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PubMed1996

Neural tube closure in the chick embryo is multiphasic.

Progression of neurulation in the chick embryo has not been well documented. To provide a detailed description, chick embryos were stained in ovo after the least manipulation possible to avoid distortion of the neural plate and folds. This allowed a morphological and morphometric description of the process of neurulation in relatively undisturbed chick embryos. Neurulation comprises several specific phases with distinct closure patterns and closure rates. The first closure event occurs, de novo, in the future mesencephalon at the 4-6 somite stage (sst 4-6). Soon afterwards, at sst 6-7, de novo closure is seen at the rhombocervical level in the form of multisite contacts of the neural folds. These contacts occur in register with the somites, suggesting that the somites may play a role in forcing elevation and apposition of the neural folds. The mesencephalic] and rhombocervical closure events define an intervening rhombencephalic neuropore, which is present for a brief period before it closes. The remaining pear-shaped posterior neuropore (PNP) narrows and displaces caudally, but its length remains constant in embryos with seven to ten somites, indicating that the caudal extension of the rhombocervical closure point and elongation of the caudal neural plate are keeping pace with each other. From sst 10 onward, the tapered cranial portion of the PNP closes fast in a zipper-like manner, and, subsequently, the wide caudal portion of the PNP closes rapidly as a result of the parallel alignment of its folds, with numerous button-like temporary contact points. A role for convergent extension in this closure event is suggested. The final remnant of the PNP closes at sst 18. Thus, as in mammals, chick neurulation involves multisite closure and probably results form several different development mechanisms at varying levels of the body axis.

Animals↗

PubMed1997

Genetic patterning of the developing mouse tail at the time of posterior neuropore closure.

Posterior neuropore (PNP) closure coincides with the end of gastrulation, marking the end of primary neurulation and primary body axis formation. Secondary neurulation and axis formation involve differentiation of the tail bud mesenchyme. Genetic control of the primary-secondary transition is not understood. We report a detailed analysis of gene expression in the caudal region of day 10 mouse embryos during primary neuropore closure. Embryos were collected at the 27-32 somite stage, fixed, processed for whole mount in situ hybridisation, and subsequently sectioned for a more detailed analysis. Genes selected for study include those involved in the key events of gastrulation and neurulation at earlier stages and more cranial levels. Patterns of expression within the tail bud, neural plate, recently closed neural tube, notochord, hindgut, mesoderm, and surface ectoderm are illustrated and described. Specifically, we report continuity of expression of the genes Wnt5a, Wnt5b, Evx1, Fgf8, RARgamma, Brachyury, and Hoxb1 from primitive streak and node into subpopulations of the tail bud and caudal axial structures. Within the caudal notochord, developing floorplate, and hindgut, HNF3alpha, HNF3beta, Shh, and Brachyury expression domains correlate directly with known genetic roles and predicted tissue interdependence during induction and differentiation of these structures. The patterns of expression of Wnt5a, Hoxb1, Brachyury, RARgamma, and Evx1, together with observations on proliferation, reveal that the caudal mesoderm is organised at a molecular level into distinct domains delineated by longitudinal and transverse borders before histological differentiation. Expression of Wnt5a in the ventral ectodermal ridge supports previous evidence that this structure is involved in epithelial-mesenchymal interaction. These results provide a foundation for understanding the mechanisms facilitating transition from primary to secondary body axis formation, as well as the factors involved in defective spinal neurulation.

Animals↗

PubMed1987

Early stages of development in the caudal neural tube of the golden Syrian hamster (Mesocricetus auratus).

Secondary neurulation is the morphogenetic process whereby the caudal segments of the neural tube are derived from cells in the embryonic tail bud. Comparative studies have demonstrated similar characteristics in the mechanism of secondary neurulation among tailless species, which are thought to be due to the evolutionary reduction in tail length (Hughes and Freeman, 1974). In order to explore this hypothesis further, light and scanning electron microscopy was used to study early stages of neurulation in the tail buds of hamster embryos. The golden Syrian hamster is a relatively common laboratory rodent with a reduced tail. In this species, secondary neurulation first became apparent in embryos with approximately 17 pairs of somites. This was well before closure of the posterior neuropore which occurred at the 21-somite stage. The lumen of the neural tube appeared to extend into the tail bud in an even and progressive fashion accompanied by reorientation and rearrangement of tail-bud cells. The mechanism appeared to be similar to that reported in long-tailed rodents.

Animals↗

PubMed1984

Histological and ultrastructural studies on the origin of caudal neural crest cells in mouse embryos.

The origin of neural crest cells was studied histologically and ultrastructurally in caudal regions of mouse embryos at 8.5-11 days of gestation (day of vaginal plug = day 0). The neural tube of caudal regions develops in two different phases, called primary and secondary neurulation. The primary (more cranial) portion of the neural tube originates from the ectodermal neural plate, whereas the secondary (most caudal) portion originates from the tail bud. We asked in this study: Do neural crest cells of caudal regions originate exclusively from the developing primary portion of the neural tube and, subsequently, migrate into areas undergoing secondary neurulation; or do some of these cells originate from the tail bud, with the secondary portion of the neural tube, forming in situ in caudal areas? Most embryos were preserved with fixative containing cetylpyridinium chloride (CPC) to facilitate the identification of neural crest cells, which stain darkly after exposure to CPC during fixation. Our results suggest that there are two sources of neural crest cells in caudal regions: the neuroectoderm of the neural folds flanking the closing posterior neuropore, and the tail bud. Neural crest cells derived from the neuroectoderm are designated as the primary neural crest, because they form in conjunction with the primary portion of the neural tube during primary neurulation, whereas neural crest cells derived from the tail bud are designated as the secondary neural crest, because they form in conjunction with the secondary portion of the neural tube during secondary neurulation.

Animals↗

PubMed1985

Neural fold and neural crest movement in the Mexican salamander Ambystoma mexicanum.

In studies of amphibian neurulation, the terms "neural ridge," "neural fold," and "neural crest" are sometimes used as synonyms. This has occasionally led to the misconception that grafting of the neural crest is equivalent to grafting of the neural fold. The neural fold, however, is composed of three parts: the neural crest, prospective neural tube tissue, and epidermis. In order to investigate how these neural fold components move during neurulation, time-lapse photography, electron microscopy, and grafting were performed. Ambystoma mexicanum embryos were photographed during neurulation at regular intervals. The photographs were analyzed to find the position of those cells at beginning of neurulation that end up on the line of fusion as the neural folds close. Posteriorly, these cells are already on the emerging neural fold. In the anterior neural folds, however, these cells are located in the lateral epidermis. Electron microscopy of the neural folds confirms the presence of epidermis. To follow the movement of the cells differentiating into melanophores (neural crest), neural fold parts were grafted into albino hosts. The crest cells differentiating into melanophores following ectopic grafting are located in the flank of the neural fold that is in contact with the neural plate. In grafts from the outside (distal) flank, no melanophores developed. Semithin sections show that the third part of the neural fold consists of apically constricted cells known to differentiate into neural tissue. Because the neural folds consist of epidermis, neural tissue, and neural crest, neural fold and neural crest cannot be used as synonyms.

Ambystoma↗

PubMed1993

Embryonic development of the mammalian caudal neural tube.

In the literature, some controversy still exists about the embryonic developmental processes involved in the formation of the caudal neural tube. Therefore, a three-dimensional and histological study concerning the normal development of the caudal neural tube was performed on both mouse and human embryos. Three developmental processes can be distinguished in caudal neural tube development: caudal neuropore closure, secondary neurulation, and degeneration and differentiation of the secondary neural tube. Caudal neuropore closure occurs at the level of somite 32-34 in both species. Therefore, primary neurulation leads to the formation of all spinal cord segments and ganglia. Secondary neurulation involves cell deposition from a cluster of neurectodermal cells at the caudal end of the closed neural tube, directly around a lumen, the lumen always in contact with the lumen of the primary neural tube. This process leads only to the formation of the primordia of the filum terminale and ventriculus terminalis and, possibly, part of the conus medullaris. Secondary neurulation is followed by a period characterized by degeneration and differentiation of the secondary neural tube. Its lumen and neural tissue will disappear, whereas part of the secondary neurectodermal cells differentiate to a fibrous layer comparable and continuous with the marginal layer of the primary neural tube. This fibrous layer represents the future filum terminale. The embryological processes indicated above can be helpful in the interpretation of congenital anomalies affecting the caudal spinal cord and spine.

Animals↗

PubMed1996

Differences in origin and fate between the cranial and caudal spinal cord during normal and disturbed human development.

Differences in histological appearance between the cranial and caudal parts of the spinal cord and associated axial organs were analyzed in 9- and 15-week-old human dysraphic fetuses and compared with normal fetuses. In human development the cranial part of the neural tube down to the lumbosacral level forms during primary neurulation, while its caudal part results from secondary neurulation. In the 9-week fetus with cervical spina bifida, the cranial spinal cord displayed a variety of morphological changes along the cranio-caudal axis. Spinal cord in the upper cervical region transformed into the area cerebrovasculosa, while the lower cervical and thoracic levels showed only disturbed differentiation of the cell layers and roof plate. The degree of the cranial spinal cord dysmorphogenesis correlated with anomalies of the underlying notochord and vertebral column. The caudal to lumbosacral region of the spinal cord appeared normal. In the case of the 15-week-old fetus with complete dysraphia, the area cerebrovasculosa was found along the whole extent of the cranial spinal cord, while more caudally, all axial organs showed a normal histological structure. Our findings confirmed a different origin for the cranial and caudal parts of the human spinal cord. The appearance of dysraphic disorders corresponded to the time of primary neurulation; therefore, they resulted in the faulty formation of the cranial spinal cord. Normally formed caudal spinal cord appears during secondary neurulation at later developmental stages.

Age Factors↗

PubMed2006

Current perspectives on the genetic causes of neural tube defects.

Neural tube defects (NTDs) are a group of severe congenital abnormalities resulting from the failure of neurulation. The pattern of inheritance of these complex defects is multifactorial, making it difficult to identify the underlying causes. Scientific research has rapidly progressed in experimental embryology and molecular genetics to elucidate the basis of neurulation. Crucial mechanisms of neurulation include the planar cell polarity pathway, which is essential for the initiation of neural tube closure, and the sonic hedgehog signaling pathway, which regulates neural plate bending. Genes influencing neurulation have been investigated for their contribution to human neural tube defects, but only genes with well-established role in convergent extension provide an exciting new set of candidate genes. Biochemical factors such as folic acid appear to be the greatest modifiers of NTDs risk in the human population. Consequently, much research has focused on genes of folate-related metabolic pathways. Variants of several such genes have been found to be significantly associated with the risk of neural tube defects in more studies. In this manuscript, we reviewed the current perspectives on the causes of neural tube defects and highlighted that we are still a long way from understanding the etiology of these complex defects.

Animals↗

PubMed2006

Effects of high dose retinoic acid on TGF-beta2 expression during pancreatic organogenesis.

The aim of this study was to investigate the effects of excess all-trans retinoic acid, a vitamin A metabolite, on pancreatic organogenesis and TGF-beta2 expression during prenatal development in rats. First group of animals used as control while a single dose of 60 mg/kg all-trans retinoic acid was ingested by the mothers, at day 8 of gestation (before the neurulation period) in group II and at day 12 of gestation (after the neurulation period) in group III, and all embryos were sacrificed at day 18 of gestation. TGF-beta2 expression was detected in the capsule, acini and Langerhans islets in the control group. In the pancreas of group II, dilatation and congestion of interlobular vessels were observed. Langerhans islet structures were completely absent. Moreover acinar TGF-beta2 immune reactivity was not determined. In group III, acinar expression of TGF-beta2 in acid was similar to that in the controls but their Langerhans islets TGF-beta2 immune reactivity was significantly less than the controls. In view of the present findings we suggest that TGF-beta2 plays important role in pancreatic morphogenesis and administration of excess all-trans retinoic acid before neurulation inhibit TGF-beta2 expression disrupted pancreatic morphogenesis particularly Langerhans islets. However, its administration after neurulation had less adverse affect on pancreatic organogenesis and TGF-beta2 immune reactivity.

Animals↗

PubMed2006

Progesterone improves the number and quality of hormone induced Fowler toad (Bufo fowleri) oocytes.

Combinations of progesterone, lutenizing hormone releasing hormone analogue (LHRHa), human chorionic gonadotrophin (hCG), and the dopamine-2 (DA2) receptor antagonist 1-[1-[4,4-bis(4-Fluorophenyl)butyl]-4-piperidinyl]-1,3-dihydro-2H-benzimidazol-2-one (Pimozide; Orap) were tested for improvement of spawning rates, oocyte numbers, fertilization and neurulation rates of the Fowler toad (Bufo fowleri). Only treatments combined with progesterone produced large numbers of oocytes. The best treatment on oocyte numbers, neurulation rates, and the number of neurulas was with 5 mg progesterone, 20 mic.g LHRHa, and 0.25 mg Pimozide. Progesterone (5 mg) with 60 mic.g LHRHa gave high spawning rates, oocyte numbers, and fertilization rates but neurulation rates were low. Progesterone alone in high repeated doses did not result in ovulation. High doses of LHRHa (60 mic.g) with hCG, progesterone, and Pimozide gave the greatest number of toads spawning, however, they resulted in low oocyte numbers, fertilization and neurulation rates. A low dose of LHRHa (4 mic.g) with hCG, or hCG alone as a second administration, and progesterone with Pimozide produced few good quality oocytes. Toads were given normal ovulatory doses of hormones 24 or 48 hrs after their initial dose, but these resulted in low oocyte numbers followed by poor fertilization. Overall, these results suggest that progesterone with a dose between 20 mic.g and 60 mic.g of LHRHa may be optimal for the induction of ovulation in these toads. Moreover, Pimozide can supplement low doses of LHRHa but not replace it.

Animals↗

PubMed2002

Neural tube closure requires Dishevelled-dependent convergent extension of the midline.

In Xenopus, Dishevelled (Xdsh) signaling is required for both neural tube closure and neural convergent extension, but the connection between these two morphogenetic processes remains unclear. Indeed normal neurulation requires several different cell polarity decisions, any of which may require Xdsh signaling. In this paper we address two issues: (1) which aspects of normal neurulation require Xdsh function; and (2) what role convergent extension plays in the closure of the neural tube. We show that Xdsh signaling is not required for neural fold elevation, medial movement or fusion. Disruption of Xdsh signaling therefore provides a specific tool for uncoupling convergent extension from other processes of neurulation. Using disruption of Xdsh signaling, we demonstrate that convergent extension is crucial to tube closure. Targeted injection revealed that Xdsh function was required specifically in the midline for normal neural tube closure. We suggest that the inherent movement of the neural folds can accomplish only a finite amount of medial progress and that convergent extension of the midline is necessary to reduce the distance between the nascent neural folds, allowing them to meet and fuse. Similar results with Xenopus strabismus implicate the planar cell polarity (PCP) signaling cascade in neural convergent extension and tube closure. Together, these data demonstrate that PCP-mediated convergent extension movements are crucial to proper vertebrate neurulation.

Adaptor Proteins, Signal Transducing↗

PubMed1996

A spinal cord fate map in the avian embryo: while regressing, Hensen's node lays down the notochord and floor plate thus joining the spinal cord lateral walls.

The spinal cord of thoracic, lumbar and caudal levels is derived from a region designated as the sinus rhomboidalis in the 6-somite-stage embryo. Using quail/chick grafts performed in ovo, we show the following. (1) The floor plate and notochord derive from a common population of cells, located in Hensen's node, which is equivalent to the chordoneural hinge (CNH) as it was defined at the tail bud stage. (2) The lateral walls and the roof of the neural tube originate caudally and laterally to Hensen's node, during the regression of which the basal plate anlage is bisected by floor plate tissue. (3) Primary and secondary neurulations involve similar morphogenetic movements but, in contrast to primary neurulation, extensive bilateral cell mixing is observed on the dorsal side of the region of secondary neurulation. (4) The posterior midline of the sinus rhomboidalis gives rise to somitic mesoderm and not to spinal cord. Moreover, mesodermal progenitors are spatially arranged along the rest of the primitive streak, more caudal cells giving rise to more lateral embryonic structures. Together with the results reported in our study of tail bud development (Catala, M., Teillet, M.-A. and Le Douarin, N.M. (1995). Mech. Dev. 51, 51-65), these results show that the mechanisms that preside at axial elongation from the 6-somite stage onwards are fundamentally similar during the complete process of neurulation.

Animals↗

PubMed2001

[Mechanisms for encoding positional information in embryonic shaping of the vertebrate brain].

The mechanisms of early embryonal shaping of the brain in man and animals were studied. Analysis of the biomechanical properties of development of nervous tissue and embryological experiments demonstrated that tangential neuroepithelial intention is the major source of positional information. Experimental changes in the neuroepithelial intention system resulted in various types of embryonal anomalies of the nervous system. Mechanism-dependent ion channels that have marked periods of sensitivity and determine the histogenetic direction of neuroblast cell differentiation were found to underlie the mechanosensitivity of the neuroepithelium. Experimental findings were compared with unique autopsy data on early development of the human brain. Human embryos were examined from neurulation to week 6 of development. Different types of human embryonal brain anomalies were shown to occur with 3 types of neurulation disorders: 1) an open preneuropore is responsible for anomalies of the forebrain and ethmoidal area; 2) arrested neurulation in the postneuropore leads to anomalies of the diencephalon, midbrain, and occipital region; 3) impaired neurulation in the caudal region is a cause of spinal cord anomalies. The above anomalies resulted from local compensatory responses of the neuroepithelium due to the lack of intentions that are characteristic of normal development of the neural tube.

Adolescent↗

PubMed2002

Methods of developmental research.

Neural tube defects (NTD) caused by abnormal neurulation are the major congenital anomalies which result in fetal or embryonic death, and medical, financial and social problems. The multifactorial events of neurulation have attracted researchers to identify the mechanisms of this disability. Research focused on NTDs is one of the major topics in developmental experiments. Mammalian, avian, amphibian and computer models are used as fundamental models to discover specific events causing NTDs. There are advantages of working on some models: rats and mice are mammalian models of neurulation; amphibians and avian embryos are simple models and more practical. Advancement in laboratory techniques has yielded more detailed information about neurulation which will assist in future with prevention and therapy of these defects.

Animals↗

PubMed1986

Gene and teratogen induced defects of early central nervous system development.

The events involved in the histogenesis of the primitive nervous system involve precise control over cell shape changes, cellular migrations, cell-cell and cell-extracellular matrix interactions. The coordinated procession of these events results in the elevation of the neural folds, and their apposition and fusion in the dorsal midline, forming the primary neural tube. This is followed by a second series of cellular migrations and rearrangements (collectively called secondary neurulation) which result in lengthening of the caudal neural tube. After a brief consideration of the mechanisms involved in neurulation, the effects of gene or teratogen induced perturbations of these events are presented and reviewed. New data are presented on neurulation in the delayed Splotch mutant embryo and on the effects of altering mesenchymal or neuroepithelial basal lamina constituents on primary and secondary neurulation.

Animals↗

PubMed1995

[The symmetrical relation of intestines, the habenular nuclei and the intestinal venous system in dorsal-doral and ventral-ventral grown parabiontic larva of mountain salamanders (Triturus alpestris)].

Embryos of the newt Triturus alpestris were fused in their dorsal regions (DD-parabionts) of their ventral regions (VV-parabionts), while the longitudinal axes were in equal direction. In these parabionts situs and symmetry of the gut, the heart, the habenular nuclei and the vitelline vein were studied. The fusion of the embryos of the DD-parabionts was performed in three developmental stages (after Harrison): phase of neurulation (14-18, N-parabionts), late phase of neurulation (19-22, E-parabionts) and tail bud stage (23-27, S-parabionts). VV-parabionts were only fused in phase of neurulation (14-18). The external development of the parabionts in most cases was normally. DD-parabionts showed a more or less pronounced deformation of their longitudinal axes. In DD-parabionts all organs developed separately in nearly all cases. In VV-parabionts a partial fusion of the heart was sometimes observed, while fusion of large part of gut occurred regularly. In DD-parabionts complete and incomplete inversions of all organs and the vitelline vein are extremely abundant in the N-parabionts, much lower in E-parabionts and nearly absent in S-parabionts. The differences are statistically of high significance. The "pair situs" symmetries of N-parabionts (DD-parabionts) show always a strong dominance of a transindividual organ- and vitellin vein-symmetry. In VV-parabionts (N-parabionts) the tendency for inversion of the asymmetric organs is statistically significant lower as in DD-parabionts. In regard to this observation there is a preference for an asymmetric "pair situs" in the heart, habenular nuclei and vitelline vein system. In "polarisied" DD-parabionts ("left" as well as "right" parabionts) the asymmetric organs as well as the vitelline vein system inversions were more often observed in the "left" parabiont compared with the "right" parabiont in N- and E-parabionts. These right-left differences partial are statistically significant (P < 0.05). The organ situs-correlation as well as the situs-correlation between vitelline vein and gut or heart, respectively, are mostly positive (concordant). The frequency of dominance of "left" organ inversions argues against a morphogenetic "left dominance" of the amphibian embryo. The determination of organ-asymmetries is irreversible only after the end of neurulation in tail-bud-stage. The results suggest the efficiency of a "symmetry-factor", which determines the organ symmetry during neurulaphase. The differences between DD- and VV-parabionts are statistically significant and point to a dorso-ventral polarity of the embryo, with a maximal morphogenetic potency in the dorsal region.

Animals↗

PubMed1997

Changes in cell adhesion and extracellular matrix molecules in spontaneous spinal neural tube defects in avian embryos.

Quail embryos (embryonic days 2-2.5) with spontaneous neural tube defects (NTDs), along with age-matched normal embryos, were examined immunocytochemically for the extracellular matrix (ECM) molecules laminin, fibronectin, and chondroitin sulfate proteoglycan, the cell adhesion molecules (CAMs) E- and N-cadherin and neural CAM (NCAM), and the neural crest marker HNK-1. The embryos with NTDs were at the lower limit of the normal stage range and the affected region was about 25% shorter than in normal embryos. Open NTDs occurred in cervical and upper thoracic level, although often the ventral neural tube was morphologically normal. Widened, irregular but closed neural tubes (lower thoracic to sacral levels) showed disorganized mesenchyme-like cells centrally and often multiple lumens. Finger-like tabs projecting from the ectoderm over the neural tube also occurred at lower thoracic to sacral levels. In open NTDs, the E-cadherin-labeled epidermis was incomplete dorsally, and was continuous with the N-cadherin-labeled neural tissue, with a sharp demarcation between E- and N-cadherin-expressing regions, as in the early stages of normal primary neurulation. A sharp inverted peak of epidermis extended ventrally, closely applied to the side of the neural tissue. The intervening matrix labeled less intensely for chondroitin sulfate proteoglycan relative to laminin and fibronectin, in comparison to control embryos. In closed NTDs, the dorsal superficial cell layer (i.e., positionally epidermis) was not separated from the underlying neural tissue by a band of matrix as in control embryos. In addition, this layer expressed E-cadherin (as in normal embryos), but coexpressed N-cadherin and NCAM, which are not normally found here at this stage. This overlap region resembled the mid-dorsal tissue at earlier stages in normal secondary neurulation in the tail-bud. The tabs of tissue appeared to be localized hypertrophy of the epidermal and neural ectoderm, and also showed codistribution of E- and N-cadherin. In all these defects, matrix molecules occurred within (rather than around) the neural and epidermal epithelia. HNK-1-labeled neural crest cells were frequently absent in regions of NTDs, in contrast to control embryos. These results show that matrix and cell adhesion molecules are disturbed in spontaneous NTDs at the time of neurulation, and therefore could be involved in the generation of the defects by altering cell adhesion-dependent morphogenetic events.

Animals↗

PubMed1993

Expression of Xenopus snail in mesoderm and prospective neural fold ectoderm.

Expression of the Xsna gene during Xenopus laevis embryogenesis has been analysed by in situ hybridisation. Like its homologue snail in Drosophila, Xsna is expressed zygotically in all early mesoderm. Expression starts during stage 9 in the dorsal marginal zone and spreads to the ventral side by stage 10. During gastrulation, each cell begins to express as it involutes so that cells newly expressing Xsna are added to the forming mesoderm mantle in an anterior-to-posterior progression. Xsna expression is then down-regulated in a tissue-specific fashion that reveals the subdivision of the mesoderm before its derivatives are overtly differentiated; e.g., the appearance of the notochord, myotomes, and pronephroi are preceded by the disappearance of Xsna mRNA, while undifferentiated mesoderm remains labelled, even into tadpole stages. Xsna is expressed in the suprablastoporal endoderm during gastrulation and in its derivatives, the prechordal and sub-notochordal endoderm, during neurulation. Relationships between Xbra, Xtwi, and Xsna expression are examined. Xsna is also expressed in the prospective neural fold ectoderm from stage 11 in a low arc above the dorsal marginal zone, precisely identifying a distinct band of cells that surrounds the prospective neural plate that we designate the neural plate border. The anterior transverse neural fold, which becomes forebrain, ceases Xsna expression during neurulation. In the longitudinal neural folds, the deep and superficial ectoderm compartments labelled by Xsna expression are the prospective neural crest and prospective roof of the neural tube, respectively. Xsna expression persists in the neural crest during migration and in some derivatives at least until metamorphosis but ceases in the roof of the neural tube soon after neurulation.

Animals↗