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‣ Mild cognitive deficits associated to neocortical microgyria in mice with genetic deletion of cellular prion protein

XIKOTA, Joao C.; RIAL, Daniel; RUTHES, Daniel; PEREIRA, Rafael; FIGUEIREDO, Ciaudia P.; PREDIGER, Rui D. S.; WALZ, Roger
Fonte: ELSEVIER SCIENCE BV Publicador: ELSEVIER SCIENCE BV
Tipo: Artigo de Revista Científica
Português
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The cellular prion protein (PrP(c)) has been implicated with the modulation of neuronal apoptosis, adhesion, neurite outgrowth and maintenance which are processes involved in the neocortical development. Malformations of cortical development (MCD) are frequently associated with neurological conditions including mental retardation, autism, and epilepsy. Here we investigated the behavioral performance of female adult PrP(c)-null mice (Prnp(%)) and their wild-type controls (Prnp(+/+)) presenting unilateral polymicrogyria, a MCD experimentally induced by neonatal freeze-lesion in the right hemisphere. injured mice from both genotypes presented similar locomotor activity but Prnp(%) mice showed a tendency to increase anxiety-related responses when compared to Prnp(+/+) animals. Additionally, injured Prnp(%) mice have a poorer performance in the social recognition task than sham-operated and Prnp(%) injured ones. Moreover the step-down inhibitory avoidance task was not affected by the procedure or the genotype of the animals. These data suggest that the genetic deletion of PrP(c) confers increased susceptibility to short-term social memory deficits induced by neonatal freezing model of polymicrogyria in mice. (C) 2008 Published by Elsevier B.V.; Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq); de Coordenacao de Aperfeigoamento de Pessoal de Nivel Superior (CAPES); Programa de Apoio aos Nucleos de Excelencia (PRONEX); Fundacao de Apoio a Pesquisa do Estado de Santa Catarina (FAPESC)

‣ Functional and structural studies of two enzymes: membrane bound kinase and Z-DNA/Z-RNA-binding protein

Rosário, Ana Lúcia Rebelo do
Fonte: Faculdade de Ciências e Tecnologia Publicador: Faculdade de Ciências e Tecnologia
Tipo: Tese de Doutorado
Publicado em //2013 Português
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Dissertação para obtenção do Grau de Doutor em Sistemas de Bioengenharia; The neocortex is a unique structure designed for higher cognitive and associative functions. Herein, we will refer to the work performed to assess the role of TAOK2α, a specific membrane bound kinase, in the mammalian neocortical development. The results obtained, delineate a pathway whereby Semaphorin3A and Neuropilin1 transduce signals through TAOK2α and c-Jun N-terminal Kinase to regulate basal dendrite development and migration in cortical neurons. This work represents the first approach aimed at understanding the mechanisms responsible for the delineation of basal and apical dendrites during pyramidal neuron development in the embryo, and how such mechanism may evolve to neocortical disconnection disorders. Additional work performed on humanTAOK2α focused at the determination of its three-dimensional structure by X-ray crystallography to elucidate its regulatory mechanism. The 20th century exciting discovery of the DNA left-handed conformation, and the fact it binds to certain classes of proteins with high affinity and specificity, indicated a biological role to it. However, a full function is still to be elucidated. The human double-stranded RNA adenosine deaminase (ADAR1) is the best characterized of all Z-DNA binding proteins...

‣ Mechanisms of neocortical development

Isaac, John T R; Feldmeyer, Dirk
Fonte: Blackwell Science Inc Publicador: Blackwell Science Inc
Tipo: Artigo de Revista Científica
Publicado em 01/05/2009 Português
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‣ Developmental alterations in the functional properties of excitatory neocortical synapses

Feldmeyer, Dirk; Radnikow, Gabriele
Fonte: Blackwell Science Inc Publicador: Blackwell Science Inc
Tipo: Artigo de Revista Científica
Português
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In the neocortex, most excitatory, glutamatergic synapses are established during the first 4–5 weeks after birth. During this period profound changes in the properties of synaptic transmission occur. Excitatory postsynaptic potentials (EPSPs) at immature synaptic connections are profoundly and progressively reduced in response to moderate to high frequency (5–100 Hz) stimulation. With maturation, this frequency-dependent depression becomes progressively weaker and may eventually transform into a weak to moderate EPSP facilitation. In parallel to changes in the short-term plasticity, a reduction in the synaptic reliability occurs at most glutamatergic neocortical synapses: immature synapses show a high probability of neurotransmitter release as indicated by their low failure rate and small EPSP amplitude variation. This high reliability is reduced in mature synapses, which show considerably higher failure rates and more variable EPSP amplitudes. During early neocortical development synaptic vesicle pools are not yet fully differentiated and their replenishment may be slow, thus resulting in EPSP amplitude depression. The decrease in the probability of neurotransmitter release may be the result of an altered Ca2+ control in the presynaptic terminal with a reduced Ca2+ influx and/or a higher Ca2+ buffering capacity. This may lead to a lower synaptic reliability and a weaker short-term synaptic depression with maturation.

‣ The development of cortical columns: role of Fragile X mental retardation protein

Bureau, Ingrid
Fonte: Blackwell Science Inc Publicador: Blackwell Science Inc
Tipo: Artigo de Revista Científica
Português
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Neuronal circuits in the brain are complex and precise. Here, I review aspects of the development of cortical columns in the rodent barrel cortex, focusing on the anatomical and functional data describing the maturation of ascending glutamatergic circuits. Projections from layer 4 to layer 3 develop into cortical columns with little macroscopic refinement. Depriving animals of normal sensory experience induces long-term synaptic depression but does not perturb this pattern of development. Mouse models of mental retardation can help us understand the mechanisms of development of cortical columns. Fmr1 knock-out (ko) mice, a model for Fragile X syndrome, lack Fragile X mental retardation protein (FMRP), a suppressor of translation present in synapses. Because FMRP expression is stimulated by neuronal activity, Fmr1-ko mice provide a model to survey the role of sensory input in brain development. Layer 4 to layer 3 projections are altered in multiple ways in the young mutant mice: connection rate is low and layer 4 cell axons are spatially diffuse. Sensory deprivation rescues the connection rate phenotype. The interaction of FMRP and neuronal activity in the development of cortical circuits is discussed.

‣ Synchronized changes to relative neuron populations in postnatal human neocortical development

Cooper, David L.; Gentle, James E.; Barreto, Ernest; Olds, James L.
Fonte: Springer Netherlands Publicador: Springer Netherlands
Tipo: Artigo de Revista Científica
Português
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Mammalian prenatal neocortical development is dominated by the synchronized formation of the laminae and migration of neurons. Postnatal development likewise contains “sensitive periods” during which functions such as ocular dominance emerge. Here we introduce a novel neuroinformatics approach to identify and study these periods of active development. Although many aspects of the approach can be used in other studies, some specific techniques were chosen because of a legacy dataset of human histological data (Conel in The postnatal development of the human cerebral cortex, vol 1–8. Harvard University Press, Cambridge, 1939–1967). Our method calculates normalized change vectors from the raw histological data, and then employs k-means cluster analysis of the change vectors to explore the population dynamics of neurons from 37 neocortical areas across eight postnatal developmental stages from birth to 72 months in 54 subjects. We show that the cortical “address” (Brodmann area/sub-area and layer) provides the necessary resolution to segregate neuron population changes into seven correlated “k-clusters” in k-means cluster analysis. The members in each k-cluster share a single change interval where the relative share of the cortex by the members undergoes its maximum change. The maximum change occurs in a different change interval for each k-cluster. Each k-cluster has at least one totally connected maximal “clique” which appears to correspond to cortical function.

‣ SOX6 controls dorsal-ventral progenitor parcellation and interneuron diversity during neocortical development

Azim, Eiman; Jabaudon, Denis; Fame, Ryann; Macklis, Jeffrey D.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Português
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The extraordinary neuronal diversity of the central nervous system emerges largely from controlled spatial and temporal segregation of cell type-specific molecular regulators. Here, we report that the transcription factor SOX6 controls the molecular segregation of dorsal (pallial) from ventral (subpallial) telencephalic progenitors, and the differentiation of cortical interneurons, regulating forebrain progenitor and interneuron heterogeneity. During corticogenesis in mice, SOX6 and highly related SOX5 expression is largely mutually exclusive in pallial and subpallial progenitors, respectively, and remains mutually exclusive in a reverse pattern in postmitotic neuronal progeny. Loss of SOX6 from pallial progenitors causes their inappropriate expression of normally subpallium-restricted developmental controls, conferring mixed dorsal-ventral identity. In postmitotic cortical interneurons, loss of SOX6 dramatically disrupts the differentiation and diversity of cortical interneuron subtypes, analogous to SOX5 control over cortical projection neuron development. These data reveal SOX6 as a novel transcription factor regulator of both progenitor and cortical interneuron diversity during neocortical development.

‣ Premutation CGG-repeat expansion of the Fmr1 gene impairs mouse neocortical development

Cunningham, Christopher L.; Martínez Cerdeño, Verónica; Navarro Porras, Eliecer; Prakash, Anish N.; Angelastro, James M.; Willemsen, Rob; Hagerman, Paul J.; Pessah, Isaac N.; Berman, Robert F.; Noctor, Stephen C.
Fonte: Oxford University Press Publicador: Oxford University Press
Tipo: Artigo de Revista Científica
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Fragile X-associated tremor/ataxia syndrome (FXTAS) is a late adult-onset neurodegenerative disorder caused by a premutation CGG-trinucleotide repeat expansion (55–200 CGG repeats) within the 5′-untranslated region of the FMR1 gene. Although FXTAS generally affects premutation carriers over 50 years of age, cognitive and psychological symptoms can appear in carriers during childhood, suggesting that the FMR1 premutation affects brain function early in life. Recent work with cultured hippocampal neurons from a premutation (Fmr1 CGG knock-in) mouse model revealed impaired development of early postnatal neurons, consistent with the developmental clinical involvement of premutation carriers. In the current work, we show that the presence of premutation CGG-repeat expansions in the mouse Fmr1 gene alters embryonic neocortical development. Specifically, embryonic premutation mice display migration defects in the neocortex and altered expression of neuronal lineage markers. The current data demonstrate that premutation alleles of the Fmr1 gene are associated with defects in developmental programs operating during prenatal stages of brain formation and provide further evidence that the FMR1 premutation has a neurodevelopmental component.

‣ Repressor element 1 silencing transcription factor (REST) controls radial migration and temporal neuronal specification during neocortical development

Mandel, Gail; Fiondella, Christopher G.; Covey, Matthew V.; Lu, Diane D.; LoTurco, Joseph J.; Ballas, Nurit
Fonte: National Academy of Sciences Publicador: National Academy of Sciences
Tipo: Artigo de Revista Científica
Português
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Neurogenesis requires mechanisms that coordinate early cell-fate decisions, migration, and terminal differentiation. Here, we show that the transcriptional repressor, repressor element 1 silencing transcription factor (REST), regulates radial migration and the timing of neural progenitor differentiation during neocortical development, and that the regulation is contingent upon differential REST levels. Specifically, a sustained presence of REST blocks migration and greatly delays—but does not prevent—neuronal differentiation, resulting in a subcortical band heterotopia-like phenotype, reminiscent of loss of doublecortin. We further show that doublecortin is a direct gene target of REST, and that its overexpression rescues, at least in part, the aberrant phenotype caused by persistent presence of REST. Our studies support the view that the targeted down-regulation of REST to low levels in neural progenitors, and its subsequent disappearance during neurogenesis, is critical for timing the spatiotemporal transition of neural progenitor cells to neurons.

‣ Neocortical development as an evolutionary platform for intragenomic conflict

Lewitus, Eric; Kalinka, Alex T.
Fonte: Frontiers Media S.A. Publicador: Frontiers Media S.A.
Tipo: Artigo de Revista Científica
Publicado em 09/04/2013 Português
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Embryonic development in mammals has evolved a platform for genomic conflict between mothers and embryos and, by extension, between maternal and paternal genomes. The evolutionary interests of the mother and embryo may be maximized through the promotion of sex-chromosome genes and imprinted alleles, resulting in the rapid evolution of postzygotic phenotypes preferential to either the maternal or paternal genome. In eutherian mammals, extraordinary in utero maternal investment in the brain, and neocortex especially, suggests that convergent evolution of an expanded mammalian neocortex along divergent lineages may be explained, in part, by parent-of-origin-linked gene expression arising from parent-offspring conflict. The influence of this conflict on neocortical development and evolution, however, has not been investigated at the genomic level. In this hypothesis and theory article, we provide preliminary evidence for positive selection in humans in the regions of two platforms of intragenomic conflict—chromosomes 15q11-q13 and X—and explore the potential relevance of cis-regulated imprinted domains to neocortical expansion in mammalian evolution. We present the hypothesis that maternal- and paternal-specific pressures on the developing neocortex compete intragenomically to influence neocortical expansion in mammalian evolution.

‣ Expression of Calcium-Binding Proteins in Layer 1 Reelin-Immunoreactive Cells during Rat and Mouse Neocortical Development

Martinez-Galan, Juan R.; Moncho-Bogani, Jose; Caminos, Elena
Fonte: SAGE Publications Publicador: SAGE Publications
Tipo: Artigo de Revista Científica
Publicado em /01/2014 Português
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Cajal-Retzius cells in layer 1 of the developing cerebral cortex and their product of secretion, reelin, an extracellular matrix protein, play a crucial role in establishing the correct lamination pattern in this tissue. As many studies into reelin signaling routes and pathological alterations are conducted in murine models, we used double-labeling and confocal microscopy to compare the distribution of the cell-specific markers, calretinin and calbindin, in reelin-immunoreactive cells during postnatal rat and mouse neocortical development. In the rat, neither calretinin nor calbindin colocalized with reelin in Cajal-Retzius cells at P0-P2. From P5 to P14, the colocalization of reelin and calretinin was commonly found in presumptive rat subpial piriform cells. These cells progressively lacked calretinin expression and persisted into adulthood as part of the pool of layer 1 reelin-positive interneurons. Conversely, in the mouse, reelin-immunoreactive Cajal-Retzius cells colocalized with calretinin and/or calbindin. Subpial piriform cells containing reelin and calretinin were identified at P5-P7, but lacked calretinin expression at P14. In adult mice, as in the rat, reelin-immunoreactive cells did not colocalize with calcium-binding proteins. Our results reveal a complex neurochemical profile of layer 1 cells in the rat neocortex...

‣ Prdm8 Regulates the Morphological Transition at Multipolar Phase during Neocortical Development

Inoue, Mayuko; Kuroda, Takao; Honda, Aya; Komabayashi-Suzuki, Mariko; Komai, Tae; Shinkai, Yoichi; Mizutani, Ken-ichi
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 29/01/2014 Português
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Here, we found that the PR domain protein Prdm8 serves as a key regulator of the length of the multipolar phase by controlling the timing of morphological transition. We used a mouse line with expression of Prdm8-mVenus reporter and found that Prdm8 is predominantly expressed in the middle and upper intermediate zone during both the late and terminal multipolar phases. Prdm8 expression was almost coincident with Unc5D expression, a marker for the late multipolar phase, although the expression of Unc5D was found to be gradually down-regulated to the point at which mVenus expression was gradually up-regulated. This expression pattern suggests the possible involvement of Prdm8 in the control of the late and terminal multipolar phases, which controls the timing for morphological transition. To test this hypothesis, we performed gain- and loss-of-function analysis of neocortical development by using in utero electroporation. We found that the knockdown of Prdm8 results in premature change from multipolar to bipolar morphology, whereas the overexpression of Prdm8 maintained the multipolar morphology. Additionally, the postnatal analysis showed that the Prdm8 knockdown stimulated the number of early born neurons, and differentiated neurons located more deeply in the neocortex...

‣ Tcf3 Represses Wnt–β-Catenin Signaling and Maintains Neural Stem Cell Population during Neocortical Development

Kuwahara, Atsushi; Sakai, Hiroshi; Xu, Yuanjiang; Itoh, Yasuhiro; Hirabayashi, Yusuke; Gotoh, Yukiko
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 15/05/2014 Português
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During mouse neocortical development, the Wnt–β-catenin signaling pathway plays essential roles in various phenomena including neuronal differentiation and proliferation of neural precursor cells (NPCs). Production of the appropriate number of neurons without depletion of the NPC population requires precise regulation of the balance between differentiation and maintenance of NPCs. However, the mechanism that suppresses Wnt signaling to prevent premature neuronal differentiation of NPCs is poorly understood. We now show that the HMG box transcription factor Tcf3 (also known as Tcf7l1) contributes to this mechanism. Tcf3 is highly expressed in undifferentiated NPCs in the mouse neocortex, and its expression is reduced in intermediate neuronal progenitors (INPs) committed to the neuronal fate. We found Tcf3 to be a repressor of Wnt signaling in neocortical NPCs in a reporter gene assay. Tcf3 bound to the promoter of the proneural bHLH gene Neurogenin1 (Neurog1) and repressed its expression. Consistent with this, Tcf3 repressed neuronal differentiation and increased the self-renewal activity of NPCs. We also found that Wnt signal stimulation reduces the level of Tcf3, and increases those of Tcf1 (also known as Tcf7) and Lef1, positive mediators of Wnt signaling...

‣ Convergent microRNA actions coordinate neocortical development

Barca-Mayo, Olga; De Pietri Tonelli, Davide
Fonte: Springer Basel Publicador: Springer Basel
Tipo: Artigo de Revista Científica
Português
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Neocortical development is a complex process that, at the cellular level, involves tight control of self-renewal, cell fate commitment, survival, differentiation and delamination/migration. These processes require, at the molecular level, the precise regulation of intrinsic signaling pathways and extrinsic factors with coordinated action in a spatially and temporally specific manner. Transcriptional regulation plays an important role during corticogenesis; however, microRNAs (miRNAs) are emerging as important post-transcriptional regulators of various aspects of central nervous system development. miRNAs are a class of small, single-stranded noncoding RNA molecules that control the expression of the majority of protein coding genes (i.e., targets). How do different miRNAs achieve precise control of gene networks during neocortical development? Here, we critically review all the miRNA–target interactions validated in vivo, with relevance to the generation and migration of pyramidal-projection glutamatergic neurons, and for the initial formation of cortical layers in the embryonic development of rodent neocortex. In particular, we focus on convergent miRNA actions, which are still a poorly understood layer of complexity in miRNA signaling...

‣ An in vitro model of human neocortical development using pluripotent stem cells: cocaine-induced cytoarchitectural alterations

Kindberg, Abigail A.; Bendriem, Raphael M.; Spivak, Charles E.; Chen, Jia; Handreck, Annelie; Lupica, Carl R.; Liu, Jinny; Freed, William J.; Lee, Chun-Ting
Fonte: The Company of Biologists Limited Publicador: The Company of Biologists Limited
Tipo: Artigo de Revista Científica
Português
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Neocortical development involves ordered specification of forebrain cortical progenitors to various neuronal subtypes, ultimately forming the layered cortical structure. Modeling of this process using human pluripotent stem cells (hPSCs) would enable mechanistic studies of human neocortical development, while providing new avenues for exploration of developmental neocortical abnormalities. Here, we show that preserving hPSCs aggregates – allowing embryoid body formation – while adding basic fibroblast growth factor (bFGF) during neuroepithelial development generates neural rosettes showing dorsal forebrain identity, including Mash1+ dorsal telencephalic GABAergic progenitors. Structures that mirrored the organization of the cerebral cortex formed after rosettes were seeded and cultured for 3 weeks in the presence of FGF18, BDNF and NT3. Neurons migrated along radial glia scaffolding, with deep-layer CTIP2+ cortical neurons appearing after 1 week and upper-layer SATB2+ cortical neurons forming during the second and third weeks. At the end of differentiation, these structures contained both glutamatergic and GABAergic neurons, with glutamatergic neurons being most abundant. Thus, this differentiation protocol generated an hPSC-based model that exhibits temporal patterning and a neuronal subtype ratio similar to that of the developing human neocortex. This model was used to examine the effects of cocaine during neocorticogenesis. Cocaine caused premature neuronal differentiation and enhanced neurogenesis of various cortical neuronal subtypes. These cocaine-induced changes were inhibited by the cytochrome P450 inhibitor cimetidine. This in vitro model enables mechanistic studies of neocorticogenesis...

‣ PAX6 does not regulate Nfia and Nfib expression during neocortical development

Bunt, Jens; Lim, Jonathan W. C.; Zhao, Lu; Mason, Sharon; Richards, Linda J.
Fonte: Nature Publishing Group Publicador: Nature Publishing Group
Tipo: Artigo de Revista Científica
Publicado em 29/05/2015 Português
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The Nuclear factor I (NFI) family of transcription factors regulates proliferation and differentiation throughout the developing central nervous system. In the developing telencephalon of humans and mice, reduced Nfi expression is associated with agenesis of the corpus callosum and other neurodevelopmental defects. Currently, little is known about how Nfi expression is regulated during early telencephalic development. PAX6, a transcription factor important for telencephalic development, has been proposed as an upstream regulator of Nfi expression in the neocortex. Here we demonstrate that, in the developing neocortex of mice, NFIA and NFIB are endogenously expressed in gradients with high caudo-medial to low rostro-lateral expression and are most highly expressed in the cortical plate. We found that this expression pattern deviates from that of PAX6, suggesting that PAX6 does not drive Nfi expression. This is supported by in vitro reporter assays showing that PAX6 over-expression does not regulate Nfi promoter activity. Similarly, we also found that in the Pax6 Small Eye mutant, no changes in Nfi mRNA or protein expression are observed in the neocortical ventricular zone where PAX6 and the NFIs are expressed. Together these data demonstrate that in mice...

‣ Building a Bigger Brain: Centriole Control of Cerebral Cortical Development

Hu, Wen Fan
Fonte: Harvard University Publicador: Harvard University
Tipo: Thesis or Dissertation
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Human genetics has identified essential roles for many centriole- and cilia-related proteins during human development. Mutations in centrosome-associated genes commonly cause microcephaly, or "small brain," and mutations in cilia-associated genes cause a diverse spectrum of diseases termed "ciliopathies." However, the functional relationships between these two crucial organelles are less well studied. The activities of centrosome-related proteins during mitosis and cytoskeletal remodeling are well-characterized, but their in vivo functions are incompletely understood. Here, we identify novel human mutations in a centrosomal gene which encodes a regulatory subunit of a microtubule interacting protein, and uncover unexpected pathways during vertebrate development. Human mutations cause severe microlissencephaly, reflecting defects in cerebral cortical neurogenesis, and loss of function in mice and zebrafish confirm essential roles in embryonic development, neurogenesis, and cell survival. Surprisingly, null mutant embryos display hallmarks of aberrant Sonic hedgehog signaling, including holoprosencephaly. Deficient induced pluripotent stem cells and lymphoblasts show defective proliferation and spindle structure, while deficient fibroblasts also demonstrate a remarkable excess of centrioles...

‣ A multi-resource data integration approach: identification of candidate genes regulating cell proliferation during neocortical development

Vied, Cynthia M.; Freudenberg, Florian; Wang, Yuting; Raposo, Alexandre A. S. F.; Feng, David; Nowakowski, Richard S.
Fonte: Frontiers Research Foundation Publicador: Frontiers Research Foundation
Tipo: Artigo de Revista Científica
Publicado em 21/08/2014 Português
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Neurons of the mammalian neocortex are produced by proliferating cells located in the ventricular zone (VZ) lining the lateral ventricles. This is a complex and sequential process, requiring precise control of cell cycle progression, fate commitment and differentiation. We have analyzed publicly available databases from mouse and human to identify candidate genes that are potentially involved in regulating early neocortical development and neurogenesis. We used a mouse in situ hybridization dataset (The Allen Institute for Brain Science) to identify 13 genes (Cdon, Celsr1, Dbi, E2f5, Eomes, Hmgn2, Neurog2, Notch1, Pcnt, Sox3, Ssrp1, Tead2, Tgif2) with high correlation of expression in the proliferating cells of the VZ of the neocortex at early stages of development (E15.5). We generated a similar human brain network using microarray and RNA-seq data (BrainSpan Atlas) and identified 407 genes with high expression in the developing human VZ and subventricular zone (SVZ) at 8-9 post-conception weeks. Seven of the human genes were also present in the mouse VZ network. The human and mouse networks were extended using available genetic and proteomic datasets through GeneMANIA. A gene ontology search of the mouse and human networks indicated that many of the genes are involved in the cell cycle...

‣ A multi-resource data integration approach: identification of candidate genes regulating cell proliferation during neocortical development

Vied, Cynthia M.; Freudenberg, Florian; Wang, Yuting; Raposo, Alexandre A. S. F.; Feng, David; Nowakowski, Richard S.
Fonte: Frontiers Media S.A. Publicador: Frontiers Media S.A.
Tipo: Artigo de Revista Científica
Publicado em 21/08/2014 Português
Relevância na Pesquisa
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Neurons of the mammalian neocortex are produced by proliferating cells located in the ventricular zone (VZ) lining the lateral ventricles. This is a complex and sequential process, requiring precise control of cell cycle progression, fate commitment and differentiation. We have analyzed publicly available databases from mouse and human to identify candidate genes that are potentially involved in regulating early neocortical development and neurogenesis. We used a mouse in situ hybridization dataset (The Allen Institute for Brain Science) to identify 13 genes (Cdon, Celsr1, Dbi, E2f5, Eomes, Hmgn2, Neurog2, Notch1, Pcnt, Sox3, Ssrp1, Tead2, Tgif2) with high correlation of expression in the proliferating cells of the VZ of the neocortex at early stages of development (E15.5). We generated a similar human brain network using microarray and RNA-seq data (BrainSpan Atlas) and identified 407 genes with high expression in the developing human VZ and subventricular zone (SVZ) at 8–9 post-conception weeks. Seven of the human genes were also present in the mouse VZ network. The human and mouse networks were extended using available genetic and proteomic datasets through GeneMANIA. A gene ontology search of the mouse and human networks indicated that many of the genes are involved in the cell cycle...

‣ Maternal-fetal unit interactions and eutherian neocortical development and evolution

Maliqueo Yevilao, Manuel Alejandro; Kaune, Heidy; Montiel, Juan F.
Fonte: Frontiers Research Foundations Publicador: Frontiers Research Foundations
Tipo: Artículo de revista
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Artículo de publicación ISI; The conserved brain design that primates inherited from early mammals differs from the variable adult brain size and species-specific brain dominances observed across mammals. This variability relies on the emergence of specialized cerebral cortical regions and sub-compartments, triggering an increase in brain size, areal interconnectivity and histological complexity that ultimately lies on the activation of developmental programs. Structural placental features are not well correlated with brain enlargement; however, several endocrine pathways could be tuned with the activation of neuronal progenitors in the proliferative neocortical compartments. In this article, we reviewed some mechanisms of eutherians maternal fetal unit interactions associated with brain development and evolution. We propose a hypothesis of brain evolution where proliferative compartments in primates become activated by "non-classical" endocrine placental signals participating in different steps of corticogenesis. Changes in the inner placental structure, along with placenta endocrine stimuli over the cortical proliferative activity would allow mammalian brain enlargement with a concomitant shorter gestation span, as an evolutionary strategy to escape from parent-offspring conflict.; Government of Chile Universidad Diego Portales...