chick and quail embryos demonstrated that the cranial neural crest cells reached the cardiac outflow tract, contributing to aorticopulmonary and truncal septation. Since an ablation of the cranial neural crest also produced the conotruncal anomalies, bis-diamine is proposed to disturb the normal migration of cardiac neural crest cells to the heart. Based on our data concerning cardiac anomalies induced by bis-diamine, we reviewed how the cardiac malformations were morphologically established in early developing rat hearts. Our data showed that 1) cardiovascular anomalies induced by bis-diamine are time- and species or strain- dependent. 2) bis-diamine reduces the number of neural crest cells migrating to participate in the conotruncal septation, 3) bis-diamine induces anomalous coronary arteries, thin ventricular walls and epicardial defects, and 4) some embryos cultured in the medium containing bis-diamine had extra-cardiac abnormalities including abnormal location of the otic placodes and delay in mid brain closure. Conclusively, bis-diamine does not appear to merely affect the cardiac development, but rather disturbs normal development of all the organs contributed to by neural crest cells. [source] Differential expression of sphingosine-1-phosphate receptors 1-5 in the developing nervous systemDEVELOPMENTAL DYNAMICS, Issue 2 2009H. Meng Abstract Sphingosine-1-phosphate (S1P) binds to G protein,coupled receptors and can regulate a wide range of cellular functions. In a previous study, we isolated two key enzymes in the S1P pathway that were expressed in migrating neural crest cells. To determine if S1P receptors are present in neural crest cells or peripheral nervous system, we examine the expression patterns of S1P receptors (S1pr1-5) in mouse, and s1pr1 and s1pr3 in chick embryos. Here, we present a comprehensive expression analysis of these receptors using in situ hybridizations, which provide spatiotemporal information. We showed that S1pr2 was expressed in migrating cranial neural crest cells and enteric neurons. S1pr1 was prominently expressed in the neuroepithelium whereas S1pr4 and S1pr5 were in neurons at later stages. On the contrary, S1pr3 was predominantly detected in non-neuronal cells within and surrounding neural structures. We also described novel expression sites for S1P receptors in the developing nervous system. Developmental Dynamics 238:487,500, 2009. © 2009 Wiley-Liss, Inc. [source] Recent advances in craniofacial morphogenesisDEVELOPMENTAL DYNAMICS, Issue 9 2006Yang Chai Abstract Craniofacial malformations are involved in three fourths of all congenital birth defects in humans, affecting the development of head, face, or neck. Tremendous progress in the study of craniofacial development has been made that places this field at the forefront of biomedical research. A concerted effort among evolutionary and developmental biologists, human geneticists, and tissue engineers has revealed important information on the molecular mechanisms that are crucial for the patterning and formation of craniofacial structures. Here, we highlight recent advances in our understanding of evo,devo as it relates to craniofacial morphogenesis, fate determination of cranial neural crest cells, and specific signaling pathways in regulating tissue,tissue interactions during patterning of craniofacial apparatus and the morphogenesis of tooth, mandible, and palate. Together, these findings will be beneficial for the understanding, treatment, and prevention of human congenital malformations and establish the foundation for craniofacial tissue regeneration. Developmental Dynamics 235:2353,2375, 2006. © 2006 Wiley-Liss, Inc. [source] Expression of chondrogenic potential of mouse trunk neural crest cells by FGF2 treatmentDEVELOPMENTAL DYNAMICS, Issue 2 2006Atsushi Ido Abstract There is a significant difference between the developmental patterns of cranial and trunk neural crest cells in the amniote. Thus, whereas cranial neural crest cells generate bone and cartilage, trunk neural crest cells do not contribute to skeletal derivatives. We examined whether mouse trunk neural crest cells can undergo chondrogenesis to analyze how the difference between the developmental patterns of cranial and trunk neural crest cells arises. Our present data demonstrate that mouse trunk neural crest cells have chondrogenic potential and that fibroblast growth factor (FGF) 2 is an inducing factor for their chondrogenesis in vitro. FGF2 altered the expression patterns of Hox9 genes and Id2, a cranial neural crest cell marker. These results suggest that environmental cues may play essential roles in generating the difference between developmental patterns of cranial and trunk neural crest cells. Developmental Dynamics 235:361,367, 2006. © 2005 Wiley-Liss, Inc. [source] Cell fate and timing in the evolution of neural crest and mesoderm development in the head region of amphibians and lungfishesACTA ZOOLOGICA, Issue 2009Rolf Ericsson Abstract Our research on the evolution of head development focuses on understanding the developmental origins of morphological innovations and involves asking questions like: How flexible (or conserved) are cell fates, patterns of cell migration or the timing of developmental events (heterochrony)? How do timing changes, or changes in life history affect head development and growth? Our ,model system' is a comparison between lungfishes and representatives from all three extant groups of amphibians. Within anuran amphibians, major changes in life history such as the repeated evolution of larval specializations (e.g. carnivory), or indeed the loss of a free-swimming larva, allows us to test for developmental constraints. Cell migration and cell fate are conserved in cranial neural crest cells in all vertebrates studied so far. Patterning and developmental anatomy of cranial neural crest and head mesoderm cells are conserved within amphibians and even between birds, mammals and amphibians. However, the specific formation of hypobranchial muscles from ventral somitic processes shows variation within tetrapods. The evolution of carnivorous larvae in terminal taxa is correlated with changes in both pattern and timing of head skeletal and muscle development. Sequence-heterochronic changes are correlated with feeding mode in terminal taxa and with phylogenetic relatedness in basal branches of the phylogeny. Eye muscles seem to form a developmental module that can evolve relatively independently from other head muscles, at least in terms of timing of muscle differentiation. [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] The function of the Egr1 transcription factor in cartilage formation and adaptation to microgravity in zebrafish, Danio rerioJOURNAL OF APPLIED ICHTHYOLOGY, Issue 2 2010M. Muller Summary Osteoporosis is one of the major concerns for an ageing human population and for passengers on long-term space flights. Teleosts represent a potentially interesting alternative for studying bone physiology. In zebrafish (Danio rerio), the cartilaginous elements that form the pharyngeal arches derive from cranial neural crest cells, whose proper patterning and morphogenesis require reciprocal interactions with other tissue types such as pharyngeal endoderm, ectoderm and mesoderm. We show how the zebrafish can be used to study the function of signal transduction pathways, such as the Fgf pathway, or that of particular genes, such as the zinc finger transcription factor Egr1, in pharyngeal skeleton formation and maintenance. We investigate the changes caused by microgravity and chemical treatments on zebrafish. We analyze early gene expression modification using whole genome microarray experiments and the long-term consequences by staining bone structures. [source] Fetal alcohol syndrome and developing craniofacial and dental structures , a reviewORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 4 2006LB Sant'Anna Structured abstract Authors ,, Sant'Anna LB, Tosello DO Objectives ,, Fetal alcohol syndrome (FAS) is a collection of signs and symptoms seen in children exposed to alcohol in the prenatal period. It is characterized mainly by a distinct pattern of craniofacial malformations, physical and mental retardation. However, with the increased incidence of FAS, there is a great variation in the clinical features of FAS. Design ,, Narrative review. Results ,, This review describes data from clinical and experimental studies, and in vitro models. Experimental studies have shown that alcohol has a direct toxic effect on the ectodermal and mesodermal cells of the developing embryo, particularly in the cells destined to give rise to dentofacial structures (i.e. cranial neural crest cells). Other effects, such as, abnormal pattern of cranial and mandibular growth and altered odontogenesis are described in detail. The exact mechanism by which alcohol induces its teratogenic effects remains still unknown. The possible mechanisms are outlined here, with an emphasis on the developing face and tooth. Possible future research directions and treatment strategies are also discussed. Conclusion ,, Early identification of children affected by prenatal alcohol exposure leads to interventions, services, and improved outcomes. FAS can be prevented with the elimination of alcohol consumption during pregnancy. We need to provide education, target high-risk groups, and make this issue a high priority in terms of public health. [source] | ||||||||||