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PubMed2005

Identification of protogenin, a novel immunoglobulin superfamily gene expressed during early chick embryogenesis.

We have identified a chick cDNA encoding the novel membrane protein, Protogenin. It has structural features of four immunoglobulin domains and five fibronectin type III domains and is closely related to the DCC/neogenin subclass of the Ig superfamily. protogenin gene is conserved among human, mouse and chick genome, and mapped on the same chromosome as other related members of the gene family such as neogenin, punc and nope. Expression of protogenin mRNA is most prominent in E1-E3 chick embryos and subsequently its expression level declines. The transcripts are found in early mesodermal cells, the neuroepithelial cell layer of the brain and the trunk neural tube, the neural layer of the retina and in the epithelial somite and dermomyotome.

Amino Acid Sequence↗

PubMed1999

GABAA receptor subunit composition and functional properties of Cl- channels with differential sensitivity to zolpidem in embryonic rat hippocampal cells.

Using flow cytometry in conjunction with a voltage-sensitive fluorescent indicator dye (oxonol), we have identified and separated embryonic hippocampal cells according to the sensitivity of their functionally expressed GABAA receptors to zolpidem. Immunocytochemical and RT-PCR analysis of sorted zolpidem-sensitive (ZS) and zolpidem-insensitive (ZI) subpopulations identified ZS cells as postmitotic, differentiating neurons expressing alpha2, alpha4, alpha5, beta1, beta2, beta3, gamma1, gamma2, and gamma3 GABAA receptor subunits, whereas the ZI cells were neuroepithelial cells or newly postmitotic neurons, expressing predominantly alpha4, alpha5, beta1, and gamma2 subunits. Fluctuation analyses of macroscopic Cl- currents evoked by GABA revealed three kinetic components of GABAA receptor/Cl- channel activity in both subpopulations. We focused our study on ZI cells, which exhibited a limited number of subunits and functional channels, to directly correlate subunit composition with channel properties. Biophysical analyses of GABA-activated Cl- currents in ZI cells revealed two types of receptor-coupled channel properties: one comprising short-lasting openings, high affinity for GABA, and low sensitivity to diazepam, and the other with long-lasting openings, low affinity for GABA, and high sensitivity to diazepam. Both types of channel activity were found in the same cell. Channel kinetics were well modeled by fitting dwell time distributions to biliganded activation and included two open and five closed states. We propose that short- and long-lasting openings correspond to GABAA receptor/Cl- channels containing alpha4beta1gamma2 and alpha5beta1gamma2 subunits, respectively.

Animals↗

PubMed1986

[Experimental teratological studies on facial anomalies induced in mice by bis(dichloroacetyl)diamine. II. Pathogenesis of bis(dichloroacetyl)diamine-induced median cleft face syndrome in mice].

The present study was performed to clarify the pathogenesis of bis(dichloroacetyl)diamine (abbreviated as bisdiamine hereafter)-induced median cleft face syndrome in mice. Bisdiamine was administered by oral intubation to pregnant Jcl: ICR mice at a dosage of 3,200 mg/kg/day at days 7.5 and 8.5 of gestation (VP = day 0). Embryos were recovered at 4, 12, 24, 48, 72 and 96 hr after bisdiamine treatment at day 8.5 of gestation and morphological differences between the bisdiamine-treated and control embryos at the specific time intervals were quantitatively examined by the light and scanning electron microscopy. First, bisdiamine caused extensive death of cranial, mainly prosencephalic and mesencephalic, neural crest cells and neuroepithelial cells. Second, the former damage resulted in reduced numbers of mesenchymal cells in the frontonasal prominences and the latter resulted in dorsolateral deviation of the nasal placodes. Consequently, the medial nasal prominences were abnormally widely spaced and then, the median cleft face syndrome was induced. In addition, the findings suggesting that bisdiamine might cause aberrant movement of neural crest cells and/or mesenchymal cells were observed.

Abnormalities, Drug-Induced↗

PubMed1997

Retinoic acid induced neural differentiation in a neuroectodermal cell line immortalized by p53 deficiency.

Neuroepithelial cell lines were established from cerebral vesicles of 9-day-old mouse embryos lacking functional p53 genes (Livingstone et al: Cell 70:923-935, 1992). All-trans retinoic acid (RA) induced bulk formation of neurons both in several p53-deficient neuroepithelial cell lines and in wild-type neural cells derived from early embryonic (E9-E12) forebrain vesicles. Forty-eight-hour treatment with 10(-6) M RA was necessary and sufficient to initiate neuron formation by p53(-/-)-progenitors, but neuronal characteristics appeared with a delay of 3-4 days. The first appearance of cells with astroglial features followed that of neurons with a further delay of 4-5 days. The establishment of neuronal phenotypes involved minimally three rounds of cell cycle. Future neurons were sorted out from substrate-attached cells and were characterized by a specific rearrangement of nestin-immunoreactive filaments. The formation of neuronal phenotypes was not synchronized within the RA-treated cell populations. The data indicate that RA, which promotes the initiation of neural differentiation, cannot function as a direct regulator of cell-fate decisions made by neural progenitor cells.

Animals↗

PubMed1990

Fibroblast growth factor stimulates the proliferation and differentiation of neural precursor cells in vitro.

We have developed an in vitro culture system to study the regulation of proliferation and differentiation of neural precursor cells contained within the neuroepithelium of embryonic day 10 mice. A number of soluble growth factors have been tested for their ability to regulate these early events and, of these factors, we have found that the fibroblast growth factors [FGFs] can directly stimulate the proliferation and survival of the neuroepithelial cells. At least 50% of the neuroepithelial cells divide in the presence of FGF whereas in the absence of FGF all of the cells die within 6 days of culture. At higher concentrations of FGF, the cells change from being nonadherent round cells in tight clusters into a more flattened cell type which adheres to the substratum. This morphological change is accompanied by the expression of both neurofilament and GFAP, which are definitive markers of the two major cell types in the central nervous system: neurons and glia. In addition a neuroepithelial cell line, which does not rely on FGF for survival or proliferation, expresses both of these markers in response to FGF. These results indicate that FGF is stimulating the differentiation of the neuroepithelial cells into mature neurons and glia.

Animals↗

PubMed1998

Process of repair in the neuroepithelium of developing rat brain during neurogenesis: chronological and quantitative observation of DNA-replicating cells.

The neuroepithelium (NE) of the cerebrum of the developing brain has been reported to 'regenerate' within a certain period after being injured. To clarify the process of repair of the NE during neurogenesis, we chronologically examined the number of cells in the neocortex, and the rate of DNA-replicating cells and the mitotic figure ratio in the NE of rats after injury. The injury was induced by transplacental administration of ethylnitrosourea (ENU), which is cytotoxic immediately after administration, to the pregnant rats on embryonic day 16. The number of living and pyknotic cells in a 220-micron width of the neocortex was evaluated in each of three groups, such as NE, subventricular zone (SVZ) + intermediate zone (IMZ) + subplate (SP), and cortical plate (CP). The 5-bromo-2-deoxyuridine (BrdU)-labeling index and the mitotic index were examined 4, 8, 16, 24, 36, and 48 h after ENU administration. Up to 16 h after ENU administration, the number of living cells per 220 microns width in the NE and SVZ + IMZ + SP decreased, but increased in CP. From 16 to 24 h, the living cell number per 220 microns width in the NE and CP was unchanged, but increased in the SVZ + IMZ + SP. From 24 to 36 h, the living cell number per 220 microns width increased in all the groups, NE, SVZ + IMZ + SP and CP. From 36 to 48 h, the living cell number per 220 microns width in the NE was unchanged, but increased in the SVZ + IMZ + SP and CP. The BrdU-labeling index reached its nadir at 8 h, but markedly increased by 16 h, and then decreased to the control level by 36 h. No mitotic figures were observed at 16 h after administration, but a significant increase in mitotic index was noted at 24 h, and after which it decreased to almost the control value by 36 h. These findings indicate: (i) that temporary arrest of neuroepithelial cell cycle occurs in the G1-phase from 4 to 8 h after ENU administration, (ii) that the cell synchronizes in the S-phase at 16 h, (iii) that a proportion of neuroepithelial cells of rat fetal neocortex at the neurogenesis stage return to neuroepithelial cell proliferation stage, to repair the NE, and (iv) that regulation of the cell kinetics of neuroepithelial cells depends on the number of cells in a certain width of NE during regeneration.

Alkylating Agents↗

PubMed1991

A morphometric and computer-assisted three-dimensional reconstruction study of neural tube formation in chick embryos.

The origin of the driving forces for neural tube formation remains uncertain but is currently thought to involve the participation of microfilament bundles situated in the apical ends of neuroepithelial cells. In the work presented here, we show how morphometric measurements that map local variations in the apical geometry of neuroepithelial cells (especially apical constriction) can provide information on the distribution of motive forces within the neuroepithelium during neural tube formation. When used in combination with computer-assisted, three-dimensional reconstruction, it becomes possible to analyze the morphometric data from a dynamic, three-dimensional perspective. As an example application of this method, we have used morphometry to evaluate the effects of ionomycin on the developing neuroepithelium. Treatment of early (stages 6-8) chick embryos with 5 microM ionomycin was found to cause rapid bending of the neuroepithelium within 1 min of exposure and a dramatic acceleration of the normal sequence of neural tube formation. Electron microscopy and morphometry revealed that this acceleration was coincident with a marked increase in the local degree of apical constriction of neuroepithelial cells, presumably a consequence of enhanced contractile activity of apical microfilament bundles. This work shows that transient elevation of free calcium levels can accelerate the usual sequential phases of NT formation. The rapidity of the response (hours of normal development reduced to minutes), increased prominence of apical microfilament bundles, and the enhanced degree of apical constriction strongly support a direct causal role for apical microfilament bundles and apical constriction of neuroepithelial cells in bending of the neuroepithelium.

Actin Cytoskeleton↗

PubMed2005

Role of IL-6 in the neural stem cell differentiation.

In the developing brain neurons, astrocytes, and oligodendrocytes are differentiated from common multipotent progenitors called neural stem cells. We have examined the effect of cytokines on mouse neuroepithelial cells that are known to contain neural stem cells. Cytokines belonging to the interleukin (IL)-6 family and those classified into the bone morphogenetic protein (BMP) family act in synergy on neuroepithelial cells to induce astrocyte differentiation. Cooperation of these two types of cytokines is explained by the formulation of a complex between their respective downstream transcription factors (signal tranducer and activator of transcription [STAT]-3 and Smad1), bridged by a transcriptional coactivator (p300). Whereas BMPs family cytokines are involved in astrocyte differentiation, they inhibit neuronal differentiation. This appears to change the fate of neural progenitor cells from neurogenesis to astrocytogenesis. Interestingly, during brain development, neuronal differentiation starts at a very early stage and continues throughout development, whereas astrocytes appear just before term. We have shown that astrocyte differentiation is largely dependent on IL-6 family cytokine-mediated STAT3 activation and that there exists a STAT3 binding element in the promoter region of the gene for the astrocyte marker glial fibrillary acidic protein. A cytosine residue in this element is highly methylated in neuroepithelial cells in a mid-gestational stage but becomes demethylated in accordance with brain development. Because this methylation inhibits STAT3 binding, we suggest that DNA methylation is a critical determinant in the developmental stage-dependent regulation of astrocytogeneis. In conclusion, fate of neural stem cells during development is regulated by cell-intrinsic programs, such as epigenetic modification (including DNA methylation), and signaling crosstalk of cell-external mediators (including IL-6 family cytokines).

Animals↗

PubMed1999

Astrocyte differentiation mediated by LIF in cooperation with BMP2.

Leukemia inhibitory factor (LIF) and bone morphogenetic protein (BMP) 2 signal via different receptor systems. We have recently demonstrated that simultaneous stimulation of fetal mouse neuroepithelial cells with these distinct types of cytokines synergistically induces astrocyte differentiation in a 2-day culture. Here we show that astrocytes spontaneously emerge in vitro without exogenously added LIF and BMP2 in the culture of neuroepithelial cells for a much longer period. This spontaneous astrocyte differentiation is completely impaired when neuroepithelial cells deficient for gp130, a signal transducing receptor component for LIF, are used. We also show that LIF and BMP2 as well as related cytokines and respective receptor molecules are expressed in fetal mouse brain and cultured neuroepithelial cells. Taken together with our previous finding that prenatal mouse brain deficient for gp130 exhibits a severe reduction of astrocytes, it is suggested that LIF acts cooperatively with BMP2 in vivo to induce astrocyte differentiation in mouse developing brain.

Animals↗

PubMedDate not supplied

Hyperplasia of bombesin-immunoreactive pulmonary neuroendocrine cells and neuroepithelial bodies in sudden infant death syndrome.

The distribution and frequency of bombesin immunoreactive neuroendocrine (NE) cells including neuroepithelial bodies (NEB) was analyzed morphometrically in lung sections from 25 infants who died of sudden infant death syndrome (SIDS) and 25 control infants. The control group included infants age-matched to those with SIDS, as well as subjects ranging in age from early to late infancy, to define the postnatal development of pulmonary NE-cell system. Quantitative analysis was performed on lung sections immunostained with monoclonal antibody against bombesin and the contents of bombesin-like peptide in lung extracts were measured by a specific radioimmunoassay (RIA). In control infants, the frequency of NE cells was high at birth but decreased dramatically during the first year of life. In SIDS infants, the frequency of NE cells, the size of NEB, and the mean concentration of bombesin-like peptide detected by RIA were significantly increased compared to those values for age-matched controls. These findings suggest hyperplasia of bombesin-immunoreactive NE-cell system in the lungs of SIDS infants. Since NEB are thought to function as hypoxia-sensitive airway chemoreceptors and since these cells are prominent in the neonates but decline postnatally, we speculate that chronic hypoxia and/or developmental delay may be responsible for this alteration in the lungs of SIDS victims. Potential dysfunction of pulmonary NE-cell system, compounded by other abnormalities in the autonomic regulation of respiration may be of importance in the pathogenesis of SIDS.

Bombesin↗

PubMed2004

Innervation of pulmonary neuroendocrine cells and neuroepithelial bodies in developing rabbit lung.

We investigated the development of innervation of the pulmonary neuroendocrine cell (PNEC) system composed of single cells and organoid cell clusters, neuroepithelial bodies (NEB) in rabbit fetal and neonatal lungs. To visualize the nerve fibers and their contacts with PNECs/NEBs, we used confocal microscopy and multilabel immunohistochemistry (IHC) with pan-neural marker, synaptic vesicle protein 2 (SV2), and serotonin (5-HT) as markers for PNECs/NEBs, and smooth muscle actin or cytokeratin to identify airway landmarks. The numbers and distribution of PNEC/NEB at different stages of lung development (E16, 18, 21, 26, and P2) and the density of innervation were quantified. First PNECs immunoreactive for 5-HT were identified in primitive airway epithelium at E18 as single cells or as small cell clusters with or without early nerve contacts. At E21 a significant increase in the number of PNECs with formation of early innervated NEB corpuscules was observed. The overall numbers of PNECs/NEBs and the density of mucosal, submucosal, and intercorpuscular innervation increased with progressing gestation and peaked postnatally (P2). At term, the majority of NEBs and single PNECs within airway mucosa possessed neural contacts. Such an extensive and complex innervation of the PNEC system indicates a multifunctional role in developing lung and during neonatal adaptation.

Animals↗

PubMed2006

Alix, making a link between apoptosis-linked gene-2, the endosomal sorting complexes required for transport, and neuronal death in vivo.

Alix/apoptosis-linked gene-2 (ALG-2)-interacting protein X is an adaptor protein involved in the regulation of the endolysosomal system through binding to endophilins and to endosomal sorting complexes required for transport (ESCRT) proteins, TSG101 and CHMP4b. It was first characterized as an interactor of ALG-2, a calcium-binding protein necessary for cell death, and several observations suggest a role for Alix in controlling cell death. We used electroporation in the chick embryo to test whether overexpressed wild-type or mutated Alix proteins influence cell death in vivo. We show that Alix overexpression is sufficient to induce cell death of neuroepithelial cells. This effect is strictly dependent on its capacity to bind to ALG-2. On the other hand, expression of Alix mutants lacking the ALG-2 or the CHMP4b binding sites prevents early programmed cell death in cervical motoneurons at day 4.5 of chick embryo development. This protection afforded by Alix mutants was abolished after deletion of the TSG101, but not of the endophilin, binding sites. Our results suggest that the interaction of the ALG-2/Alix complex with ESCRT proteins is necessary for naturally occurring death of motoneurons. Therefore, Alix represents a molecular link between the endolysosomal system and the cell death machinery.

Adaptor Proteins, Vesicular Transport↗

PubMed2005

Embryonic cerebrospinal fluid collaborates with the isthmic organizer to regulate mesencephalic gene expression.

Early in development, the behavior of neuroepithelial cells is controlled by several factors acting in a developmentally regulated manner. Recently it has been shown that diffusible factors contained within embryonic cerebrospinal fluid (CSF) promote neuroepithelial cell survival, proliferation, and neurogenesis in mesencephalic explants lacking any known organizing center. In this paper, we show that mesencephalic and mesencephalic+isthmic organizer explants cultured only with basal medium do not express the typically expressed mesencephalic or isthmic organizer genes analyzed (otx2 and fgf8, respectively) and that mesencephalic explants cultured with embryonic CSF-supplemented medium do effect such expression, although they exhibit an altered pattern of gene expression, including ectopic shh expression domains. Other trophic sources that are able to maintain normal neuroepithelial cell behavior, i.e., fibroblast growth factor-2, fail to activate this ectopic shh expression. Conversely, the expression pattern of the analyzed genes in mesencephalic+isthmic organizer explants cultured with embryonic cerebrospinal fluid-supplemented medium mimics the pattern for control embryos developed in ovo. We demonstrate that embryonic CSF collaborates with the isthmic organizer in regulation of the expression pattern of some characteristic neuroectodermal genes during early stages of central nervous system (CNS) development, and we suggest that this collaboration is not restricted to the maintenance of neuroepithelial cell survival. Data reported in this paper corroborate the hypothesis that factors contained within embryonic CSF contribute to the patterning of the CNS during early embryonic development.

Animals↗

PubMed2002

Tissue-specific RNA interference in postimplantation mouse embryos with endoribonuclease-prepared short interfering RNA.

RNA interference (RNAi) using double-stranded RNA has been used for the systematic analysis of gene function in invertebrate organisms. Here we have explored the use of short interfering RNA (siRNA) to knock down gene expression during the development of mammalian postimplantation embryos. The developing CNS system of embryonic day 10 mouse embryos was used as a model tissue. siRNA prepared by endoribonuclease digestion (esiRNA) was injected into the lumen of the neural tube at specific regions and delivered into neuroepithelial cells by directed electroporation. Injected and electroporated embryos were grown for 1 day in whole-embryo culture and the effects of RNAi were examined. esiRNA directed against beta-galactosidase (beta-gal), coelectroporated into neuroepithelial cells together with reporter plasmids expressing GFP and beta-gal, abolished expression of beta-gal but not GFP, showing the specificity of the esiRNA-mediated RNAi. To demonstrate RNAi of endogenous gene expression, we used heterozygous embryos of a knock-in mouse line expressing GFP from the Tis21 locus, a gene turned on in neuroepithelial cells that switch from proliferation to neurogenesis. GFP-directed esiRNA electroporated into neuroepithelial cells of such embryos blocked the GFP expression normally occurring on the onset of neurogenesis. Taken together, our data indicate that esiRNA delivered in a tissue-specific manner by topical injection followed by directed electroporation can efficiently silence endogenous gene expression in mammalian postimplantation embryos.

Animals↗

PubMed1986

An examination of the evidence for the existence of preformed pathways in the neural tube of Xenopus laevis.

We have examined the neural tube in Xenopus laevis tadpoles to investigate the anatomical guidance elements which may be present in the presumptive marginal zone. With appropriate fixation protocols the neuroepithelial cells appeared in contact; electron microscopic observations failed to show any specialized intercellular spaces preceding the growing axons. The first fibres were found in the intercellular clefts between the neuroepithelial cells near the surface of the neural tube. Reconstructions of the neural tube from examination of serial 1 micron sections showed that the intercellular clefts are non-aligned at this stage and branching. Scanning electron microscopy of the surface of the neural tube confirmed that the intercellular spaces are non-aligned and often branch caudal to the growing front of descending axons. Thus to grow in a consistent direction the developing axons may have to make consistent and selective (specific) selections of pathway at numerous branch points if their growth is restricted to these intercellular clefts. As more axons grow along the neural tube, the intercellular clefts become wider, and the neuroepithelial cells bounding the clefts become indented. At later stages many fibres were observed with both scanning and transmission electron microscopy to grow along the surface of the neural tube. These changes in neuroepithelial cell morphology and fibre pathway allow axons to form bundles which take a fairly straight course in contrast to the winding path which must be taken by the first axons to grow through the intercellular clefts.

Animals↗

PubMed1985

Ultrastructural changes in the neural tube of 10-day-old mouse embryos exposed to colchicine and hydroxyurea.

The ultrastructural changes in the neural tube of 10-day-old mouse embryos were investigated between 1.5 hr and 4 hr after application of either 1 mg/kg colchicine (Col) or 500 mg/kg hydroxyurea (HU) or simultaneous application of both substances. During the investigated period, the shape of the nuclei of the neuroepithelial cells had changed from elongated to round after Col application. The chromatin in the nuclei was condensed and arranged in clusters. A breakdown of polysomes into ribosomes and an enlargement of the rough ER was observed in the cytoplasm. At the luminal surface, bleb-like cytoplasmic processes of the neuroepithelial cells containing monoribosomes protruded into the lumen. No cell necroses were visible in the neural tube after Col application. A condensation of chromatin in the nuclei of some neuroepithelial cells was visible 1.5 hr after HU application. Shortly thereafter, cell necroses appeared in the neural tube and 4 hr after HU application the entire spinal cord was strongly damaged. After simultaneous application of Col and HU, the ultrastructural changes in the neuroepithelial cells of the neural tube did not differ from the results obtained after Col application alone. In contrast to the results obtained after HU application alone, no necroses occurred after simultaneous application of Col and HU.

Abnormalities, Drug-Induced↗

PubMed1982

The influence of colchicine on the cytotoxic effect of hydroxyurea in the embryonic spinal cord of the mouse.

The development of necroses and the course of the mitotic index in the embryonic spinal cord of 10-day-old mouse embryos (NMRI) were investigated between 1.5 h and 4 h after either an intraperitoneal application of 500 mg/kg hydroxyurea (HU) or 1 mg/kg colchicine or a simultaneous application of both substances. One h and 30 min after colchicine application, the mitotic index of the neuroepithelial cells had decreased (5.22%; control 7.7%). Subsequently, the mitotic index increased, reaching a maximum of 10.35% 2 h and 30 min after colchicine application. Between 1 h and 30 min and 4 h after HU application, the mitotic index decreased from 4.6% to 0.61% (control 7.7%). First necroses of neuroepithelial cells were observed 1 h and 50 min after HU application. 4 h after HU treatment, 34.38% of the neuroepithelial cells were necrotic. After simultaneous application of HU and colchicine, the decrease of the mitotic index was similar to the decrease after HU application alone. No necroses were observed in the embryonic spinal cord during a 4 h period after simultaneous application of HU and colchicine. After colchicine, as well as after simultaneous HU and colchicine application, the shape of the nuclei of the neuroepithelial cells changed from oval to round and the chromatin was condensed. Mechanisms for the inhibition of the cytotoxic but not the cytokinetic effects of HU by colchicine are discussed.

Animals↗

PubMed1995

Dorsal and ventral cell types can arise from common neural tube progenitors.

To challenge the developmental potential of dorsal neural tube cells and test whether single neuroepithelial cells can give rise to the full range of neural tube derivatives, we grated a notochord lateral to the closing neural folds. This results in juxtaposition of dorsal and ventral cell types, by inducing floor plate cells and motor neurons dorsally. Clonal analysis with the vital dye lysinated rhodamine dextran showed that both "dorsal" and "ventral" neural tube derivatives can arise from a single precursor. Cells as diverse as sensory ganglion cells, presumptive pigment cells, roof plate cells, motor neurons, and floor plate cells were observed in the same clone. The presence of such diversity within single clones indicates that the responses to dorsal and ventral signals are not mutually exclusive; even in the early neural tube, neuroepithelial cells are not restricted to form only dorsal or ventral neural tube derivatives.

Animals↗