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PubMed2003

Interplay between Notch signaling and the homeoprotein Xiro1 is required for neural crest induction in Xenopus embryos.

The neural crest is a population of cells that originates at the interface between the neural plate and non-neural ectoderm. Here, we have analyzed the role that Notch and the homeoprotein Xiro1 play in the specification of the neural crest. We show that Xiro1, Notch and the Notch target gene Hairy2A are all expressed in the neural crest territory, whereas the Notch ligands Delta 1 and Serrate are expressed in the cells that surround the prospective crest cells. We have used inducible dominant-negative and activator constructs of both Notch signaling components and Xiro1 to analyze the role of these factors in neural crest specification without interfering with mesodermal or neural plate development. Activation of Xiro1 or Notch signaling led to an enlargement of the neural crest territory, whereas blocking their activity inhibited the expression of neural crest markers. It is known that BMPs are involved in the induction of the neural crest and, thus, we assessed whether these two elements might influence the expression of Bmp4. Activation of Xiro1 and of Notch signaling upregulated Hairy2A and inhibited Bmp4 transcription during neural crest specification. These results, in conjunction with data from rescue experiments, allow us to propose a model wherein Xiro1 lies upstream of the cascade regulating Delta 1 transcription. At the early gastrula stage, the coordinated action of Xiro1, as a positive regulator, and Snail, as a repressor, restricts the expression of Delta 1 at the border of the neural crest territory. At the late gastrula stage, Delta 1 interacts with Notch to activate Hairy2A in the region of the neural fold. Subsequently, Hairy2A acts as a repressor of Bmp4 transcription, ensuring that levels of Bmp4 optimal for the specification of the neural plate border are attained in this region. Finally, the activity of additional signals (WNTs, FGF and retinoic acid) in this newly defined domain induces the production of neural crest cells. These data also highlight the different roles played by BMP in neural crest specification in chick and Xenopus or zebrafish embryos.

Animals↗
PubMed1992

Ultrastructure of hyaline, border, and vacuole cells in chick inner ear.

The sense organ for hearing in birds, the basilar papilla, is capable of replacing lost or damaged hair cells and supporting cells through regeneration. Potential candidates for precursor-cell populations include cells within the auditory receptor epithelium and nonsensory cells inferior to the sensory epithelium. Ultrastructural characteristics of hyaline cells, border cells, and vacuole cells, nonsensory cells which border or lie inferior to the receptor epithelium proper, were studied with transmission electron microscopy. Data were obtained from normal neonatal and adult chickens. Several rows of epithelial cells separate hyaline cells from inferiorly located organ supporting cells and hair cells. Ultrastructural characteristics and location of these epithelial cells differentiate them from organ supporting cells and hyaline cells; consequently, we have termed them "border cells." Synaptic specializations are observed between neural elements and border cells, and gap junctions are found between adjacent border cells, between border cells and neighboring organ supporting cells, and between juxtaposed border and hyaline cells. Hyaline cells, in contrast to border cells, are highly specialized. Dense bundles of filaments are present in hyaline cells from the basal one-half of the papilla, and an unusual structure, a rough tubular aggregate, is present in hyaline-cell cytoplasm. Pre- and postsynaptic specializations are observed between neural elements and hyaline cells, and gap-junctional complexes link neighboring hyaline cells. Vacuole cells lie inferior to the hyaline cells and rest on the inferior fibrocartilaginous plate. They are unspecialized morphologically. Their only remarkable morphological feature is the abundance of spherical vacuoles within their cytoplasmic matrix.

Animals↗
PubMed1996

Neural crest formation in Xenopus laevis: mechanisms of Xslug induction.

A study of the induction of the prospective neural crest in Xenopus laevis embryos has been carried out, using the expression of Xslug as a specific marker for the neural crest. We have analyzed the competence and the specification of the neural crest. The competence to express Xslug was analyzed using two different approaches: (1) in vitro culture of conjugates of dorsal mesoderm and ectoderm taken from embryos at different ages and (2) grafts of equivalent pieces of ectoderm in the neural fold region of a gastrula or a neurula. Similar results were obtained with both methods: the ectoderm loses the competence to respond to neural fold induction at the end of gastrulation. Neural crest specification was analyzed by culturing a region of the ectoderm that contained the prospective neural crest and analyzing Xslug expression. Our results show that neural folds are specified autonomously to express Xslug by the end of gastrulation. By grafting labeled neural plate into lateral epidermis we have shown that neural crest can be induced by an interaction between neural plate and epidermis. Furthermore, neural crest cells come from both tissues. We have discarded the possibility that these neural crest cells are induced by a signal coming from the underlying lateral plate, by a homeogenetic signal coming from the host neural plate, or by regeneration of crest cells from the dissected neural plate. We propose a model to explain how the neural crest cells are induced at the border of the neural plate in X. laevis.

Animals↗
PubMed2005

The transcriptional control of trunk neural crest induction, survival, and delamination.

Trunk neural crest cells are generated at the border between the neural plate and nonneural ectoderm, where they initiate a distinct program of gene expression, undergo an epithelial-mesenchymal transition (EMT), and delaminate from the neuroepithelium. Here, we provide evidence that members of three families of transcription induce these properties in premigratory neural crest cells. Sox9 acts to provide the competence for neural crest cells to undergo an EMT and is required for trunk neural crest survival. In the absence of Sox9, cells apoptose prior to or shortly after delamination. Slug/Snail, in the presence of Sox9, is sufficient to induce an EMT in neural epithelial cells, while FoxD3 regulates the expression of cell-cell adhesion molecules required for neural crest migration. Together, the data suggest a model in which a combination of transcription factors regulates the acquisition of the diverse properties of neural crest cells.

Animals↗
PubMed2007

Border-ownership-dependent tilt aftereffect in incomplete figures.

A recent physiological finding of neural coding for border ownership (BO) that defines the direction of a figure with respect to the border has provided a possible basis for figure-ground segregation. To explore the underlying neural mechanisms of BO, we investigated stimulus configurations that activate BO circuitry through psychophysical investigation of the BO-dependent tilt aftereffect (BO-TAE). Specifically, we examined robustness of the border ownership signal by determining whether the BO-TAE is observed when gestalt factors are broken. The results showed significant BO-TAEs even when a global shape was not explicitly given due to the ambiguity of the contour, suggesting a contour-independent mechanism for BO coding.

Algorithms↗
PubMed2005

Zebrafish narrowminded disrupts the transcription factor prdm1 and is required for neural crest and sensory neuron specification.

Specification of both neural crest cells and Rohon-Beard (RB) sensory neurons involves a complex series of interactions between the neural and non-neural ectoderm. The molecular mechanisms directing this process are not well understood. The zebrafish narrowminded (nrd) mutation is unique, since it is one of two mutations in which defects are observed in both cell populations: it leads to a complete absence of RB neurons and a reduction in neural crest cells and their derivatives. Here, we show that nrd is a mutation in prdm1, a SET/zinc-finger domain transcription factor. A Morpholino-mediated depletion of prdm1 phenocopies the nrd mutation, and conversely overexpression of prdm1 mRNA rescues the nrd RB sensory neuron and neural crest phenotype. prdm1 is expressed at the border of the neural plate within the domain where neural crest cells and RB sensory neurons form. Analysis of prdm1 function by overexpression indicates that prdm1 functions to promote the cell fate specification of both neural crest cells and RB sensory neurons, most likely as a downstream effector of the BMP signaling pathway.

Animals↗
PubMed2003

Neural crest induction by paraxial mesoderm in Xenopus embryos requires FGF signals.

At the border of the neural plate, the induction of the neural crest can be achieved by interactions with the epidermis, or with the underlying mesoderm. Wnt signals are required for the inducing activity of the epidermis in chick and amphibian embryos. Here, we analyze the molecular mechanisms of neural crest induction by the mesoderm in Xenopus embryos. Using a recombination assay, we show that prospective paraxial mesoderm induces a panel of neural crest markers (Slug, FoxD3, Zic5 and Sox9), whereas the future axial mesoderm only induces a subset of these genes. This induction is blocked by a dominant negative (dn) form of FGFR1. However, neither dnFGFR4a nor inhibition of Wnt signaling prevents neural crest induction in this system. Among the FGFs, FGF8 is strongly expressed by the paraxial mesoderm. FGF8 is sufficient to induce the neural crest markers FoxD3, Sox9 and Zic5 transiently in the animal cap assay. In vivo, FGF8 injections also expand the Slug expression domain. This suggests that FGF8 can initiate neural crest formation and cooperates with other DLMZ-derived factors to maintain and complete neural crest induction. In contrast to Wnts, eFGF or bFGF, FGF8 elicits neural crest induction in the absence of mesoderm induction and without a requirement for BMP antagonists. In vivo, it is difficult to dissociate the roles of FGF and WNT factors in mesoderm induction and neural patterning. We show that, in most cases, effects on neural crest formation were parallel to altered mesoderm or neural development. However, neural and neural crest patterning can be dissociated experimentally using different dominant-negative manipulations: while Nfz8 blocks both posterior neural plate formation and neural crest formation, dnFGFR4a blocks neural patterning without blocking neural crest formation. These results suggest that different signal transduction mechanisms may be used in neural crest induction, and anteroposterior neural patterning.

Animals↗
PubMed2003

Development of melanocyte precursors from the vertebrate neural crest.

Pigment cells that differentiate in the vertebral skin arise from the neural crest (NC), a transitory structure formed at the dorsal borders of the neural plate and which gives rise to migratory cells of multiple fates. How NC cells become committed to the melanocytic lineage and what factors control the survival, proliferation and differentiation of melanocyte precursors remain largely unknown. These issues are of great importance for understanding the mechanisms of several pigment cell pathologies including melanomas. Recent in vivo and in vitro analyses of the fate of single NC cells have indicated that multipotent cells yield melanocyte precursors that become spatially and temporally segregated from other, non melanogenic, NC-derived cell types. The proper development of subsets of NC precursors is governed by environmental local cytokines acting in a paracrine manner. The conjunction of recent studies in mammals and birds reviewed here focuses on the action of endothelin 3 in controlling both the emergence and the maintenance of the NC-derived melanocyte phenotype.

Animals↗
PubMed2005

Early steps in neural crest specification.

The neural crest is a multipotent cell population that arise at the border of the neural plate and non-neural ectoderm. Studies conducted in a number of model organisms including chickens, frogs, zebrafish and mice have been instrumental in elucidating this molecular mechanisms underlying neural crest formation. Signaling molecules of the Wnt, BMP, and FGF families and their downstream effectors have been shown to mediate neural crest induction. Transcription factors including members of the Snail and SoxE gene families as well as FoxD3, c-Myc and others have been implicated in specification of the neural crest. These studies represent an important step in understanding the regulatory interactions involved in generating this complex and interesting cell type.

Animals↗
PubMed2004

BMP receptor IA is required in mammalian neural crest cells for development of the cardiac outflow tract and ventricular myocardium.

The neural crest is a multipotent, migratory cell population arising from the border of the neural and surface ectoderm. In mouse, the initial migratory neural crest cells occur at the five-somite stage. Bone morphogenetic proteins (BMPs), particularly BMP2 and BMP4, have been implicated as regulators of neural crest cell induction, maintenance, migration, differentiation and survival. Mouse has three known BMP2/4 type I receptors, of which Bmpr1a is expressed in the neural tube sufficiently early to be involved in neural crest development from the outset; however, earlier roles in other domains obscure its requirement in the neural crest. We have ablated Bmpr1a specifically in the neural crest, beginning at the five-somite stage. We find that most aspects of neural crest development occur normally; suggesting that BMPRIA is unnecessary for many aspects of early neural crest biology. However, mutant embryos display a shortened cardiac outflow tract with defective septation, a process known to require neural crest cells and to be essential for perinatal viability. Surprisingly, these embryos die in mid-gestation from acute heart failure, with reduced proliferation of ventricular myocardium. The myocardial defect may involve reduced BMP signaling in a novel, minor population of neural crest derivatives in the epicardium, a known source of ventricular myocardial proliferation signals. These results demonstrate that BMP2/4 signaling in mammalian neural crest derivatives is essential for outflow tract development and may regulate a crucial proliferation signal for the ventricular myocardium.

Animals↗
PubMed2001

xPitx1 plays a role in specifying cement gland and head during early Xenopus development.

Xenopus Pitx1 is a homeobox gene whose family members are structurally and functionally conserved in organisms as diverse as Drosophila, chick, mouse, human, and frog. Present as a maternal transcript, the gene is zygotically expressed during gastrulation in a dorsal streak of cells. This streak restricts to a small circular domain underlying the center of presumptive neural plate. Shortly thereafter, a crescent of expression develops at the border of anterior neural ectoderm, and as the central plate domain diminishes, the crescent coalesces to define the presumptive cement gland. Expression remains high throughout cement gland development, and subsequently expands to include ectodermal cells involved in stomodeal invagination. During early organogenesis, expression ensues in developing eye, posterior lateral mesoderm, and first branchial arch derivatives. Ectopic expression of xPitx1 causes head deformities including enlarged cement gland, ectopic cement glands, and posterior deformities or, in extreme cases, inhibition of recognizable structures posterior to the cement gland. Expression of markers such as XCG-1, xOtx2, xPax6, neuralbeta tubulin, and xTwist suggest that increases in cement gland and lower mandibular size are likely at the expense of other head tissues. Paradoxically, overexpression is sufficient to partially rescue embryos that are axially perturbed by ultraviolet irradiation or retinoic acid administration. Ectopic expression of xPitx1 in ectodermal explants directly promotes cement gland development as there was no evidence that mesodermal or neural tissue was present in explants.

Amino Acid Sequence↗
PubMed1999

Neural tube defects along the Texas-Mexico border, 1993-1995.

In response to a 1991 anencephaly cluster in Cameron County, Texas, a surveillance and neural tube defect (NTD) recurrence prevention project for NTDs was implemented in the 14 Texas-Mexico border counties. For 1993-1995, NTD-affected pregnancies were identified at all gestational ages through active surveillance of multiple case-ascertainment sources. There were 87 cases of anencephaly, 96 cases of spina bifida, and 14 cases of encephalocele for respective rates of 6.4, 7.1, and 1.1 per 10,000 live births. Of the 197 NTD case-women, 93% were Hispanic. The overall, Hispanic, and Anglo NTD rates were, respectively, 14.6, 14.9, and 10.6 per 10,000 live births. The NTD rate for El Paso County (9.8 per 10,000), the most northwestern Texas county, was significantly lower (p = 0.001) than the aggregate rate for the rest of the Texas border (17.1 per 10,000). The overall Texas border rate was significantly higher (p < 0.001) than a recently estimated rate of 9.3 for California and minimally higher than a recently adjusted rate of 11.3 for the Metropolitan Atlanta Congenital Defects Program counties (p = 0.052), both of which now reflect all gestational ages. Of the 197 Texas border cases, 85% (168 cases) reached a gestational age of > or =20 weeks. Excluding cases of <20 weeks' gestation in the rate had a more marked effect on reducing the anencephaly rate (4.9 per 10,000) than the spina bifida rate (6.7 per 10,000). A country of birth was known for 153 (83%) of the 184 Hispanic case-women: 63% were born in Mexico; 24%, in Texas; and 11%, elsewhere in the United States. Rates for Mexico-born Hispanic women (15.1 per 10,000) were significantly higher than rates for United States-born Hispanic women (9.5 per 10,000) (p = 0.006).

Adult↗
PubMed2000

Snail-related transcriptional repressors are required in Xenopus for both the induction of the neural crest and its subsequent migration.

The neural crest is a transient population of precursor cells that arises at the border between the neural plate and prospective epidermis in vertebrate embryos. The earliest known response to neural-crest-inducing signals is the expression of the zinc-finger transcription factors slug and snail. Although it is widely believed that these transcription factors play an essential role in neural crest development, relatively little is understood about their mechanism of action during this process. We have previously shown that overexpression of XSlug leads to expanded expression of neural crest markers and an excess of at least one neural crest derivative, melanocytes. In order to further investigate XSlug function, we overexpressed mutant constructs in which the DNA-binding domain was fused to either the activation domain from Gal4 or the repressor domain from Drosophila Engrailed. The Engrailed repressor fusion was found to mimic the effects of wild-type XSlug, indicating that XSlug functions as a transcriptional repressor during neural crest formation. In contrast, overexpression of either the activation domain fusion or the DNA-binding domain alone was found to inhibit XSlug function. Using a hormone-inducible inhibitory mutant, we show that inhibition of XSlug function at early stages prevents the formation of neural crest precursors, while inhibition at later stages interferes with neural crest migration, demonstrating for the first time that this transcriptional repressor is required during multiple stages of neural crest development.

Animals↗
PubMed2005

Agreement and disagreement among fate maps of the chick neural plate.

Fate maps are essential to understand embryonic development; they provide a background for deducing maps of differential cellular specification in the context of other experimental data and molecular expression patterns. Due to its accessibility, the chick neural plate has been fate-mapped many times, albeit without complete agreement with respect to its shape, extent and fated subdivisions. In this review, we first comment about avian neural plate fate maps reported since the early period of experimental embryology, referring to the different methods followed. We next review a perfected fate-mapping methodology, which recently allowed us rather precise delimitation of the chick neural plate at stages 3d/4. This leads to a general discussion about the apparent border of the neural plate and the prospective main rostrocaudal and longitudinal divisions of the neural tube.

Animals↗
PubMed1990

Identification of early developing axon projections from spinal interneurons in the chick embryo with a neuron specific beta-tubulin antibody: evidence for a new 'pioneer' pathway in the spinal cord.

The early development of interneurons in the chick embryo spinal cord was studied using a monoclonal antibody against a neuron-specific beta-tubulin isoform. Early developing interneurons were divided into two cell groups on the basis of their location and the pattern of growth of their axons. One group is composed of cells that establish a primitive longitudinal pathway (PL-cells), whereas the other group contains cells constituting a circumferential pathway (C-cells). The onset of axonal development in both cell groups occurs at stage (st.) 15 (embryonic day, (E), 2) in the branchial segments, which is prior to axonogenesis of motoneurons. PL-cells develop in the region between the floor plate and the motoneuron nucleus. Their axons are the first neuronal processes ('pioneer axons') to arrive in the ventrolateral marginal zone and they project both rostrally and caudally to establish a primitive longitudinal association pathway at the ventrolateral surface of the neural tube. This pathway is formed before axons of C-cells arrive in the ventrolateral region. The first C-cells are initially located in the most dorsal portion of the neural tube, whereas later appearing C-cells are also located in both intermediate and ventral regions of the neural tube. The axons of C-cells project ventrally, without fasciculating, along the lateral border of the neural tube. Some of their axons enter the ipsilateral ventrolateral longitudinal pathway at st. 17. We often observed apparent contacts and interactions between preexisting axons of PL-cells and newly arriving axons of C-cells. The axons of commissural C-cells first enter the floor plate at st. 17 and cross the midline at st. 18. Axons of C cells begin to join the contralateral ventrolateral longitudinal pathway at st. 18+ to st. 19. In the floor plate region, contacts between growth cones and axons were often observed. However, axons in the floor plate at these stages were not fasciculated. These observations establish the timing and pattern of growth of axons from two specific populations of early developing interneurons in the chick spinal cord. Additionally, we have identified an early and apparently previously undescribed 'pioneer' pathway that constitutes the first longitudinal pathway in the chick spinal cord.

Animals↗
PubMed1995

Tissue boundaries and cell behavior during neurulation.

We have analyzed the dynamics of the boundaries between the neural plate and the epidermis and between the neural plate and the notoplate. Our experiments confirm that these two boundaries have important roles in neurulation. Measurements of the lengths of neural fold (the boundary between epidermis and neural plate) in embryos of axolotls and newts reveal that neural folds abutting the prospective brain decrease in length while neural folds abutting the prospective spinal cord increase in length during neurulation. We tested the proposition that boundaries of the neural plate with epidermis and with notoplate are essential for proper neurulation. Cuts made along the boundaries with epidermis or with notoplate stop, or greatly diminish, neural plate elongation and tube formation. Explanting the axolotl neural plate without any bordering epidermis stops plate elongation and prevents neural tube closure, but neural plates explanted with a rim of epidermis elongate and close into tubes. Cutting the notoplate boundary stops midline elongation in the newt embryo or diminishes it in the axolotl embryo. We conclude that the notoplate boundary and part of the boundary of the epidermis that abuts the prospective spinal cord organize cell behavior to elongate the neural plate and help close the neural tube. The boundary of the neural plate with the epidermis is essential for tube closure both because it organizes plate elongation in the spinal cord region and because cell behavior becomes organized at the boundary such that neural folds are raised and a rolling moment is produced that helps form the neural tube.

Ambystoma↗
PubMed2004

Neural induction requires BMP inhibition only as a late step, and involves signals other than FGF and Wnt antagonists.

A dominant molecular explanation for neural induction is the 'default model', which proposes that the ectoderm is pre-programmed towards a neural fate, but is normally inhibited by endogenous BMPs. Although there is strong evidence favouring this in Xenopus, data from other organisms suggest more complexity, including an involvement of FGF and modulation of Wnt. However, it is generally believed that these additional signals also act by inhibiting BMPs. We have investigated whether BMP inhibition is necessary and/or sufficient for neural induction. In the chick, misexpression of BMP4 in the prospective neural plate inhibits the expression of definitive neural markers (Sox2 and late Sox3), but does not affect the early expression of Sox3, suggesting that BMP inhibition is required only as a late step during neural induction. Inhibition of BMP signalling by the potent antagonist Smad6, either alone or together with a dominant-negative BMP receptor, Chordin and/or Noggin in competent epiblast is not sufficient to induce expression of Sox2 directly, even in combination with FGF2, FGF3, FGF4 or FGF8 and/or antagonists of Wnt signalling. These results strongly suggest that BMP inhibition is not sufficient for neural induction in the chick embryo. To test this in Xenopus, Smad6 mRNA was injected into the A4 blastomere (which reliably contributes to epidermis but not to neural plate or its border) at the 32-cell stage: expression of neural markers (Sox3 and NCAM) is not induced. We propose that neural induction involves additional signalling events that remain to be identified.

Animals↗
PubMed1996

Rhombomere of origin determines autonomous versus environmentally regulated expression of Hoxa-3 in the avian embryo.

We have investigated the pattern and regulation of Hoxa3 expression in the hindbrain and associated neural crest cells in the chick embryo, using whole mount in situ hybridization in conjunction with DiI labeling of neural crest cells and microsurgical manipulations. Hoxa3 is expressed in the neural plate and later in the neural tube with a rostral border of expression corresponding to the boundary between rhombomeres (r) 4 and 5. Initial expression is diffuse and becomes sharp after boundary formation. Hoxa3 exhibits uniform expression within r5 after formation of rhombomeric borders. Cell marking experiments reveal that neural crest cells migrating caudally, but not rostrally, from r5 and caudally from r6 express Hoxa3 in normal embryo. Results from transposition experiments demonstrate that expression of Hoxa3 in r5 neural crest cells is not strictly cell-autonomous. When r5 is transposed with r4 by rostrocaudal rotation of the rhomobomeres, Hoxa3 is expressed in cells migrating lateral to transposed r5 and for a short time, in condensing ganglia, but not by neural crest within the second branchial arch. Since DiI-labeled cells from transposed r5 are present in the second arch, Hoxa3-expressing neural crest cells from r5 appear to down-regulate their Hoxa3 expression in their new environment. In contrast, when r6 is transposed to the position of r4 after boundary formation, Hoxa3 is maintained in both migrating neural crest cells and those positioned within the second branchial arch and associated ganglia. These results suggest that Hoxa3 expression is cell-autonomous in r6 and its associated neural crest. Our results suggest that neural crest cells expressing the same Hox gene are not eqivalent; they respond differently to environmental signals and exhibit distinct degrees of cell autonomy depending upon their rhombomere of origin.

Animals↗