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Skeletogenic Fate of Zebrafish Cranial and Trunk Neural Crest  [PDF]
Erika Kague, Michael Gallagher, Sally Burke, Michael Parsons, Tamara Franz-Odendaal, Shannon Fisher
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047394
Abstract: The neural crest (NC) is a major contributor to the vertebrate craniofacial skeleton, detailed in model organisms through embryological and genetic approaches, most notably in chick and mouse. Despite many similarities between these rather distant species, there are also distinct differences in the contribution of the NC, particularly to the calvariae of the skull. Lack of information about other vertebrate groups precludes an understanding of the evolutionary significance of these differences. Study of zebrafish craniofacial development has contributed substantially to understanding of cartilage and bone formation in teleosts, but there is currently little information on NC contribution to the zebrafish skeleton. Here, we employ a two–transgene system based on Cre recombinase to genetically label NC in the zebrafish. We demonstrate NC contribution to cells in the cranial ganglia and peripheral nervous system known to be NC–derived, as well as to a subset of myocardial cells. The indelible labeling also enables us to determine NC contribution to late–forming bones, including the calvariae. We confirm suspected NC origin of cartilage and bones of the viscerocranium, including cartilages such as the hyosymplectic and its replacement bones (hymandibula and symplectic) and membranous bones such as the opercle. The cleithrum develops at the border of NC and mesoderm, and as an ancestral component of the pectoral girdle was predicted to be a hybrid bone composed of both NC and mesoderm tissues. However, we find no evidence of a NC contribution to the cleithrum. Similarly, in the vault of the skull, the parietal bones and the caudal portion of the frontal bones show no evidence of NC contribution. We also determine a NC origin for caudal fin lepidotrichia; the presumption is that these are derived from trunk NC, demonstrating that these cells have the ability to form bone during normal vertebrate development.
Phenothiourea Sensitizes Zebrafish Cranial Neural Crest and Extraocular Muscle Development to Changes in Retinoic Acid and IGF Signaling  [PDF]
Brenda L. Bohnsack, Donika Gallina, Alon Kahana
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0022991
Abstract: 1-phenyl 2-thiourea (PTU) is a tyrosinase inhibitor commonly used to block pigmentation and aid visualization of zebrafish development. At the standard concentration of 0.003% (200 μM), PTU inhibits melanogenesis and reportedly has minimal other effects on zebrafish embryogenesis. We found that 0.003% PTU altered retinoic acid and insulin-like growth factor (IGF) regulation of neural crest and mesodermal components of craniofacial development. Reduction of retinoic acid synthesis by the pan-aldehyde dehydrogenase inhibitor diethylbenzaldehyde, only when combined with 0.003% PTU, resulted in extraocular muscle disorganization. PTU also decreased retinoic acid-induced teratogenic effects on pharyngeal arch and jaw cartilage despite morphologically normal appearing PTU-treated controls. Furthermore, 0.003% PTU in combination with inhibition of IGF signaling through either morpholino knockdown or pharmacologic inhibition of tyrosine kinase receptor phosphorylation, disrupted jaw development and extraocular muscle organization. PTU in and of itself inhibited neural crest development at higher concentrations (0.03%) and had the greatest inhibitory effect when added prior to 22 hours post fertilization (hpf). Addition of 0.003% PTU between 4 and 20 hpf decreased thyroxine (T4) in thyroid follicles in the nasopharynx of 96 hpf embryos. Treatment with exogenous triiodothyronine (T3) and T4 improved, but did not completely rescue, PTU-induced neural crest defects. Thus, PTU should be used with caution when studying zebrafish embryogenesis as it alters the threshold of different signaling pathways important during craniofacial development. The effects of PTU on neural crest development are partially caused by thyroid hormone signaling.
Emergence and migration of trunk neural crest cells in a snake, the California Kingsnake (Lampropeltis getula californiae)
Michelle Reyes, Katrina Zandberg, Iska Desmawati, Maria E de Bellard
BMC Developmental Biology , 2010, DOI: 10.1186/1471-213x-10-52
Abstract: In this study, we show for the first time ever trunk neural crest migration in a snake by labeling it with DiI and immunofluorescence. As in birds and mammals, we find that early migrating trunk neural crest cells use both a ventromedial pathway and an inter-somitic pathway in the snake. However, unlike birds and mammals, we also observed large numbers of late migrating neural crest cells utilizing the inter-somitic pathway in snake.We found that while trunk neural crest migration in snakes is very similar to that of other amniotes, the inter-somitic pathway is used more extensively by late-migrating trunk neural crest cells in snake.The neural crest is a group of multipotent cells that emerge after an epithelial-to-mesenchymal transition from the dorsal neural tube early after neural tube closure. These cells give rise to a wide variety of neuronal and glial derivatives in the peripheral nervous system, as well as parts of the head skeleton and endocrine organs [1,2]. In jawed, anamniote vertebrates like sharks and teleosts, neural crest cells also give rise to electrosensory organs [3] and fin mesenchyme [4]. The neural crest in the trunk portion of an embryo has been found to follow different migratory pathways in different organisms. In amniotes trunk neural crest cells will follow two main courses: a ventromedial pathway through the rostral part of somites, and a dorsolateral pathway between somites and ectoderm [5]. In amphibians, trunk neural crest follows a dorsal pathway into the fin and a ventral pathway between the neural tube and the caudal portion of the somite [6]. In zebrafish, trunk neural crest predominantly migrates between the neural tube and somites as in amphibians [7,8].The origin of the neural crest was an important event in vertebrate given that it forms most of the craniofacial skeleton [9]. Agnathans (like lampreys) [10,11], teleosts (bony fish) and amphibians clearly possess identifiable cranial neural crest streams that are similar to tho
An Essential Role of Variant Histone H3.3 for Ectomesenchyme Potential of the Cranial Neural Crest  [PDF]
Samuel G. Cox,Hyunjung Kim,Aaron Timothy Garnett,Daniel Meulemans Medeiros,Woojin An,J. Gage Crump
PLOS Genetics , 2012, DOI: 10.1371/journal.pgen.1002938
Abstract: The neural crest (NC) is a vertebrate-specific cell population that exhibits remarkable multipotency. Although derived from the neural plate border (NPB) ectoderm, cranial NC (CNC) cells contribute not only to the peripheral nervous system but also to the ectomesenchymal precursors of the head skeleton. To date, the developmental basis for such broad potential has remained elusive. Here, we show that the replacement histone H3.3 is essential during early CNC development for these cells to generate ectomesenchyme and head pigment precursors. In a forward genetic screen in zebrafish, we identified a dominant D123N mutation in h3f3a, one of five zebrafish variant histone H3.3 genes, that eliminates the CNC–derived head skeleton and a subset of pigment cells yet leaves other CNC derivatives and trunk NC intact. Analyses of nucleosome assembly indicate that mutant D123N H3.3 interferes with H3.3 nucleosomal incorporation by forming aberrant H3 homodimers. Consistent with CNC defects arising from insufficient H3.3 incorporation into chromatin, supplying exogenous wild-type H3.3 rescues head skeletal development in mutants. Surprisingly, embryo-wide expression of dominant mutant H3.3 had little effect on embryonic development outside CNC, indicating an unexpectedly specific sensitivity of CNC to defects in H3.3 incorporation. Whereas previous studies had implicated H3.3 in large-scale histone replacement events that generate totipotency during germ line development, our work has revealed an additional role of H3.3 in the broad potential of the ectoderm-derived CNC, including the ability to make the mesoderm-like ectomesenchymal precursors of the head skeleton.
Ets-1 Confers Cranial Features on Neural Crest Delamination  [PDF]
Eric Théveneau, Jean-Loup Duband, Muriel Altabef
PLOS ONE , 2007, DOI: 10.1371/journal.pone.0001142
Abstract: Neural crest cells (NCC) have the particularity to invade the environment where they differentiate after separation from the neuroepithelium. This process, called delamination, is strikingly different between cranial and trunk NCCs. If signalings controlling slow trunk delamination start being deciphered, mechanisms leading to massive and rapid cranial outflow are poorly documented. Here, we show that the chick cranial NCCs delamination is the result of two events: a substantial cell mobilization and an epithelium to mesenchyme transition (EMT). We demonstrate that ets-1, a transcription factor specifically expressed in cranial NCCs, is responsible for the former event by recruiting massively cranial premigratory NCCs independently of the S-phase of the cell cycle and by leading the gathered cells to straddle the basal lamina. However, it does not promote the EMT process alone but can cooperate with snail-2 (previously called slug) to this event. Altogether, these data lead us to propose that ets-1 plays a pivotal role in conferring specific cephalic characteristics on NCC delamination.
Retinoic Acid Upregulates Ret and Induces Chain Migration and Population Expansion in Vagal Neural Crest Cells to Colonise the Embryonic Gut  [PDF]
Johanna E. Simkin, Dongcheng Zhang, Benjamin N. Rollo, Donald F. Newgreen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0064077
Abstract: Vagal neural crest cells (VNCCs) arise in the hindbrain, and at (avian) embryonic day (E) 1.5 commence migration through paraxial tissues to reach the foregut as chains of cells 1–2 days later. They then colonise the rest of the gut in a rostrocaudal wave. The chains of migrating cells later resolve into the ganglia of the enteric nervous system. In organ culture, E4.5 VNCCs resident in the gut (termed enteric or ENCC) which have previously encountered vagal paraxial tissues, rapidly colonised aneural gut tissue in large numbers as chains of cells. Within the same timeframe, E1.5 VNCCs not previously exposed to paraxial tissues provided very few cells that entered the gut mesenchyme, and these never formed chains, despite their ability to migrate in paraxial tissue and in conventional cell culture. Exposing VNCCs in vitro to paraxial tissue normally encountered en route to the foregut conferred enteric migratory ability. VNCC after passage through paraxial tissue developed elements of retinoic acid signalling such as Retinoic Acid Binding Protein 1 expression. The paraxial tissue's ability to promote gut colonisation was reproduced by the addition of retinoic acid, or the synthetic retinoid Am80, to VNCCs (but not to trunk NCCs) in organ culture. The retinoic acid receptor antagonist CD 2665 strongly reduced enteric colonisation by E1.5 VNCC and E4.5 ENCCs, at a concentration suggesting RARα signalling. By FACS analysis, retinoic acid application to vagal neural tube and NCCs in vitro upregulated Ret; a Glial-derived-neurotrophic-factor receptor expressed by ENCCs which is necessary for normal enteric colonisation. This shows that early VNCC, although migratory, are incapable of migrating in appropriate chains in gut mesenchyme, but can be primed for this by retinoic acid. This is the first instance of the characteristic form of NCC migration, chain migration, being attributed to the application of a morphogen.
The role of the neural crest in the normal and abnormal heart development  [PDF]
Mashtalir M.A.,Tverdokhleb I.V.,Kozlov V.A.
Морфолог?я , 2007,
Abstract: The data about participation of the neural crest in the normal and abnormal cardiogenesis are summarized in the review. The main morphological phenomena which accompany the interaction of the neural crest cells and embryonic heart are the migration of the dense mesenchyme originated from neural crest from pharyngeal arches to the trunk of heart as well as apoptotic processes. After chemical teratogens treatment such as retinoic acid and ethyl alcohol the distant relationship between neural crest and heart and also the migration of neural crest cells to the heart were changed. The decrease of inten-sity of the apoptotic processes in the heart, the delay of reduction of the conotruncal and atrioventricular myocardium and lesion of mesenchyme structures were determined morphologically. The ethanol and retinoic acid treatment cause also the abnormalities in the interventricular foramen closure, in the development of conductive system, and heart valves. We suggest that these abnormalities are mediated by the neural crest cells.
Histone deacetylase-4 is required during early cranial neural crest development for generation of the zebrafish palatal skeleton
April DeLaurier, Yukio Nakamura, Ingo Braasch, Vishesh Khanna, Hiroyuki Kato, Shigeyuki Wakitani, John H. Postlethwait, Charles B. Kimmel
BMC Developmental Biology , 2012, DOI: 10.1186/1471-213x-12-16
Abstract: We identify hdac4 in zebrafish and characterize its function in craniofacial morphogenesis. The gene is present as a single copy, and the deduced Hdac4 protein sequence shares all known functional domains with human HDAC4. The zebrafish hdac4 transcript is widely present in migratory cranial neural crest (CNC) cells of the embryo, including populations migrating around the eye, which previously have been shown to contribute to the formation of the palatal skeleton of the early larva. Embryos injected with hdac4 morpholinos (MO) have reduced or absent CNC populations that normally migrate medial to the eye. CNC-derived palatal precursor cells do not recover at the post-migratory stage, and subsequently we found that defects in the developing cartilaginous palatal skeleton correlate with reduction or absence of early CNC cells. Palatal skeletal defects prominently include a shortened, clefted, or missing ethmoid plate, and are associated with a shortening of the face of young larvae.Our results demonstrate that Hdac4 is a regulator of CNC-derived palatal skeletal precursors during early embryogenesis. Cleft palate resulting from HDAC4 mutations in human patients may result from defects in a homologous CNC progenitor cell population.
Divergent roles for Eph and Ephrin in Avian Cranial Neural Crest
Dan O Mellott, Robert D Burke
BMC Developmental Biology , 2008, DOI: 10.1186/1471-213x-8-56
Abstract: To distinguish neural crest from bordering ectoderm and head mesenchyme, we have co-labelled embryos for Eph or ephrin RNA and a neural crest marker protein. Throughout their migration avian cranial neural crest cells express EphA3, EphA4, EphA7, EphB1, and EphB3 and move along pathways bordered by non-neural crest cells expressing ephrin-B1. In addition, avian cranial neural crest cells express ephrin-B2 and migrate along pathways bordered by non-neural crest cells expressing EphB2. Thus, the distribution of avian Eph receptors and ephrins differs from those reported in other vertebrates. In stripe assays when explanted cranial neural crest were given the choice between FN or FN plus clustered ephrin-B1 or EphB2 fusion protein, the cells strongly localize to lanes containing only FN. This preference is mitigated in the presence of soluble ephrin-B1 or EphB2 fusion protein.These findings show that avian cranial neural crest use Eph and ephrin receptors as other vertebrates in guiding migration. However, the Eph receptors are expressed in different combinations by neural crest destined for each branchial arch and ephrin-B1 and ephrin-B2 appear to have opposite roles to those reported to guide cranial neural crest migration in mice. Unlike many of the signalling, specification, and effector pathways of neural crest, the roles of Eph receptors and ephrins have not been rigorously conserved. This suggests diversification of receptor and ligand expression is less constrained, possibly by promiscuous binding and use of common downstream pathways.A defining feature of vertebrates is the neural crest (NC), a transient group of cells that originate within the dorsal neuroectoderm of the neural tube during embryonic development [1]. Following an epithelial to mesenchyme transition in which they lose affinity for the neuroectodermal epithelium, NC cells individualize and gain the capacity to migrate through the underlying mesoderm. Hindbrain cranial neural crest (CNC) cells mi
An Assessment of the Long-Term Effects of Simulated Microgravity on Cranial Neural Crest Cells in Zebrafish Embryos with a Focus on the Adult Skeleton  [PDF]
Sara C. Edsall, Tamara A. Franz-Odendaal
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0089296
Abstract: It is becoming increasingly important to address the long-term effects of exposure to simulated microgravity as the potential for space tourism and life in space become prominent topics amongst the World’s governments. There are several studies examining the effects of exposure to simulated microgravity on various developmental systems and in various organisms; however, few examine the effects beyond the juvenile stages. In this study, we expose zebrafish embryos to simulated microgravity starting at key stages associated with cranial neural crest cell migration. We then analyzed the skeletons of adult fish. Gross observations and morphometric analyses show that exposure to simulated microgravity results in stunted growth, reduced ossification and severe distortion of some skeletal elements. Additionally, we investigated the effects on the juvenile skull and body pigmentation. This study determines for the first time the long-term effects of embryonic exposure to simulated microgravity on the developing skull and highlights the importance of studies investigating the effects of altered gravitational forces.
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