Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neural Plate”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed2003

Localization of cartilage linking protein 1 during primary neurulation in the chick embryo.

Primary neurulation is a form-shaping event during the early development of the vertebrate embryo in which the neural plate is rolled up into the neural tube, the rudiment of the central nervous system. In an effort to identify genes specifically expressed in tissues lateral to the chick neural plate--tissues known to generate extrinsic forces for primary neurulation--we designed a subtractive scheme and identified a positive clone as the gene encoding chick cartilage linking protein 1 (CRTL1). CRTL1 (also known as link protein) is a small glycoprotein of the extracellular matrix that was originally identified for its role in stabilizing aggregates of aggrecan and hyaluronan in cartilage. In addition to being expressed in cartilage, CRTL1 is also immunolocalized in several noncartilaginous tissues as assessed with the 4B6 monoclonal antibody. Using the 4B6 antibody and the G9 riboprobe derived from our subtraction, we report the detailed distribution of CRTL1 protein and crtl1 transcripts during primary neurulation in chick embryos. This report emphasizes and briefly discusses important differences between the RNA expression pattern and the domains of accumulation of the protein. CRTL1 prominently accumulates in the basal lamina of the epidermal ectoderm just lateral to the neural plate. Based on the crucial role of the interface between this tissue and the neuroepithelium in the formation of the neural folds, and because of the biophysical role of hyaluronan in tissue morphogenesis, we propose that crtl1 represents is an excellent candidate neurulation gene, worthy of further study.

Animals↗
PubMed1976

Changes in the shape of the developing vertebrate nervous system analyzed experimentally, mathematically and by computer simulation.

Two forces are necessary and sufficient to produce the transformation of the newt neural plate from a hemispheric sheet of cells one cell thick to a keyhole shape. These forces are: (1) a regionally programmed shrinkage of the surface of the neural plate (accomplished by contraction of the apical surfaces of the neural plate cells and elongation of these cells perpendicular to the plate); and (2) displacement of the whole sheet caused by elongation of either the notochord or the overlying neural plate cells in the antero-posterior direction. A computer simulation and mathematical analysis ("morphodynamics"), together with experiments and observations on embryos, were used to deduce the morphogenesis of the neural plate from these forces.

Animals↗
PubMed2003

Expression pattern of a basic helix-loop-helix transcription factor Xhairy2b during Xenopus laevis development.

We report on the temporal and spatial expression pattern of the Xenopus laevis hairy2b ( Xhairy2b) transcription factor. Xhairy2b transcripts are present maternally, and expressed throughout the prospective ectoderm prior to the gastrula stage. During gastrulation, Xhairy2b expression is restricted to the deep layer of the Spemann organizer and three distinct regions in the prospective neuroectoderm, neural plate border, notoplate and anterior neural plate. At later stages, Xhairy2b expression is localized to prechordal plate, presomitic mesoderm, neural tube, neural crest derivatives and several tissue territories of the central nervous system. The analyses of Xhairy2b and several other hairy-related genes suggest potential roles for Xhairy2b in the formation of boundaries in neural tissue territories.

Animals↗
PubMed2003

A novel inducible element, activated by contact with Rathke's pouch, is present in the regulatory region of the Rpx/Hesx1 homeobox gene.

Reciprocal inductive interactions are postulated to play a role in the determination and differentiation of the pituitary gland and the ventral hypothalamus. The homeobox gene Rpx/Hesxl is expressed during gastrulation in the anterior endoderm, prechordal plate, and the prospective cephalic neural plate, and at later stages of development in Rathke's pouch, the primordium of the pituitary. We have defined the regulatory elements necessary for proper spatial and temporal expression during development in transgenic mice using lacZ reporter genes. Proper spatial and temporal expression in the anterior endoderm prechordal plate and anterior neural plate can be recapitulated with as little as 568 bp of upstream sequence and intragenic sequence containing the first exon and intron. Late-stage expression in Rathke's pouch requires additional negative and positive regulatory elements. Interestingly, deletion analysis uncovered an element that directs transgene expression to a region of the hypothalamus that lies in direct contact with Rathke's pouch. In vitro tissue recombination experiments have established that this expression is induced by contact with the pouch. We propose that this element may be present in other genes that normally respond to signals emanating from the pouch during the development of the hypothalamic-pituitary axis. The Rpx-lacZ transgenic mice provide a novel model system for the molecular dissection of inductive cell signaling during pituitary development.

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↗
PubMed2000

Neuroectodermal specification and regionalization of the Spemann organizer in Xenopus.

During gastrulation in Xenopus convergence and extension movements, mediated by mediolateral intercalations, are the driving force for early neural plate morphogenesis. Here we show that the winged helix transcriptional regulator, Xfd-12' is dynamically expressed in medial neural plate precursors that undergo convergence and extension movements. These medial neuraxial progenitors are specified in and beyond the Spemann organizer prior to specification of the basal anlage of the neural plate. The initiation of Xfd-12' expression coincides with the induction of mesendoderm by Nodal-related growth factors at the late blastula stage. Comparative expression analysis suggests that cellular rearrangements at the pre-gastrulation stage account for regionalization of the Spemann organizer into head and trunk organizer compartments, the latter in which medial neural plate progenitors reside. While the maintenance of Xfd-12' expression in the dorsal non-involuting marginal zone requires FGF signalling, its subsequent positioning along the medial aspect of the neuraxis depends on signalling by Wnt and Nodal-related family members. Based on these findings we propose that XFD-12' is a trunk organizer component that might control convergence and extension movements of medial neural plate precursors during gastrulation.

Animals↗
PubMed1983

Early epochal maps of two different cell adhesion molecules.

N-CAM, the neural cell-adhesion molecule, has previously been found to be expressed during several epochs of development and function, first as an early marker in embryo-genesis, later during organogenesis, and finally in adult life. L-CAM, the liver cell-adhesion molecule, has now been localized in embryonic and adult tissues of the chicken by fluorescent antibody techniques. In the early embryonic epoch, L-CAM and N-CAM appeared in epiblastic and hypoblastic tissues. L-CAM was distributed thereafter across all three germ layers. By the onset of neurulation, however, L-CAM disappeared in the region of the neural plate and N-CAM increased in amount in that region. L-CAM appeared strongly on all budding endodermal structures (liver, pancreas, lung, thyroid, parathyroid, thymus, and bursa of Fabricius) whereas N-CAM appeared most strongly in the neural plate, neural tube, and in cardiac mesoderm but was not found in endodermal derivatives. In placodes, both L-CAM and N-CAM were present until the formation of definitive neural structures, at which time L-CAM disappeared. In kidney precursors, the two CAMs followed a complex reciprocal pattern of appearance and disappearance. For the most part, however, the distributions of the two molecules did not overlap during organogenesis. Like N-CAM, L-CAM persisted in a distinctive pattern of expression in adult tissues. During embryonic development, the two different CAMs were distributed on tissues derived from more than two-thirds of the early embryonic surface. Interpretation of maps summarizing CAM distributions over a defined developmental epoch suggested a key role for both L-CAM and N-CAM in embryonic induction. Consistent with this interpretation and with the fact that the continuity of germ layers is lost when organ rudiments are formed, neither of the CAMs was limited in distribution to a single germ layer. The regions of the early epochal maps that lacked both L-CAM and N-CAM comprised some portions of the splanchnopleure and somatopleure. Certain adult tissues that derive from this lateral plate mesoderm such as smooth muscle also lacked L-CAM and N-CAM. Such observations suggest that at least one more CAM may exist in these and similarly derived tissues.

Animals↗
PubMed1979

Histogenesis of experimental open neural defects in the early chick embryo.

The chick embryo is a useful experimental model for investigating neural dysraphism. Windowing at 26 h incubation is by itself teratogenic, resulting in predominantly neural tube defects. A histological study of a regular series of specimens between pre-neurulation and later stages was undertaken. Open brain defects occurred at every stage after the expected closure of the anterior neuropore, suggesting that they arose by non-closure, myeloschisis was preceded by a characteristic triangular shape of the rhomboid sinus. Serial sections revealed regular open defects, with separation between the neural plate and tail-bud sources of neural tissue, but continuity of the neural plate into the caudal region. These findings suggest that myeloschisis arises by nonclosure of the neural folds. The establishment of myeloschisis was followed by local separation of the notochord from an open area of neural tube, but not by overgrowth of neural tissue. Myelodysplasia appeared at about the time of expected closure of the rhomboid sinus. Serial sections revealed irregular open defects, with complete absence of neural plate material and formation of the cord tissue from tailbud material alone. The lesions were accompanied by extensive cystic and hemorrhagic changes in local mesoderm, with reduction in somite volume. There was no associated notochordal separation.

Animals↗
PubMed1996

The role of bone morphogenetic proteins in vertebral development.

This study first shows a striking parallel between the expression patterns of the Bmp4, Msx1 and Msx2 genes in the lateral ridges of the neural plate before neural tube closure and later on, in the dorsal neural tube and superficial midline ectoderm. We have previously shown that the spinous process of the vertebra is formed from Msx1- and 2-expressing mesenchyme and that the dorsal neural tube can induce the differentiation of subcutaneous cartilage from the somitic mesenchyme. We show here that mouse BMP4- or human BMP2-producing cells grafted dorsally to the neural tube at E2 or E3 increase considerably the amount of Msx-expressing mesenchymal cells which are normally recruited from the somite to form the spinous process of the vertebra. Later on, the dorsal part of the vertebra is enlarged, resulting in vertebral fusion and, in some cases (e.g. grafts made at E3), in the formation of a 'giant' spinous process-like structure dorsally. In strong contrast, BMP-producing cells grafted laterally to the neural tube at E2 exerted a negative effect on the expression of Pax1 and Pax3 genes in the somitic mesenchyme, which then turned on Msx genes. Moreover, sclerotomal cell growth and differentiation into cartilage were then inhibited. Dorsalization of the neural tube, manifested by expression of Msx and Pax3 genes in the basal plate contacting the BMP-producing cells, was also observed. In conclusion, this study demonstrates that differentiation of the ventrolateral and dorsal parts of the vertebral cartilage is controlled by different molecular mechanisms. The former develops under the influence of signals arising from the floor plate-notochord complex. These signals inhibit the development of dorsal subcutaneous cartilage forming the spinous process, which requires the influence of BMP4 to differentiate.

Animals↗
PubMed1998

XBF-2 is a transcriptional repressor that converts ectoderm into neural tissue.

We have identified Xenopus Brain Factor 2 (XBF-2) as a potent neuralizing activity in an expression cloning screen. In ectodermal explants, XBF-2 converts cells from an epidermal to a neural fate. Such explants contain neurons with distinct axonal profiles and express both anterior and posterior central nervous system (CNS) markers. In striking contrast to X-ngnR-1a or X-NeuroD, ectopic expression of XBF-2 in Xenopus embryos results in an expansion of the neural plate to the ventral midline. The enlarged neural plate consists predominantly of undifferentiated neurons. XBF-2 lies downstream of the BMP antagonists noggin, cerberus, and gremlin since ectodermal explants expressing these molecules exhibit strong expression of XBF-2. While XBF-2 does not upregulate the expression of secreted neural inducers, it downregulates the transcription of BMP-4, an epidermal inducer. We show that XBF-2 acts as a transcriptional repressor and that its effects can be phenocopied with either the engrailed or hairy repressor domain fused to the XBF-2 DNA-binding domain. A fusion of the DNA-binding domain to the activator domain of VP16 blocks the effects of XBF-2 and prevents neural plate development in the embryo. This provides evidence that a transcriptional repressor can affect both regional neural development and neurogenesis in vertebrates.

Amino Acid Sequence↗
PubMed1998

Neurulation in amniote vertebrates: a novel view deduced from the use of quail-chick chimeras.

Two apparently different mechanisms successively contribute to the formation of the neural tube in the avian embryo: bending of the neural plate during the primary neurulation in the cephalo-cervico-thoracic region and cavitation of the medullary cord during the secondary neurulation in the lumbo-sacral region. During both these processes, gastrulation continues by the caudal regression of Hensen's node--also called cordoneural hinge in the secondary neurulation. Labeling of Hensen's node or cordoneural hinge by the quail chick marker system revealed that this structure, which is the equivalent of the dorsal blastoporal lip of the Amphibian embryo, i.e., of the Spemann's organizer, gives rise to the midline cells of the three germ layers: the floor plate of the neural tube, the notocord and the dorsal cells of the intestinal endoderm. Caudally to the organizer, both in primary and secondary neurulation, the presumptive territory of the alar plates of the future neural tube overlies the precursors of the paraxial mesoderm. Regression of Hensen's node bisects the ectoderm in two bilateral neural plates leaving in its wake the floor plate, the notocord and the dorsal endoderm.

Animals↗
PubMed2002

An amphioxus winged helix/forkhead gene, AmphiFoxD: insights into vertebrate neural crest evolution.

During amphioxus development, the neural plate is bordered by cells expressing many genes with homologs involved in vertebrate neural crest induction. However, these amphioxus cells evidently lack additional genetic programs for the cell delaminations, migrations, and differentiations characterizing definitive vertebrate neural crest. We characterize an amphioxus winged helix/forkhead gene (AmphiFoxD) closely related to vertebrate FoxD genes. Phylogenetic analysis indicates that the AmphiFoxD is basal to vertebrate FoxD1, FoxD2, FoxD3, FoxD4, and FoxD5. One of these vertebrate genes (FoxD3) consistently marks neural crest during development. Early in amphioxus development, AmphiFoxD is expressed medially in the anterior neural plate as well as in axial (notochordal) and paraxial mesoderm; later, the gene is expressed in the somites, notochord, cerebral vesicle (diencephalon), and hindgut endoderm. However, there is never any expression in cells bordering the neural plate. We speculate that an AmphiFoxD homolog in the common ancestor of amphioxus and vertebrates was involved in histogenic processes in the mesoderm (evagination and delamination of the somites and notochord); then, in the early vertebrates, descendant paralogs of this gene began functioning in the presumptive neural crest bordering the neural plate to help make possible the delaminations and cell migrations that characterize definitive vertebrate neural crest.

Animals↗
PubMed1994

Investigation of DNA synthesis in experimentally induced Long-Evans rat myeloschisis by the BrdU/antiBrdU technique.

The volume and DNA synthesis of the neuroepithelium in induced myeloschisis in Long-Evans rats as shown by hematoxylin-eosin and BrdU/antiBrdU immunohistochemical staining patterns were examined at different stages of embryonal development. On day 14 of gestation, control animals contained BrdU-incorporating cells mainly at the alar plate of the closed neural tube. On the same day, the everted neural plate of rats with myeloschisis showed active, diffuse uptake of BrdU in the cells of the matrix layer, although an increase in the volume of the everted neural plate was not yet identifiable. On day 21 of gestation, rats with myeloschisis showed a marked increase in the volume of the neuroepithelium compared with controls. Our investigations suggest that, in myeloschisis, more neuroepithelial cells than normal retain their capability for DNA synthesis on day 14 of gestation, and the overgrowth of the neuroepithelium found on day 21 is possibly a secondary effect of failure of neural tube closure.

Animals↗
PubMed2003

A dual role for Sonic hedgehog in regulating adhesion and differentiation of neuroepithelial cells.

In vertebrates, the nervous system arises from a flat sheet of epithelial cells, the neural plate, that gradually transforms into a hollow neural tube. This process, called neurulation, involves sequential changes in cellular interactions that are precisely coordinated both spatially and temporally by the combined actions of morphogens. To gain further insight into the molecular events regulating cell adhesion during neurulation, we investigated whether the adhesive and migratory capacities of neuroepithelial cells might be modulated by Sonic hedgehog (Shh), a signaling molecule involved in the control of cell differentiation in the ventral neural tube. When deposited onto extracellular matrix components in vitro, neural plates explanted from avian embryos at early neurulation readily dispersed into monolayers of spread cells, thereby revealing their intrinsic ability to migrate. In the presence of Shh added in solution to the culture medium, the explants still exhibited the same propensity to disperse. In contrast, when Shh was immobilized to the substrate or produced by neuroepithelial cells themselves after transfection, neural plate explants failed to disperse and instead formed compact structures. Changes in the adhesive capacities of neuroepithelial cells caused by Shh could be accounted for by inactivation of surface beta1-integrins combined with an increase in N-cadherin-mediated cell adhesion. Furthermore, immobilized Shh promoted differentiation of neuroepithelial cells into motor neurons and floor plate cells with the same potency as soluble Shh. However, the effect of Shh on the neuroepithelial cell adhesion was discernible and apparently independent from its differentiation effect and was not mediated by the signaling cascade elicited by the Patched-Smoothened receptor and involving the Gli transcription factors. Thus, our experiments indicate that Shh is able to control sequentially adhesion and differentiation of neuroepithelial cells through different mechanisms, leading to a coordinated regulation of the various cell interactions essential for neural tube morphogenesis.

Animals↗
PubMed1997

The role in neural patterning of translation initiation factor eIF4AII; induction of neural fold genes.

Expression of the RNA-helicase translation initiation factor, eIF4AII, in animal cap explants of Xenopus specifically upregulates genes expressed early in the neural plate border such as Xsna, Xslu, Pax-3 and XANF and also the cement gland marker XCG-1. eIF4AII is expressed specifically in the prospective neurectoderm from stage 11.5 and appears to have a significant role in mediating early patterning of the neurectoderm. It is induced by all known neural inducing regimes including secreted factors such as noggin, follistatin and chordin, transcription factors such as XlPou-2 and constructs that overcome repression of neural induction (tBMP-4R, lim-m3 and Xbra delta 304). It is also upregulated when neurulization occurs in embryonic ectoderm that has been disaggregated and reaggregated. While high amounts of injected mRNA of the neural inducers noggin, tBMP-4R and Xlpou-2 downregulate Xslu and upregulate the neural plate NCAM, smaller amounts of these mRNAs activate expression of eIF4AII and Xslu and suppress expression of epidermal keratin in animal cap assays. Ectopic expression of eIF4AII mRNA also upregulates transcription of the PKC alpha and beta genes. The sensitivity of the upregulation of neurectodermal markers to GF109203X indicates that the activity of a calcium activated protein kinase C (PKC) is also required. Furthermore ectopic expression of mouse eIF4AII mRNA upregulates the endogenous eIF4AII gene by a process that requires the activity of PKC. The effects of eIF4AII appear to be direct as conditional expression of eIF4AII in animal cap explants at the equivalent of stage 11.5 induces the endogenous eIF4AII and neural fold genes within 40 minutes. Expression of eIF4AII and activation of PKC sensitizes the embryonic ectoderm to the neuralising effect of noggin. We suggest that in developing embryos the neuralizing signal emanating from the organiser at first induces eIF4AII and the prospective neural crest in an arc low on the dorsal aspect of the embryo. As the neuralizing signal increases in intensity close to the organizer region, the tissue becomes committed to a neural plate phenotype. Expression of Xash-3A may suppress further expression of neural plate border genes within the prospective neural plate thereby subdividing the neurectoderm into two distinct regions.

Animals↗
PubMed2001

foxD5a, a Xenopus winged helix gene, maintains an immature neural ectoderm via transcriptional repression that is dependent on the C-terminal domain.

Xenopus foxD5a, the full-length fork head gene previously described as a PCR fragment (XFLIP), is first detectable at stage II of oogenesis. Low-abundance maternal transcripts are localized to the animal hemisphere of the cleavage embryo, and protein can be translocated to the nucleus prior to the onset of zygotic transcription. Zygotic expression is strongest in the presumptive neural ectoderm at gastrula and neural plate stages, but there is minor paraxial mesodermal expression during primary gastrulation that becomes significant in the tail bud during secondary gastrulation. Expression of foxD5a in animal cap explants induces elongation and expression of mesodermal, neural-inducing, and early neural-specifying genes, indicating a role in dorsal axis formation. Zygotic foxD5a expression is induced strongly by siamois, moderately by cerberus, weakly by Wnt8 and noggin, and not by chordin in animal cap explants. Expression of foxD5a in whole embryos has differential dorsal and ventral effects. Ventral mRNA injection induces partial secondary axes composed of expanded mesodermal and epidermal tissues, but does not induce ectopic neural tissues. Dorsal mRNA injection causes hypertrophy of the neural plate and expansion of early neural genes (sox3 and otx2), but this is not the result of increased proliferation or expanded neural-inducing mesoderm. The neural plate appears to be maintained in an immature state because otx2 expression is expanded and expression of en2, Krox20, proneural genes (Xnrgn1, neuroD) and a neural differentiation gene (n-tubulin) is repressed in foxD5a-expressing cells. These results indicate that foxD5a maintains an undifferentiated neural ectoderm after neural induction. Expression of foxD5a constructs fused with the engrailed repressor domain or with the VP16 activation domain demonstrates that FoxD5a acts as a transcriptional repressor in axis formation and neural plate expansion. Deletion constructs indicate that this activity requires the C-terminal domain of the protein.

Amino Acid Sequence↗
PubMed2000

Temporospatial patterns of apoptosis in chick embryos during the morphogenetic period of development.

We examined the temporospatial pattern of naturally occurring apoptosis in chick embryos to five days of incubation (H.H. stages 1-25; Hamburger and Hamilton, 1951) using TUNEL labeling. The initial TUNEL-positive structure was the embryonic shield at stage 1. Apoptotic cells became ubiquitously present within embryos by stage 3, which is early in gastrulation. Until stage 6, TUNEL-positive cells were restricted to the headfold region. In embryos of stages 7-8, most cell death was localized at the most anterior neural plate. TUNEL-positive neural plate, notochord and somites appeared at stage 9. Otic and optic regions became TUNEL-positive at stage 11. The aggregation of cells from which the tail bud arises contains apoptotic cells from stage 11 onwards. At stage 16, scattered TUNEL-positive cells appeared in the branchial arches. Three streams of apoptotic neural crest cells in the cranial region became most clearly visible at stage 18. The secondary neural tube from which caudal structures develop contains apoptotic cells at stage 14. Apoptotic cells are present in the branchial arches and lateral body wall for extended periods, stages 16-25 and 25 respectively. At stages 24-25, intense positive regions of cell death were confined to the caudal regions of the arches, to limb and tail buds and to the lateral body wall, the latter in relation to body wall closure. The new findings in this study are discussed along with past studies to provide the temporospatial pattern of cell death during early chick development.

Animals↗
PubMed1991

Changes in neural and lens competence in Xenopus ectoderm: evidence for an autonomous developmental timer.

The ability of a tissue to respond to induction, termed its competence, is often critical in determining both the timing of inductive interactions and the extent of induced tissue. We have examined the lens-forming competence of Xenopus embryonic ectoderm by transplanting it into the presumptive lens region of open neural plate stage embryos. We find that early gastrula ectoderm has little lens-forming competence, but instead forms neural tissue, despite its location outside the neural plate; we believe that the transplants are being neuralized by a signal originating in the host neural plate. This neural competence is not localized to a particular region within the ectoderm since both dorsal and ventral portions of early gastrula ectoderm show the same response. As ectoderm is taken from gastrulae of increasing age, its neural competence is gradually lost, while lens competence appears and then rapidly disappears during later gastrula stages. To determine whether these developmental changes in competence result from tissue interactions during gastrulation, or are due to autonomous changes within the ectoderm itself, ectoderm was removed from early gastrulae and cultured for various periods of time before transplantation. The loss of neural competence, and the gain and loss of lens competence, all occur in ectoderm cultured in vitro with approximately the same time course as seen in ectoderm in vitro. Thus, at least from the beginning of gastrulation onwards, changes in competence occur autonomously within ectoderm. We propose that there is a developmental timing mechanism in embryonic ectoderm that specifies a sequence of competences solely on the basis of the age of the ectoderm.

Animals↗