TY - JOUR. T1 - Establishment of a Kit-negative cell line of melanocyte precursors from mouse neural crest cells. AU - Kawa, Yoko. AU - Soma, Yoshinao. AU - Nakamura, Masayuki. AU - Ito, Masaru. AU - Kawakami, Tamihiro. AU - Baba, Takako. AU - Sibahara, Kuniko. AU - Ohsumi, Kayoko. AU - Ooka, Shiho. AU - Watabe, Hidenori. AU - Ono, Hirotake. AU - Hosaka, Eri. AU - Kimura, Satoko. AU - Kushimoto, Tsuneto. AU - Mizoguchi, Masako. PY - 2005/6. Y1 - 2005/6. N2 - We previously established a mouse neural crest cell line named NCCmelb4, which is positive for Kit and negative for tyrosinase. NCCmelb4 cells were useful to study the effects of extrinsic factors such as retinoic acids and vitamin D3 on melanocyte differentiation, but in order to study the development of melanocytes from multipotent neural crest cells, cell lines of melanocyte progenitors in earlier developmental stages are needed. In the present study, we established an immortal cell line named NCC-melb4M5 that was derived from NCCmelb4 ...
Within the hindbrain region, neural crest cell migration is organized into three streams that follow the segmentation of the neuroepithelium into distinct rhombomeric compartments. Although the streaming of neural crest cells is known to involve signals derived from the neuroepithelium, the molecular properties underlying this process are poorly understood. Here, we have mapped the expression of the signaling component of two secreted class III Semaphorins, Semaphorin (Sema) 3A and Sema 3F, at time points that correspond to neural crest cell migration within the hindbrain region of the chick. Both Semaphorins are expressed within rhombomeres at levels adjacent to crest-free mesenchyme and expression of the receptor components essential for Semaphorin activity by neural crest cells suggests a function in restricting neural crest cell migration. By using bead implantation and electroporation in ovo, we define a role for both Semaphorins in the maintenance of neural crest cell streams in proximity to the
Greiner, Johannes, Hauser, Stefan, Widera, Darius, Qunneis, Firas, Müller, Janine, Zander, Christin, Martin, Ina, Mallah, Jana, Prante, Christian, Schwarze, Hartmut, Prohaska, Wolfgang, Beyer, André, Rott, Karsten, Hütten, Andreas, Gölzhäuser, Armin, Sudhoff, Holger, Kaltschmidt, Christian, and Kaltschmidt, Barbara. "Efficient animal-serum free 3D cultivation method for adult human neural crest-derived stem cell therapeutics". European Cells & Materials 22 (2011): 403-419 ...
Our data implicate Disc1 in the transcriptional repression of foxd3 and sox10, two transcription factors that are crucial for multiple steps of CNC development. Evidence points to a role for Foxd3 as a transcriptional repressor crucial for the maintenance of neural crest progenitor pools, neural crest migration and the differentiation of some neural crest derivatives (Cheung et al., 2005; Lister et al., 2006; Montero-Balaguer et al., 2006; Stewart et al., 2006; Teng et al., 2008). Zebrafish foxd3 mutants have normal numbers of premigratory neural crest, but delayed neural crest migration and depletion of certain neural crest derivatives (Lister et al., 2006; Stewart et al., 2006). Interestingly, the only neural crest derivative with foxd3 expression during and after terminal differentiation is peripheral glia (Kelsh et al., 2000), indicating a possible role for this transcription factor in the differentiation of this derivative. Similar to the Disc1 morphants reported here, colgate (hdac1) ...
TY - JOUR. T1 - Neural crest cell differentiation and carcinogenesis. T2 - Capability of goldfish erythrophoroma cells for multiple differentiation and clonal polymorphism in their melanogenic variants. AU - Matsumoto, Jiro. AU - Wada, Kumiko. AU - Akiyama, Toyoko. PY - 1989/5. Y1 - 1989/5. N2 - Multiple differentiation shown by a single cell line (GEM 81) of goldfish erythrophoroma (tumors of integumental erythrophores) cells after administration of chemical induction in vitro includes 1) melanogenesis, 2) formation of reflecting platelets, 3) synthesis of pteridines heterogeneous to this species, 4) formation of dermal skeletons such as teeth and fin rays, 5) production of neuronal characters, and 6) genesis of lentoid bodies. Melanogenic cells, highest in inducibility, also show remarkable phenotypic diversification in their cell morphology, pigmentation, and physiologic response. In this paper, the following findings are presented; a) multiple differentiation shown by erythrophoroma cells ...
Neural crest cells (NCCs) are a multipotent, migratory cell population that generates an astonishingly diverse array of cell types during vertebrate development. The trunk neural crest has long been considered of particular significance. First, it has been held that the trunk neural crest has a morphogenetic role, acting to coordinate the development of the peripheral nervous system, secretory cells of the endocrine system and pigment cells of the skin. Second, the trunk neural crest additionally has skeletal potential. However, it has been demonstrated that a key role of the trunk neural crest streams is to organize the innervation of the intestine. Although trunk NCCs have a limited capacity for self-renewal, sometimes they become neural-crest-derived tumor cells and reveal the fact that that NCCs and tumor cells share the same molecular machinery. In this review we describe the routes taken by trunk NCCs and consider the signals and cues that pattern these trajectories. We also discuss recent
Neural crest cell migration in the hindbrain is segmental, with prominent streams of migrating cells adjacent to rhombomeres (r) r2, r4 and r6, but not r3 or r5. This migratory pattern cannot be explained by the failure of r3 and r5 to produce neural crest, since focal injections of the lipophilic dye, DiI, into the neural folds clearly demonstrate that all rhombomeres produce neural crest cells. Here, we examine the dynamics of hindbrain neural crest cell emigration and movement by iontophoretically injecting DiI into small numbers of cells. The intensely labeled cells and their progeny were repeatedly imaged using low-light-level epifluorescence microscopy, permitting their movement to be followed in living embryos over time. These intravital images definitively show that neural crest cells move both rostrally and caudally from r3 and r5 to emerge as a part of the streams adjacent to r2, r4, and/or r6. Within the first few hours, cells labeled in r3 move within and/or along the dorsal neural ...
Because of its unique ability to generate a wide variety of both neural and nonneural derivatives, the neural crest is an ideal model system to study the factors regulating cell lineage decisions in stem and progenitor cells. The use of various cell culture techniques and in vivo functional assays, including cell type-specific gene manipulation in mouse, helped to identify signaling factors involved in this process. Moreover, it became apparent that the biological functions of growth factors acting on neural crest cells depend on the context provided by the extracellular microenvironment. Thus, signaling molecules have to be viewed as parts of complex networks that change with time and location. Neural crest cells have to integrate these signals to ensure the generation of appropriate numbers of differentiating progeny. It will be important to determine how such signaling networks are established and how they elicit multiple signaling responses in neural crest cells to activate appropriate ...
The neural crest is a multipotent cell population that migrates from the dorsal edge of the neural tube to various parts of the embryo where it differentiates into a remarkable variety of different cell types. Initial induction of neural crest is mediated by a combination of BMP, Wnt, FGF, Retinoic acid and Notch/Delta signaling. The two-signal model for neural crest induction suggests that BMP signaling induces the competence to become neural crest. The second signal involves Wnt acting through the canonical pathway and leads to expression of neural crest markers such as slug. Wnt signals from the neural plate, non-neural ectoderm and paraxial mesoderm have all been suggested to play a role in neural crest induction. We show that Xenopus frizzled7 (Xfz7) is expressed in the dorsal ectoderm including early neural crest progenitors and is a key mediator of the Wnt inductive signal. We demonstrate that Xfz7 expression is induced in response to a BMP antagonist, noggin, and that Xfz7 can induce ...
Neural crest cells are a group of temporary, multipotent (can give rise to some other types of cells but not all) cells that are pinched off during the formation of the neural tube (precursor to the spinal cord and brain) and therefore are found at the dorsal (top) region of the neural tube during development. They are derived from the ectoderm germ layer, but are sometimes called the fourth germ layer because they are so important and give rise to so many other types of cells. They migrate throughout the body and create a large number of differentiated cells such as neurons, glial cells, pigment-containing cells in skin, skeletal tissue cells in the head, and many more. Cardiac neural crest cells (CNCCs) are a type of neural crest cells that migrate to the circumpharyngeal ridge (an arc-shape ridge above the pharyngeal arches) and then into the 3rd, 4th and 6th pharyngeal arches and the cardiac outflow tract (OFT). They extend from the otic placodes (the structure in developing embryos that ...
Neural crest cells were transplanted from one position in the body to another position. They developed into neural crest derivates from their new position. Neural crest cells are apparently pluripotent, as they give rise to the cell types expected from the position to which they have been transplanted.. For example, any neural crest cell can give rise to parasympathetic ganglia if transplanted to a certain position. Thus, neural crest cells must respond to environmental cues during their migration and subsequent differentiation. These environmental cues are often identical to the cues used by axons. ...
Neural crest cells are both highly migratory and significant to vertebrate organogenesis. However, the signals that regulate neural crest cell migration remain unclear. In this study, we test the function of differential screening-selected gene aberrant in neuroblastoma (DAN), a bone morphogenetic protein (BMP) antagonist we detected by analysis of the chick cranial mesoderm. Our analysis shows that, before neural crest cell exit from the hindbrain, DAN is expressed in the mesoderm, and then it becomes absent along cell migratory pathways. Cranial neural crest and metastatic melanoma cells avoid DAN protein stripes in vitro. Addition of DAN reduces the speed of migrating cells in vivo and in vitro, respectively. In vivo loss of function of DAN results in enhanced neural crest cell migration by increasing speed and directionality. Computer model simulations support the hypothesis that DAN restrains cell migration by regulating cell speed. Collectively, our results identify DAN as a novel factor ...
Trunk neural crest migration in the zebrafish is confined to the centre of the medial surface of each somite and the pattern of migration is determined before neural crest cells contacts the sclerotome cells. Unlike other animals such as mice and birds, the sclerotome only makes up an inconsequential part of the somites in zebrafish and did not disrupt neural crest migration and DRG development[84]. It has been demonstrated that the myotome of the zebrafish contributes more in the establishment of neural crest cell migration patterns together with neural crest cells[85]. In particular, the adaxial cells, the first cells to develop and migrate from the myotome, helps in the regulation of trunk neural crest migration patterns. These slow muscle precursors have been shown to be crucial for normal migration patterns as their removal resulted in the accumulation of trunk neural crest cells at the level of the notochord[86]. Another key aspect in the proper development of DRG neurons in zebrafish lies ...
Neural crest cells are a group of multipotent stem cell that migrate to various locations and give rise to many diverse cell types in the vertebrate body. The ENS arises from "vagal" neural crest stem cells that originate from the post-otic dorsal neural tube. Vagal neural crest cells are multipotent and can give rise to the outflow tract of the heart, enteric ganglia, sympathetic ganglia, as well as pigment cells of the skin. To become enteric ganglia during development, vagal neural crest migrate ventrally from the neural tube and enter the primitive foregut tissue. They then migrate along the rostrocaudal extent of the gut in response to microenvironmental signaling cues to until they eventually reach the hindgut. These enteric neural crest cells (ENC) eventually give rise to a diverse array of neurons and glia that form the enteric ganglia ...
Massachusetts General Hospital and Harvard Medical School Purpose: Vertebrate neural crest development depends on pluripotent, migratory neural crest (NC) cells. Isolation and culture of zebrafish NC cells has not been previously reported. In vitro culture of NC cells allows evaluation of in vivo findings in a more controlled environment. Here we report for the first time the isolation, in vitro culture and characterization of NC cells from zebrafish embryos. We apply the NC culture to determine if these cells possess stem cell or progenitor cell properties of multi-lineage differentiation, maintenance and renewal.. Methods: NC cells were isolated from transgenic sox10::egfp embryos using FACS and cultured in a complex proliferation medium, on substrates coated with extra cellular matrix proteins, with growth factors to induce differentiation into various lineages. NC multi-lineage differentiation was determined by immunocytochemistry and RT-PCR, cell migration was assessed by wound healing ...
Neural Crest Cell Emigration and Migration Neural crest cells are among the most migratory cell type in vertebrate embryos. We are characterizing the machinery responsible for neural crest cell movement, the nature of the neural crest epithelial to mesenchymal transition to form a migratory cell type and the role of the migratory environment in influencing migratory pathway choices. A variety of cell labeling techniques, including DiI-labeling, microsurgical grafts and confocal time-lapse microscopy, are used to follow the pathways of neural crest migration in in a number of vertebrate species. ...
Purpose: : Long thin sympathetic axons transport tissue plasminogen activator(t-PA) to the eye. There it is released in response to adrenergic stimulations. The t-PA is synthesized and packaged in transport vesicles in superior cervical sympathetic ganglion neuron cell bodies(1) .Plasmin activated by t-PA has long been thought to accelerate the trabecular outflow of aqueous humor. Our purpose here is to map the neural crest origins of cells able to produce t-PA within the eye. Methods: : A promoter mouse line- whose human t-PA Cre transgene is specifically expressed by sympathetic nerves and all other crest derivatives(2)- was crossed with a Lac Z reporter expressing the enhanced green fluorescent protein(EGFP) transgene. PCR sorted pups showed both t-PA promoter and EGFP expressions confined within crest-derived cells. Cryosections were viewed by confocal and UV microscopy ,and immunostained for t-PA antigen.Cultured human uveal melanocytes were stimlated with phenylephrine to confirm a t-PA ...
The neural crest is an embryonic stem cell population whose migratory behaviour has been likened to malignant invasion. The neural crest, as does cancer, undergoes an epithelial-to-mesenchymal transition and migrates to colonize almost all the tissues of the embryo. Neural crest cells exhibit collective cell migration, moving in streams of high directionality. The migratory neural crest streams are kept in shape by the presence of negative signals in their vicinity. The directionality of the migrating neural crest is achieved by contact-dependent cell polarization, in a phenomenon called contact inhibition of locomotion. Two cells experiencing contact inhibition of locomotion move away from each other after collision. However, if the cell density is high only cells exposed to a free edge can migrate away from the cluster leading to the directional migration of the whole group. Recent work performed in chicks, zebrafish and frogs has shown that the non-canonical Wnt-PCP (planar cell polarity) ...
Analysis of early human neural crest development[3] "The outstanding migration and differentiation capacities of neural crest cells (NCCs) have fascinated scientists since Wilhelm His described this cell population in 1868. Today, after intense research using vertebrate model organisms, we have gained considerable knowledge regarding the origin, migration and differentiation of NCCs. However, our understanding of NCC development in human embryos remains largely uncharacterized, despite the role the neural crest plays in several human pathologies. Here, we report for the first time the expression of a battery of molecular markers before, during, or following NCC migration in human embryos from Carnegie Stages (CS) 12 to 18. Our work demonstrates the expression of Sox9, Sox10 and Pax3 transcription factors in premigratory NCCs, while actively migrating NCCs display the additional transcription factors Pax7 and AP-2alpha. Importantly, while HNK-1 labels few migrating NCCs, p75(NTR) labels a large ...
The neural crest is an embryonic cell population that gives rise to much of the vertebrate craniofacial skeleton, and its evolutionary origin is generally regarded as a key step in the diversification of vertebrates. Neural crest fate maps have been generated for a number of osteichthyan model systems (e.g. mouse, chick, frog and zebrafish). However, nothing is known about the fates of neural crest cells in chondrichthyans. We have developed methods for long-term lineage tracing of cell populations in early skate embryos, and we are using these methods to generate fate maps of chondrichthyan cranial and trunk neural crest cells. This work will allow us to infer primitive fates of neural crest cells in the last common ancestor of jawed vertebrates (e.g. neural crest vs. mesodermal contributions to the craniofacial skeleton and pectoral girdle, and the skeletogenic potential of trunk neural crest cells), thereby resolving a number of outstanding controversies relating to the early evolution of the ...
Coordinating the balance between progenitor self-renewal and myogenic differentiation is required for a regulated expansion of the developing muscles. Previous observation that neural crest cells (NCCs) migrate throughout the somite regions, where trunk skeletal muscles first emerge, suggests a potential role for these cells in influencing early muscle formation. However, specific signaling interactions between NCCs and skeletal muscle cells remain unknown. Here we show that mice with specific NCC and peripheral nervous system defects display impaired survival of skeletal muscle and show skeletal muscle progenitor cell (MPC) depletion due to precocious commitment to differentiation. We show that reduced NCC-derived Neuregulin1 (Nrg1) in the somite region perturbs ErbB3 signaling in uncommitted MPCs. Using a combination of explant culture experiments and genetic ablation in the mouse, we demonstrate that Nrg1 signals provided by the NCC lineage play a critical role in sustainable myogenesis, by ...
Gene regulatory network model of cranial neural crest cell (CNCC) development, adaped from PMID: 19575671. Most interactions in the model are proposed to regulate transcription of core factors involved involved in neural crest and downstream progenitor specification. Transcriptional regulation arrows are proposed to promote transcription, unless a graphical T-bar is present at the end of the arrow (commented to be inhibitors of transcriptional regulation). Additional gene information was obtained from http://www.ncbi.nlm.nih.gov/books/NBK53143 ...
PURPOSE OF REVIEW Metastatic melanoma is the most aggressive skin cancer and despite tremendous efforts and considerable progress in clinical treatment of melanoma patients within recent years, it remains a deadly disease. Current treatments affect melanoma cells indiscriminately, while accumulating evidence suggests that melanoma might be a disease of stem cells. This review aims to summarize the important accomplishments in the field and to emphasize the common molecular and cellular mechanisms regulating self-renewal of neural crest stem cells (NCSCs) and melanoma cells. RECENT FINDINGS A growing number of publications highlight the existence of phenotypic and functional similarities between embryonic NCSCs and melanoma cells. These studies provide compelling evidence that the propagation of melanoma cells critically depends on genes instrumental in neural crest development. The example of Sox10 and Rac1 genes provides detailed illustration of how interfering with these important genes for ...
During vertebrate embryogenesis, the cranial neural crest (CNC) forms at the neural plate border and subsequently migrates and differentiates into many types of cells. The transcription factor Snai2, which is induced by canonical Wnt signaling to be expressed in the early CNC, is pivotal for CNC induction and migration in Xenopus. However, snai2 expression is silenced during CNC migration, and its roles at later developmental stages remain unclear. We generated a transgenic X. tropicalis line that expresses enhanced green fluorescent protein (eGFP) driven by the snai2 promoter/enhancer, and observed eGFP expression not only in the pre-migratory and migrating CNC, but also the differentiating CNC. This transgenic line can be used directly to detect deficiencies in CNC development at various stages, including subtle perturbation of CNC differentiation. In situ hybridization and immunohistochemistry confirm that Snai2 is re-expressed in the differentiating CNC. Using a separate transgenic Wnt reporter line
Differentiation of Neural-Crest-Derived Intermediate Pluripotent Progenitors into Committed Periodontal Populations Involves Unique Molecular Signature Changes, Cohort Shifts, and Epigenetic Modifications. Smit Jayant Dangaria, Yoshihiro Ito, Xianghong Luan, Thomas G.H. Diekwisch. Stem Cells Dev. 2011 January; 20(1): 39-52. Published online 2010 July 6. doi: 10.1089/scd.2010.0180. PMCID: PMC3128775 ...
The human cornea contains stem cells that can be induced to express markers consistent with multipotency in cell culture; however, there have been no studies demonstrating that human corneal keratocytes are multipotent. The objective of this study is to examine the potential of human fetal keratocytes (HFKs) to differentiate into neural crest-derived tissues when challenged in an embryonic environment. HFKs were injected bilaterally into the cranial mesenchyme adjacent to the neural tube and the periocular mesenchyme in chick embryos at embryonic days 1.5 and 3, respectively. The injected keratocytes were detected by immunofluorescence using the human cell-specific marker, HuNu. HuNu-positive keratocytes injected along the neural crest pathway were localized adjacent to HNK-1-positive migratory host neural crest cells and in the cardiac cushion mesenchyme. The HuNu-positive cells transformed into neural crest derivatives such as smooth muscle in cranial blood vessels, stromal keratocytes, and ...
2Vertebrate Body Plan Group, RIKEN Center for Developmental Biology. Cephalic neural crest cells play essential roles in craniofacial development. Otx2 is a gene that plays central roles in head development and is also expressed in the cephalic neural crest cells. We have previously reported Otx2 heterozygotes exhibit a variety of craniofacial defects in C57BL/6 background, but not in CBA background (Genes Dev. 9, 2646-, 1995). Here we report (1) cis-regulatory elements that are identified by making transgenic embryos with LacZ gene as a reporter (Deve, 124, 3929, 1997), (2) components of cranial nerves and skeltons that are regulated by Otx2 and their implication in vertebrate body plan, (3) mapping of a modifier gene that is responsible for the difference of the Otx2 phenotype between C57BL/6 and CBA backgrounds.. ...
1. Ohno S. Evolution by gene duplication. New York: Springer-Verlag. 1970 2. Furlong RF, Holland PWH. Were vertebrate octoploid. Phil Trans R Soc Lond B. 2002 ;357:531-544 3. Gans C, Northcutt RG. Neural crest and the origin of vertebrates: a new head. Science. 1983 ;220:268-274 4. Jeffery WR, Strickier AG, Yamamoto Y. Migratory neural crest-like cells form body pigmentation in a urochordate embryo. Nature. 2004 ;431:696-699 5. Holland ND, Panganiban G, Henyey EL, Holland LZ. Sequence and developmental expression of AmphiDll, an amphioxus Distal-less gene transcribed in the ectoderm, epidermis and nervous system: insights into evolution of craniate forebrain and neural crest. Development. 1996 ;122:2911-2920 6. Wada H, Holland PWH, Sato S, Yamamoto H, Satoh N. Neural tube is partially dorsalized by overexpression of HrPax-37: the ascidian homologue of Pax-3 and Pax-7. Dev Biol. 1997 ;187:240-252 7. Wada H. Origin and evolution of the neural crest: a hypothetical reconstruction of its ...
The sense of smell in vertebrates is detected by specialized sensory neurons derived from the peripheral nervous system. Classically, it has been presumed that the olfactory placode forms all olfactory sensory neurons. In contrast, we show that the cranial neural crest is the primary source of microvillous sensory neurons within the olfactory epithelium of zebrafish embryos. Using photoconversion-based fate mapping and live cell tracking coupled with laser ablation, we followed neural crest precursors as they migrated from the neural tube to the nasal cavity. A subset that coexpressed Sox10 protein and a neurogenin1 reporter ingressed into the olfactory epithelium and differentiated into microvillous sensory neurons. Timed loss-of-function analysis revealed a critical role for Sox10 in microvillous neurogenesis. Taken together, these findings directly demonstrate a heretofore unknown contribution of the cranial neural crest to olfactory sensory neurons in zebrafish and provide important insights ...
2Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4472 USA. Wnt1 signaling has been implicated as one factor involved in neural crest-derived melanocyte (NC-M) development. Mice deficient for both Wnt1 and Wnt3a have a marked deficiency in trunk neural crest derivatives including NC-Ms (1). We have used cell lineage-directed gene targeting of Wnt signaling genes to examine the effects of Wnt signaling in mouse neural crest development. Gene expression was directed to cell-lineages by infection with subgroup A avian leukosis virus vectors (RCAS) (2) in lines of transgenic mice that express the retrovirus receptor tv-a (2). Transgenic mice with tva in either nestin expressing neural precuror cells (line Ntva) or dopachrome tautomerase (DCT) expressing melanoblasts (line DCTtva) were analyzed. We over-stimulated Wnt signaling in two ways: directed gene transfer of Wnt1 to Ntva+ cells and transfer of b-catenin to DCTtva+ NC-M precursor ...
Stem cells from adult tissues were considered for a long time as promising tools for regenerative therapy of neurological diseases, including spinal cord injuries (SCI). Indeed, mesenchymal (MSCs) and neural crest stem cells (NCSCs) together constitute the bone marrow stromal stem cells (BMSCs) that were used as therapeutic options in various models of experimental SCI. However, as clinical approaches remained disappointing, we thought that reducing BMSC heterogeneity should be a potential way to improve treatment efficiency and reproducibility. We investigated the impact of pure populations of MSCs and NCSCs isolated from adult bone marrow in a mouse model of spinal cord injury. We then analyzed the secretome of both MSCs and NCSCs, and its effect on macrophage migration in vitro. We first observed that both cell types induced motor recovery in mice, and modified the inflammatory reaction in the lesion site. We also demonstrated that NCSCs but especially MSCs were able to secrete chemokines and attract
article{63622856-3178-483f-a762-c592e0b05bcc, abstract = {PURPOSE. Structures derived from periocular mesenchyme arise by complex interactions between neural crest and mesoderm. Defects in development or function of structures derived from periocular mesenchyme result in debilitating vision loss, including glaucoma. The determination of long-term fates for neural crest and mesoderm in mammals has been inhibited by the lack of suitable marking systems. In the present study, the first long-term fate maps are presented for neural crest and mesoderm in a mammalian eye. METHODS. Complementary binary genetic approaches were used to mark indelibly the neural crest and mesoderm in the developing eye. Component one is a transgene expressing Cre recombinase under the control of an appropriate tissue-specific promoter. The second component is the conditional Cre reporter R26R, which is activated by the Cre recombinase expressed from the transgene. Lineage-marked cells were counterstained for expression of ...
Definition of neural crest in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is neural crest? Meaning of neural crest as a legal term. What does neural crest mean in law?
The member of Rho family of small GTPases Cdc42 plays important and conserved roles in cell polarity and motility. The Cdc42ep family proteins have been identified to bind to Cdc42, yet how they interact with Cdc42 to regulate cell migration remains to be elucidated. In this study, we focus on Cdc42ep1, which is expressed predominantly in the highly migratory neural crest cells in frog embryos. Through morpholino-mediated knockdown, we show that Cdc42ep1 is required for the migration of cranial neural crest cells. Loss of Cdc42ep1 leads to rounder cell shapes and the formation of membrane blebs, consistent with the observed disruption in actin organization and focal adhesion alignment. As a result, Cdc42ep1 is critical for neural crest cells to apply traction forces at the correct place to migrate efficiently. We further show that Cdc42ep1 is localized to two areas in neural crest cells: in membrane protrusions together with Cdc42 and in perinuclear patches where Cdc42 is absent. Cdc42 directly ...
This study demonstrates, for the first time, an essential function of IdoA in early embryonic development and cell migration in vivo. The spatio-temporal expression of Dse in the Xenopus embryo suggested a role of DS-epi1 in ectoderm and NC development. The blockage of epimerase activity and IdoA biosynthesis upon the knockdown of DS-epi1 did not affect the allocation of neural and epidermal fates or the formation of NC progenitors. However, DS-epi1 deficiency altered the expression of neural-plate-border- and NC-specific transcription factors and decreased the extent of NC cell migration, which led to defects in craniofacial skeleton, melanocyte and dorsal fin formation. The functional links between DS-epi1 and EMT and between DS-epi1 cell adhesion on fibronectin, as established in this study for normal NC development, might have implications for neurocristopathies and cancer.. Our study demonstrates that, in Xenopus embryos, DS-epi1 is important for the formation of isolated IdoA moieties ...
Induces expression of a number of neural crest marker genes as part of a heterodimer with isoform b of pbx1, to specify neural crest cell fate. Binds to a highly conserved region in the promoter of the neural crest marker gene zic3.
During development neural crest cells give rise to a wide variety of specialized cell types in response to cytokines from surrounding tissues. Depending on the cranial-caudal level of their origin, different populations of neural crest cells exhibit
Another active area of research focuses on neural crest cells (NCCs). There is growing evidence that cilia are present on the surface of NCCs and their derivatives, and skeletal ciliopathies may be caused by abnormal NCC development. The hypothesis that we are currently testing is that factors that influence NCC identity or migration may be targeted for treatment of ciliopathies and other NCC-derived defects (including specific tumours). Chemical and genetic screening is undertaken to identify novel genes and Food and Drug Administration (FDA)-approved drugs that influence NCC development in zebrafish embryos, and these factors are tested for their ability to treat skeletal ciliopathies (e.g. craniosynostosis) in model organisms and to inhibit growth of NCC-derived tumour cell lines. ...
PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.
Takahashi KF, Kiyoshima T, Kobayashi I, Xie M, Yamaza H, Fujiwara H, Ookuma Y, Nagata K, Wada H, Sakai T, Terada Y, Sakai H; Protogenin, a new member of the immunoglobulin superfamily, is implicated in the development of the mouse lower first molar.; BMC Dev Biol, 2010 PubMed Europe PMC ...
Neuroblastoma is a common childhood tumor derived from neural crest precursor cells. In the present study, we investigated the expression and function of embryonic stem cell-expressed Ras (ERas), a novel Ras family protein previously reported as the
Neural crest cells are a type of migratory cells that are responsible for the formation of many different anatomical structures...
Molecular markers that are specifically expressed in neural crest or mesoderm precursors have not been described for the mammalian ocular primordia. Therefore, we examined the protein expression patterns of several transcription factors previously implicated in ocular development to determine their expression profiles between the two embryonic precursor pools. The homeodomain transcription factor PITX2 is associated with ocular defects in humans and is essential for ocular development in mice. 2 13 32 33 PITX2 expression labeled the neural crest, beginning initially in the presumptive anterior segment and quickly extending to the periphery of the optic cup in Wnt1Cre;R26R embryos by E11.5 (Fig. 2A) . In contrast, PITX2 expression had marked all β-gal-labeled mesoderm in αGsuCre;R26R embryos at E11.5, before these cells entered the ocular field (Fig. 2B) . By E12.5, PITX2 expression had spread to all ocular neural crest (data not shown). The forkhead transcription factor FOXC1 is also essential ...
Rationale: Vascular smooth muscle cell (VSMC) differentiation from neural crest cells (NCCs) is critical for cardiovascular development, but the mechanisms remain largely unknown. Objective: TGF-β function in VSMC differentiation from NCCs is controversial. We therefore determined the role and the mechanism of a TGF-β downstream signaling intermediate Smad2 in NCC differentiation to VSMCs. Methods and Results: By using Cre/loxP system, we generated NCC tissue-specific Smad2 knockout mouse model and found that Smad2 deletion resulted in defective NCC differentiation to VSMCs in aortic arch arteries during embryonic development and caused vessel wall abnormality in adult carotid arteries where the VSMCs are derived from NCCs. The abnormalities included missing one layer of VSMCs in the media of the arteries with distorted and thinner elastic lamina, leading to a thinner vessel wall as compared to the wild type vessel. Mechanistically, Smad2 interacted with MRTFB to regulate VSMC marker gene ...
Bone morphogenetic protein 4, or BMP4, is a transforming growth factor that causes the cells of the ectoderm to differentiate into skin cells. Without BMP4 the ectoderm cells would develop into neural cells. Axial mesoderm cells under the ectoderm secrete inhibitory signals called chordin, noggin and follistatin. These inhibitory signals prevent the action of BMP4, which would normally make the cells ectoderm; as a result, the overlying cells take their normal course and develop into neural cells. The cells in the ectoderm that circumscribe these neural cells do not receive the BMP4 inhibitor signals and as a result BMP4 induces these cells to develop into skin cells.[8] Neural plate border specifiers are induced as a set of transcription factors. Distalless-5, PAX3 and PAX7 prevent the border region from becoming either neural plate or epidermis.[1] These induce a second set of transcription factors called neural crest specifiers, which cause cells to become neural crest cells. In a newly ...
J:175786 Ho AT, Hayashi S, Brohl D, Aurade F, Rattenbach R, Relaix F, Neural Crest Cell Lineage Restricts Skeletal Muscle Progenitor Cell Differentiation through Neuregulin1-ErbB3 Signaling. Dev Cell. 2011 Aug 16;21(2):273-87 ...
Shop Heart- and neural crest derivatives-expressed protein ELISA Kit, Recombinant Protein and Heart- and neural crest derivatives-expressed protein Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
Neurons of the sympathetic chain belong to the second order neurons in the efferent pathway of the sympathetic part of the autonomic nervous system. These are derived from the multipotent neural crest cells. (Yntemma and Hammond, 1947; Weston, 1970; Anderson; 1989; Stemple and Anderson, 1992). These cells migrate ventrally beside the cranial half of the sclerotome, where it forms the dorsal root ganglion (Leikola 1976) and migrate further ventralward to form sympathetic chain ganglia (Goldstein and Kalcheim, 1991). The migration of the neural crest cells to form sympathetic chain is controlled by the expression of Hox-C genes (Breier et al, 1988).. Formation of sympathetic chain is noted around 9mm stage of the human embryo (Keibel and Mall, 1912). Neurons to the human sympathetic chian are contributed by the ventrimedial aspect of the dorsal root ganglion (Keibel and Mall, 1912; Mitchell, 1953) and are also derived from the ventral aspect of the neural tube which pass along the ventral nerve ...
Principal Investigator:YAMASHITA Noriko, Project Period (FY):1991 - 1993, Research Category:Grant-in-Aid for General Scientific Research (C), Research Field:Morphological basic dentistry
Collective cell migration is often considered in the context of just one population of cells on the move, but can often actually involve several cell types, raising obvious questions about how such mass movement is coordinated. By studying the interaction between neural crest (NC) cells and placodal cells in developing Xenopus laevis and zebrafish embryos, Eric Theveneau et al. have identified a chase-and-run behaviour that ensures successful neural crest migration and placode segregation, and gained insight into the underlying molecular mechanisms.. The playground antics of placode cells and NC cells could be seen both in vivo and in vitro. By labelling both cell types in embryos, the researchers saw that placode cells moved randomly until NC cells arrived on the scene, at which point they ran away, leaving gaps in the placode region. In co-culture studies, placodal cells were seen to encourage NC cells - by secreting the chemoattractant Sdf1 - to chase them, but once the NC cells got ...