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PubMed1994

Cloning and structure of a chicken zinc finger cDNA: restricted expression in developing neural crest cells.

The cloning, DNA sequence analysis and expression pattern of a chicken cDNA, cKr2, is described. cKr2 is a 4492-bp cDNA that encodes a 1173-amino-acid (aa) protein with two domains: the N-terminal portion contains 16 zinc fingers (Zf) of the 2Cys + 2His class, while the C-terminal domain contains a stretch of 181 aa which consists of seven consecutive sequence repeats each being 24 aa in length. The aa sequence repeats harbor a putative DNA-binding helix-turn-helix motif. Northern and Western blotting experiments indicate cKr2 expression from days 2 to 12 of development. In situ hybridization and immunohistochemical analyses using an anti-cKr2 antibody and the HNK-1 antibody, a marker of neural crest cells, revealed cKr2 activity in cephalic and trunk neural crest-derived cells. cKr2 is expressed predominantly in differentiating Schwann cells lining the nerves which innervate the branchial arches and limb buds, in cells of the sympathetic ganglia and aortic plexus, and in putative neuroblasts of dorsal root ganglia. The nuclear localization of the cKr2-encoded protein is consistent with its presumed role as a transcription factor.

Amino Acid Sequence↗

PubMed2004

Midkine and pleiotrophin in neural development and cancer.

The midkine (MK) family consists of only two members, namely heparin-binding growth factors MK and pleiotrophin (PTN). During embryogenesis, MK is highly expressed in the mid-gestational period, whereas PTN expression reaches the maximum level around birth. Both proteins are localized in the radial glial processes of the embryonic brain, along which neural stem cells migrate and differentiate. Zebrafish and Xenopus MK can induce neural tissues. In addition, deposits of MK and/or PTN are found in neurodegenerative diseases, such as Alzheimer's disease and multiple system atrophy. Both molecules are induced in reactive astrocytes by ischemic insults. In this context, it is interesting that LDL receptor-related protein is a receptor for MK and PTN, and this receptor has been implicated in the pathogenesis of Alzheimer's disease. MK and PTN share receptors, and show similar biological activities that include fibrinolytic, anti-apoptotic, mitogenic, transforming, angiogenic, and chemotactic ones. These activities explain how these molecules are involved in carcinogenesis. MK is detected in human carcinoma specimens from pre-cancerous stages to advanced stages. Strong expression of PTN is also detected in several carcinomas, although, in general, MK is expressed more intensely and in a wide range of carcinomas than PTN. The blood MK level is frequently elevated in advanced human carcinomas, decreases after surgical removal of the tumors, and is correlated with prognostic factors. Thus, it is a good market for evaluating the progress of carcinomas. Furthermore, antisense oligonucleotides for MK and ribozymes for PTN show anti-tumor activity. Therefore, MK and PTN are candidate molecular targets for therapy for human carcinomas.

Animals↗

PubMed2005

Retardation of removal of radiation-induced apoptotic cells in developing neural tubes in macrophage galactose-type C-type lectin-1-deficient mouse embryos.

MGL1/CD301a is a C-type lectin that recognizes galactose and N-acetylgalactosamine as monosaccharides and is expressed on limited populations of macrophages and dendritic cells at least in adult mice. In this study, pregnant mice with Mgl1+/- genotype were mated with Mgl1+/- or Mgl1-/- genotype males, and the embryos were used to assess a hypothesis that this molecule plays an important role in the clearance of apoptotic cells. After X-ray irradiation at 1 Gy of developing embryos at 10.5 days post coitus (d.p.c.), the number of Mgl1-/- pups was significantly reduced as compared with Mgl1+/+ pups. Distributions of MGL1-positive cells, MGL2-positive cells, and apoptotic cells were histologically examined in irradiated Mgl1+/+ embryos. MGL1-positive cells were detected in the neural tube in which many cells undergo apoptosis, whereas MGL2-positive cells were not observed. Biotinylated recombinant MGL1 bound a significant portion of the apoptotic cells. When Mgl1+/+ and Mgl1-/- embryos were examined for the presence of apoptotic cells, similar numbers of apoptotic cells gave rise, but the clearance of these cells was slower in Mgl1-/- embryos than in Mgl1+/+ embryos. These results strongly suggest that MGL1/CD301a is involved in the clearance of apoptotic cells. This process should be essential in the repair and normal development of X-ray-irradiated embryos.

Animals↗

PubMed1998

Control of neural development and function in a thermoregulatory network by the LIM homeobox gene lin-11.

We show here that the lin-11 LIM homeobox gene is expressed in nine classes of head, ventral cord, and tail neurons and functions at a late step in the development of a subset of these neurons. In a lin-11 null mutant, all lin-11-expressing neurons are generated. Several of these neurons, however, exhibit neuroanatomical as well as functional defects. In the lateral head ganglion, lin-11 functions in a neural network that regulates thermosensory behavior. It is expressed in the AIZ interneuron that processes high temperature input and is required for the function of AIZ in the thermoregulatory neural network. Another LIM homeobox gene, ttx-3, functions in the antagonistic thermoregulatory interneuron AIY (). Thus, distinct LIM genes specify the functions of functionally related antagonistic interneurons within a neural network dedicated for thermoregulatory processes. Both ttx-3 and lin-11 expression are maintained throughout adulthood, suggesting that these LIM homeobox genes play a role in the functional maintenance of this neural circuit. We propose that particular LIM homeobox genes specify the distinct features of functionally related neurons that generate patterned behaviors.

Animals↗

PubMed1992

A labile period in the determination of the anterior-posterior axis during early neural development in Xenopus.

The process by which the vertebrate central nervous system acquires its regional properties remains a central problem in developmental biology. It is generally argued that at early gastrula stages the dorsal mesoderm possesses precise anterior-posterior positional information, which is subsequently imparted to the overlying ectoderm. However, using regionally specific gene probes to monitor regional responses in Xenopus embryos, we find that anterior-posterior properties are not fixed until early neurula stages. During gastrulation the regional inducing capacities of the dorsal mesoderm as well as the regional responses of the presumptive neural ectoderm are activated along the entire anterior-posterior axis when these properties are assayed in recombinant and explant experiments, respectively. Restriction of regional inducing capacity in the mesoderm and responsiveness in the neural ectoderm occur only at neural plate stages.

Animals↗

PubMed1995

Boundaries and inhibitory molecules in developing neural tissues.

Numerous studies of the past decade have illuminated the importance of intercellular adhesion events for neural pattern formation. It has been documented that members of the Ig and cadherin gene superfamilies, that glycoproteins and, probably to some extent, proteoglycans of the extracellular matrix play a role in this context. Recent observations suggest that, in addition to adhesive interactions, repulsive and/or inhibitory phenoma are also of importance in regulating neural pattern formation. Several molecules are under study which are considered possible mediators of inhibitory interactions in the nervous system. The hypothesis has been advanced that some of these might be partially responsible for restrictive, boundary-like properties ascribed to glial cells in developing and regenerating tissues. The current review summarizes these studies and focusses on molecular aspects of boundary and compartmentation phenomena.

Animals↗

PubMed2005

Role of Folbp1 in the regional regulation of apoptosis and cell proliferation in the developing neural tube and craniofacies.

Folic acid is essential for many cellular reactions, including synthesis of nucleotides and regulation of cell cycle. Folic acid-binding protein one (Folbp1), a membrane-bounded protein, is the primary mediator of folic acid transport. Mice deficient in Folbp1 gene die in utero with multiple malformations, including severe exencephaly and craniofacial defects. Fusion of the neural tube and craniofacies require precisely regulated interactions of apoptosis, cell proliferation, and differentiation. To understand the role of Folbp1 in regulating the fusions of these primordia, levels of dead and proliferating precursor cells from Folbp1 embryos were quantified before the fusion processes. Massive apoptosis was detected in the Folbp1-/- defective tissues, with Bax and activated caspase-3 distributed evenly across the apico-basal axis of the lateral neural plate. 5-Bromodeoxyuridine (BrdU) and PCNA labeling assays revealed a reduced cell proliferation as well. However, telomerase activity was unaltered, arguing against telomere shortening and consequently, chromosomal instability, as the cause of the apoptosis. Notably, Islet-1 and 2H3 immunohistochemistry demonstrated the presence of differentiating neuronal cells, albeit in decreased numbers. Interestingly, Folbp1-/- embryos also elaborated novel neural structures that sprouted orthogonally from the embryonic neuraxis. Assays on the defective craniofacies exhibited similar phenomena, suggesting the neural crest precursor population that gives rise to both these structures is selectively vulnerable to Folbp1 inactivation. The results demonstrate a prominent role of Folbp1 in the regional regulation of apoptosis and cell proliferation that underlies the aberrant neural tube and craniofacial defects.

Animals↗

PubMed2000

Dm1-MMP, a matrix metalloproteinase from Drosophila with a potential role in extracellular matrix remodeling during neural development.

We have cloned and characterized a cDNA encoding Dm1-MMP, the first matrix metalloproteinase (MMP) identified in Drosophila melanogaster. The isolated cDNA encodes a protein of 541 residues that has a domain organization identical to that of most vertebrate MMPs including a signal sequence, a prodomain with the activation locus, a catalytic domain with a zinc-binding site, and a COOH-terminal hemopexin domain. Northern blot analysis of Dm1-MMP expression in embryonic and larval adult tissues revealed a strong expression level in the developing embryo at 10-22 h, declining thereafter and being undetectable in adults. Western blot analysis confirmed the presence of pro- and active forms of Dm1-MMP in vivo during larval development. In situ hybridization experiments demonstrated that Dm1-MMP is expressed in a segmented pattern in cell clusters at the midline during embryonic stage 12-13, when neurons of the central nervous system start to arise. Recombinant Dm1-MMP produced in Escherichia coli exhibits a potent proteolytic activity against synthetic peptides used for analysis of vertebrate MMPs. This activity is inhibited by tissue inhibitors of metalloproteinases and by synthetic MMP inhibitors such as BB-94. Furthermore, Dm1-MMP is able to degrade the extracellular matrix and basement membrane proteins fibronectin and type IV collagen. On the basis of these data, together with the predominant expression of Dm1-MMP in embryonic neural cells, we propose that this enzyme may be involved in the extracellular matrix remodeling taking place during the development of the central nervous system in Drosophila.

Amino Acid Sequence↗

PubMed2005

Common fragile sites, extremely large genes, neural development and cancer.

Common fragile sites (CFSs) are large regions of profound genomic instability found in all individuals. They are biologically significant due to their role in a number of genomic alterations that are frequently found in many different types of cancer. The first CFS to be cloned and characterized was FRA3B, the most active CFS in the human genome. Instability within this region extends for over 4.0 Mbs and contained within the center of this CFS is the FHIT gene spanning 1.5 Mbs of genomic sequence. There are frequent deletions and other alterations within this gene in multiple tumor types and the protein encoded by this gene has been demonstrated to function as a tumor suppressor in vitro and in vivo. In spite of this, FHIT is not a traditional mutational target in cancer and many tumors have large intronic deletions without any exonic alterations. There are several other very large genes found within CFS regions including Parkin (1.37 Mbs in FRA6E), GRID2 (1.47 Mbs within 4q22.3), and WWOX (1.11 Mbs within FRA16D). These genes also appear to function as tumor suppressors but are not traditional mutational targets in cancer. Each of these genes is highly conserved and the regions spanning them are CFSs in mice. We have now examined lists of the largest human genes and found forty that span over one megabase. Many of these are derived from chromosomal bands containing CFSs. BACs within these genes are being utilized as FISH probes to determine if these are also CFS genes. Thus far we have identified the following as CFS genes: CNTNAP2 (2.3 Mbs in FRA7I), DMD (2.09 Mbs in FRAXC), LRP1B (1.9 Mbs in FRA2F), CTNNA3 (1.78 Mbs in FRA10D), DAB1 (1.55 Mbs in FRA1B), and IL1RAPL1 (1.36 Mbs in FRAXC). Although, these genes are also not traditional mutational targets in cancer they do exhibit loss of expression in multiple tumor types suggesting that they may also function as tumor suppressors. Many of the large CFS genes are involved in neurological development. Parkin is mutated in autosomal recessive juvenile Parkinsonism and deletions in mice are associated with the mouse mutant Quaking (viable). Spontaneous mouse mutants in GRID2 and DAB1 are associated with Lurcher and Reelin, respectively. In humans, alterations in IL1RAPL1 cause X-linked mental retardation and loss of WWOX is associated with Tau phosphorylation. We propose that the instability-induced alterations in these genes contribute to cancer development in a two-step process. Initial alterations will primarily occur within intronic regions, as these genes are greater than 99% intronic. These are not benign. Instead, they alter the repertoire of transcripts produced from these genes. As cancer progresses deletions will begin to encompass exons resulting in gene inactivation. These two types of alterations occurring in multiple large CFS genes may contribute significantly to the heterogeneity observed in cancer. There are also important potential linkages between normal neurological development and the development of cancer mediated by alterations in these genes.

Acid Anhydride Hydrolases↗

PubMed1999

Iron deficiency and neural development: an update.

In Latin America, 10-30% of reproductive age females and upwards of 40-70% of pregnant women may be iron deficient. The true prevalence in young children and infants is often hard to determine because of problems in survey design, data collection, or sampling. There is little doubt, however, that iron deficiency anemia is a significant nutritional problem in many infants within the first 5 years of life. Numerous intervention studies have been performed across the world with varying success and it is clear that in nearly all situations it is a preventable disease with preventable consequences. One such consequence is the alteration in cognition that occurs in iron deficient individuals during the early parts of their life cycle and perhaps at later times as well. While iron deficiency was once presumed to exert most of its deleterious effects only if anemia was present, it is now clear that many organs show morphologic, physiologic, and biochemical changes before there is any drop in hemoglobin concentration. Iron deficiency is associated with alterations in many metabolic processes that may impact brain functioning; among them are mitochondria electron transport, neurotransmitter synthesis and degradation, protein synthesis, organogenesis, and others. It is necessary to separate the developmental aspects of iron deficiency and neural functioning from the aspects of iron deficiency that could occur at any time in life. A number of reviews have discussed the links between brain iron and neuropathology, brain iron, nutrition, and development, and iron status and cognition. New knowledge concerning the acquisition of iron by the brain in early life is being generated by numerous research groups. In the next decade a much clearer understanding of the role of brain iron on neural functioning will probably emerge.

Animals↗

PubMed1987

Two forms of 1B236/myelin-associated glycoprotein, a cell adhesion molecule for postnatal neural development, are produced by alternative splicing.

The structures of two rat brain-specific 1B236 mRNAs, alternative splice products from a single gene regulated differently during postnatal brain development, were deduced from full-length cDNA clones. The 626- and 582-amino acid-long encoded proteins are indistinguishable from two forms of myelin-associated glycoprotein, a cell adhesion molecule involved in axonal-glial and glial-glial interactions in postnatal brain development, particularly in myelination. The two proteins share a single membrane-spanning domain and a glycosylated N terminus but differ in the structures of their C termini. The N terminus consists of five domains related in sequence to each other and to immunoglobulin-like molecules, especially the neural cell adhesion molecule N-CAM, suggesting a common structure for cell adhesion molecules.

Aging↗

PubMed1979

Acetylcholinesterase in human amniotic fluid: An index of fetal neural development?

Acetylcholinesterase (AChE) activity was detected in amniotic fluid either sampled by amniocentesis at 14--23 weeks gestation or collected at normal parturition. Activity ranged from 0.2 to 8.9 u/l in the earlier samples and from 0.2 to 4.2 u/l in the later samples. Since the fetal but not the maternal serum contained AChE activity, we suggest that the AChE in the amniotic fluid is derived from the fetus. AChE is released from both neural and nonneural tissues, and the release of the enzyme from both sources may diminish as the nervous system matures. The amount of AChE found in amniotic fluid may be affected by abnormalities of the nervous system. Amniotic fluid from two fetuses with spina bifida contained AChE activity: one, with a gestational age of 21 weeks, was in the upper levels of the normal range (4.5 u/l), whereas the other, at 36 weeks, contained 1.9 times more activity than the next highest sample. In a 20-week fetus with anencephaly, the AChE activity in the amniotic fluid was increased 2.8-fold over the activity of the highest "normal" sample.

Acetylcholinesterase↗

PubMed1989

A novel heat-stable 205 kDa microtubule-associated protein is involved in the neural development of the rat brain.

A novel microtubule associated protein (MAP) was identified with a monoclonal antibody (mAb) among rat brain microtubule (MT) proteins. This MAP, which is found in a heat-stable MAP fraction, is co-polymerized with tubulin from rat brain homogenates both in cycled and in taxol-driven assembly purifications. When the heat-stable fraction of MT proteins and purified tubulin are assembled in vitro without taxol, 205 kDa MAP is identified in the MT pellet. Immunofluorescent studies using the mAb against this MAP on sections of a rat spinal cord, hippocampus, retina and cerebellar cortex, showed that 205 kDa MAP was localized in not only neural cell bodies, dendrites, and axons, but also in glial cells. This 205 kDa MAP is clearly distinct from previously reported MAPs as to molecular mass, heat stability, immunoreactivity, distribution among tissues or within a neuron, and the developmental aspect of the postnatal cerebellar cortex. As for development, the 205 kDa MAP has already been seen to appear at postnatal day 3. Throughout the postnatal development of the cerebellar cortex, 205 kDa MAP is expressed in developing Purkinje cells, with the staining reaction being particularly intense in the more superficially positioned parallel fiber profiles. This points out the possible important functions of 205 kDa MAP in the morphogenesis of parallel fiber axons.

Animals↗

PubMed1988

Endogenous opioid systems and neural development: ultrastructural studies in the cerebellar cortex of infant and weanling rats.

Endogenous opioid systems participate in regulating the development of the nervous system. Opioid antagonists like naltrexone (NTX) perturb the relationship between endogenous opioids and opioid receptors quite effectively and reveal the function(s) of endogenous opioid systems during neuro-ontogeny. In this study, the effects of NTX, as well as the repercussions of modulation of endogenous opioid systems during critical stages of neural ontogeny, have been examined at the electron microscopic level of resolution in infant (10 day) and weanling (21 day) rats. Preweaning rats were subjected to complete (50 mg/kg NTX) or intermittent (1 mg/kg NTX) daily receptor blockade. Extensive ultrastructural examinations were conducted on the external germinal (granule), molecular, Purkinje, internal granule, and medullary layers of the cerebellar cortex. The NTX groups had striking similarities in morphology to that of controls at postnatal days 10 and 21. These results support the hypothesis that endogenous opioid systems act as trophic factors as they regulate growth; their effects on cell growth and survival, however, do not alter the basic ultrastructural morphology of the cells. Moreover, these data further strengthen the validity of paradigms utilizing opioid antagonists to explore the relationship of endogenous opioid-opioid receptor interactions and neural morphogenesis.

Aging↗

PubMed1996

Hormonal and non-hormonal regulation of glutamine synthetase in the developing neural retina.

Two isoforms of the glucocorticoid receptor, with apparent molecular mass of 90 and 95 kDa, are expressed in embryonic chicken neural retina. The 95-kDa receptor represents a hyperphosphorylated form of the 90-kDa receptor. Activation of the glucocorticoid receptor by cortisol results in a dose-dependent increase in receptor phosphorylation, translocation of receptor molecules into the nucleus and a decline in the total amount of the receptor. Activation of the glucocorticoid receptor can also be observed in the developing retinal tissue in ovo. At late embryonic ages, when the systemic level of glucocorticoids increases, a substantial quantity of receptor molecules becomes translocated into the nucleus, the relative level of the 95-kDa isoform increases, and the total amount of receptor declines. Activation of the receptor molecules in ovo correlates directly with an increase in transcription of the glucocorticoid-inducible gene, glutamine synthetase. The close correlation between the increase in systemic glucocorticoids, activation of glucocorticoid receptor molecules and induction of glutamine synthetase gene transcription suggests that glucocorticoids are directly involved in the developmental control of glutamine synthetase expression. Long-term organ culturing of embryonic retinal tissue in the absence of hormone results in an increase in glutamine synthetase expression. This increase, which is only 5 to 10% of that observed in ovo, is not mediated by activated receptor molecules and represents a mechanism for non-hormonal regulation of glutamine synthetase.

Animals↗

PubMed2001

Neural development, cell-cell signaling, and the "two-hit" hypothesis of schizophrenia.

To account for the complex genetics, the developmental biology, and the late adolescent/early adulthood onset of schizophrenia, the "two-hit" hypothesis has gained increasing attention. In this model, genetic or environmental factors disrupt early central nervous system (CNS) development. These early disruptions produce long-term vulnerability to a "second hit" that then leads to the onset of schizophrenia symptoms. The cell-cell signaling pathways involved in nonaxial induction, morphogenesis, and differentiation in the brain, as well as in the limbs and face, could be targets for a "first hit" during early development. These same pathways, redeployed for neuronal maintenance rather than morphogenesis, may be targets for a "second hit" in the adolescent or adult brain. Furthermore, dysregulation of cell-cell signaling by a "first hit" may prime the CNS for a pathologic response to a "second hit" via the same signaling pathway. Thus, parallel disruption of cell-cell signaling in both the developing and the mature CNS provides a plausible way of integrating genetic, developmental, and environmental factors that contribute to vulnerability and pathogenesis in schizophrenia.

Brain↗

PubMedDate not supplied

Cytokines regulate the cellular phenotype of developing neural lineage species.

The patterns and mechanisms of action of inductive signals that orchestrate neural lineage commitment and differentiation in the mammalian brain are incompletely understood. To examine these developmental issues, we have utilized several culture systems including conditionally immortalized cell lines, subventricular zone progenitor cells and primary neuronal cultures. A neural stem and progenitor cell line (MK31) was established from murine embryonic hippocampus by retroviral transduction of temperature-sensitive alleles of the simian virus 40 large tumor antigen. At the non-permissive temperature for antigen expression (39 degrees C) in serum-free media, the neural stem cells give rise to a series of increasingly mature neuronal progenitor and differentiated cellular forms under the influence of a subset of hematolymphopoietic cytokines (interleukins 5, 7, 9 and 11), when individually co-applied with transforming growth factor alpha, after pretreatment with basic fibroblast growth factor. These cellular forms elaborated a series of progressively more mature neurofilament proteins, a sequential pattern of ligand-gated channels, and inward currents and generation of action potentials with mature physiological properties. Because the factors regulating the development of central nervous system astrocytes have been so difficult to define, we have chosen to focus, in this manuscript, on the elaboration of this cell type. At 39 degrees C, application of a subfamily of bone morphogenetic proteins of the transforming growth factor beta superfamily of growth factors sanctioned the selective expression of astrocytic progenitor cells and mature astrocytes, as defined by sequential elaboration of the Yb subunit of glutathione-S-transferase and glial fibrillary acidic protein. These lineage-specific cytokine inductive relationships were verified using subventricular zone neural progenitor cells generated by the application of epidermal growth factor, alone or in combination with basic fibroblast growth factor, to dissociated cellular cultures derived from early embryonic murine brain, a normal non-transformed developmental population. Finally, application of a different series of cytokines from five distinct factor classes (basic fibroblast growth factor, platelet-derived growth factor-AA, insulin-like growth factor 1, neurotrophin 3 and representative gp130 receptor subunit-related ligands) caused the elaboration of oligodendroglial progenitor species and post-mitotic oligodendrocytes, defined by progressive morphological maturation and the expression of increasingly advanced oligodendroglial and oligodendrocyte lineage markers. In addition, seven different gp130-associated neuropoietic (ciliary neurotrophic factor, leukemia inhibitory factor, oncostatin-M) and hematopoietic (interleukins 6, 11, 12, granulocyte-colony stimulating factor) cytokines exhibited differential trophic effects on oligodendroglial lineage maturation and factor class interactions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2002

Tramtrack co-operates to prevent inappropriate neural development in Drosophila.

Each sensory organ of the Drosophila peripheral nervous system is derived from a single sensory organ precursor cell (SOP). These originate in territories defined by expression of the proneural genes of the Achaete-Scute complex (AS-C). Formation of ectopic sensilla outside these regions is prevented by transcriptional repression of proneural genes. We demonstrate that the BTB/POZ-domain transcriptional repressor Tramtrack (Ttk) co-operates in this repression. Ttk is expressed ubiquitously, except in proneural clusters and SOPs. Ttk over-expression represses proneural genes and sensilla formation. Loss of Ttk enhances bristle-promoting mutants. Using neural repression as an assay, we dissected functional domains of Ttk, confirming the importance of the bric-à-brac-tramtrack-broad complex (BTB) motif. We show that the Ttk BTB domain is a protein-protein interaction motif mediating tetramer formation.

Animals↗