Academic literature on the topic 'Basal radial glia cell'
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Journal articles on the topic "Basal radial glia cell"
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Pereida-Jaramillo, Elizabeth, Gabriela B. Gómez-González, Angeles Edith Espino-Saldaña, and Ataúlfo Martínez-Torres. "Calcium Signaling in the Cerebellar Radial Glia and Its Association with Morphological Changes during Zebrafish Development." International Journal of Molecular Sciences 22, no. 24 (December 16, 2021): 13509. http://dx.doi.org/10.3390/ijms222413509.
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Radial glial cells are a distinct non-neuronal cell type that, during development, span the entire width of the brain walls of the ventricular system. They play a central role in the origin and placement of neurons, since their processes form structural scaffolds that guide and facilitate neuronal migration. Furthermore, glutamatergic signaling in the radial glia of the adult cerebellum (i.e., Bergmann glia), is crucial for precise motor coordination. Radial glial cells exhibit spontaneous calcium activity and functional coupling spread calcium waves. However, the origin of calcium activity in relation to the ontogeny of cerebellar radial glia has not been widely explored, and many questions remain unanswered regarding the role of radial glia in brain development in health and disease. In this study we used a combination of whole mount immunofluorescence and calcium imaging in transgenic (gfap-GCaMP6s) zebrafish to determine how development of calcium activity is related to morphological changes of the cerebellum. We found that the morphological changes in cerebellar radial glia are quite dynamic; the cells are remarkably larger and more elaborate in their soma size, process length and numbers after 7 days post fertilization. Spontaneous calcium events were scarce during the first 3 days of development and calcium waves appeared on day 5, which is associated with the onset of more complex morphologies of radial glia. Blockage of gap junction coupling inhibited the propagation of calcium waves, but not basal local calcium activity. This work establishes crucial clues in radial glia organization, morphology and calcium signaling during development and provides insight into its role in complex behavioral paradigms.
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Li, Zhen, William A. Tyler, Ella Zeldich, Gabriel Santpere Baró, Mayumi Okamoto, Tianliuyun Gao, Mingfeng Li, Nenad Sestan, and Tarik F. Haydar. "Transcriptional priming as a conserved mechanism of lineage diversification in the developing mouse and human neocortex." Science Advances 6, no. 45 (November 2020): eabd2068. http://dx.doi.org/10.1126/sciadv.abd2068.
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How the rich variety of neurons in the nervous system arises from neural stem cells is not well understood. Using single-cell RNA-sequencing and in vivo confirmation, we uncover previously unrecognized neural stem and progenitor cell diversity within the fetal mouse and human neocortex, including multiple types of radial glia and intermediate progenitors. We also observed that transcriptional priming underlies the diversification of a subset of ventricular radial glial cells in both species; genetic fate mapping confirms that the primed radial glial cells generate specific types of basal progenitors and neurons. The different precursor lineages therefore diversify streams of cell production in the developing murine and human neocortex. These data show that transcriptional priming is likely a conserved mechanism of mammalian neural precursor lineage specialization.
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Moore, Rachel, and Paula Alexandre. "Delta-Notch Signaling: The Long and The Short of a Neuron’s Influence on Progenitor Fates." Journal of Developmental Biology 8, no. 2 (March 26, 2020): 8. http://dx.doi.org/10.3390/jdb8020008.
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Maintenance of the neural progenitor pool during embryonic development is essential to promote growth of the central nervous system (CNS). The CNS is initially formed by tightly compacted proliferative neuroepithelial cells that later acquire radial glial characteristics and continue to divide at the ventricular (apical) and pial (basal) surface of the neuroepithelium to generate neurons. While neural progenitors such as neuroepithelial cells and apical radial glia form strong connections with their neighbours at the apical and basal surfaces of the neuroepithelium, neurons usually form the mantle layer at the basal surface. This review will discuss the existing evidence that supports a role for neurons, from early stages of differentiation, in promoting progenitor cell fates in the vertebrates CNS, maintaining tissue homeostasis and regulating spatiotemporal patterning of neuronal differentiation through Delta-Notch signalling.
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Kullmann, Jan A., Sophie Meyer, Fabrizia Pipicelli, Christina Kyrousi, Felix Schneider, Nora Bartels, Silvia Cappello, and Marco B. Rust. "Profilin1-Dependent F-Actin Assembly Controls Division of Apical Radial Glia and Neocortex Development." Cerebral Cortex 30, no. 6 (December 20, 2019): 3467–82. http://dx.doi.org/10.1093/cercor/bhz321.
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Abstract Neocortex development depends on neural stem cell proliferation, cell differentiation, neurogenesis, and neuronal migration. Cytoskeletal regulation is critical for all these processes, but the underlying mechanisms are only poorly understood. We previously implicated the cytoskeletal regulator profilin1 in cerebellar granule neuron migration. Since we found profilin1 expressed throughout mouse neocortex development, we here tested the hypothesis that profilin1 is crucial for neocortex development. We found no evidence for impaired neuron migration or layering in the neocortex of profilin1 mutant mice. However, proliferative activity at basal positions was doubled in the mutant neocortex during mid-neurogenesis, with a drastic and specific increase in basal Pax6+ cells indicative for elevated numbers of basal radial glia (bRG). This was accompanied by transiently increased neurogenesis and associated with mild invaginations resembling rudimentary neocortex folds. Our data are in line with a model in which profilin1-dependent actin assembly controls division of apical radial glia (aRG) and thereby the fate of their progenies. Via this mechanism, profilin1 restricts cell delamination from the ventricular surface and, hence, bRG production and thereby controls neocortex development in mice. Our data support the radial cone hypothesis” claiming that elevated bRG number causes neocortex folds.
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Penisson, Maxime, Mingyue Jin, Shengming Wang, Shinji Hirotsune, Fiona Francis, and Richard Belvindrah. "Lis1 mutation prevents basal radial glia-like cell production in the mouse." Human Molecular Genetics 31, no. 6 (October 12, 2021): 942–57. http://dx.doi.org/10.1093/hmg/ddab295.
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Abstract Human cerebral cortical malformations are associated with progenitor proliferation and neuronal migration abnormalities. Progenitor cells include apical radial glia, intermediate progenitors and basal (or outer) radial glia (bRGs or oRGs). bRGs are few in number in lissencephalic species (e.g. the mouse) but abundant in gyrencephalic brains. The LIS1 gene coding for a dynein regulator, is mutated in human lissencephaly, associated also in some cases with microcephaly. LIS1 was shown to be important during cell division and neuronal migration. Here, we generated bRG-like cells in the mouse embryonic brain, investigating the role of Lis1 in their formation. This was achieved by in utero electroporation of a hominoid-specific gene TBC1D3 (coding for a RAB-GAP protein) at mouse embryonic day (E) 14.5. We first confirmed that TBC1D3 expression in wild-type (WT) brain generates numerous Pax6+ bRG-like cells that are basally localized. Second, using the same approach, we assessed the formation of these cells in heterozygote Lis1 mutant brains. Our novel results show that Lis1 depletion in the forebrain from E9.5 prevented subsequent TBC1D3-induced bRG-like cell amplification. Indeed, we observe perturbation of the ventricular zone (VZ) in the mutant. Lis1 depletion altered adhesion proteins and mitotic spindle orientations at the ventricular surface and increased the proportion of abventricular mitoses. Progenitor outcome could not be further altered by TBC1D3. We conclude that disruption of Lis1/LIS1 dosage is likely to be detrimental for appropriate progenitor number and position, contributing to lissencephaly pathogenesis.
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Zhang, Sanguo, Huanhuan Joyce Wang, Jia Li, Xiao-Ling Hu, and Qin Shen. "Radial Glial Cell-Derived VCAM1 Regulates Cortical Angiogenesis Through Distinct Enrichments in the Proximal and Distal Radial Processes." Cerebral Cortex 30, no. 6 (January 6, 2020): 3717–30. http://dx.doi.org/10.1093/cercor/bhz337.
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Abstract Angiogenesis in the developing cerebral cortex accompanies cortical neurogenesis. However, the precise mechanisms underlying cortical angiogenesis at the embryonic stage remain largely unknown. Here, we show that radial glia-derived vascular cell adhesion molecule 1 (VCAM1) coordinates cortical vascularization through different enrichments in the proximal and distal radial glial processes. We found that VCAM1 was highly enriched around the blood vessels in the inner ventricular zone (VZ), preventing the ingrowth of blood vessels into the mitotic cell layer along the ventricular surface. Disrupting the enrichment of VCAM1 surrounding the blood vessels by a tetraspanin-blocking peptide or conditional deletion of Vcam1 gene in neural progenitor cells increased angiogenesis in the inner VZ. Conversely, VCAM1 expressed in the basal endfeet of radial glial processes promoted angiogenic sprouting from the perineural vascular plexus (PNVP). In utero, overexpression of VCAM1 increased the vessel density in the cortical plate, while knockdown of Vcam1 accomplished the opposite. In vitro, we observed that VCAM1 bidirectionally affected endothelial cell proliferation in a concentration-dependent manner. Taken together, our findings identify that distinct concentrations of VCAM1 around VZ blood vessels and the PNVP differently organize cortical angiogenesis during late embryogenesis.
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Shohayeb, Belal, Uda Ho, Yvonne Y. Yeap, Robert G. Parton, S. Sean Millard, Zhiheng Xu, Michael Piper, and Dominic C. H. Ng. "The association of microcephaly protein WDR62 with CPAP/IFT88 is required for cilia formation and neocortical development." Human Molecular Genetics 29, no. 2 (December 9, 2019): 248–63. http://dx.doi.org/10.1093/hmg/ddz281.
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Abstract WDR62 mutations that result in protein loss, truncation or single amino-acid substitutions are causative for human microcephaly, indicating critical roles in cell expansion required for brain development. WDR62 missense mutations that retain protein expression represent partial loss-of-function mutants that may therefore provide specific insights into radial glial cell processes critical for brain growth. Here we utilized CRISPR/Cas9 approaches to generate three strains of WDR62 mutant mice; WDR62 V66M/V66M and WDR62R439H/R439H mice recapitulate conserved missense mutations found in humans with microcephaly, with the third strain being a null allele (WDR62stop/stop). Each of these mutations resulted in embryonic lethality to varying degrees and gross morphological defects consistent with ciliopathies (dwarfism, anophthalmia and microcephaly). We find that WDR62 mutant proteins (V66M and R439H) localize to the basal body but fail to recruit CPAP. As a consequence, we observe deficient recruitment of IFT88, a protein that is required for cilia formation. This underpins the maintenance of radial glia as WDR62 mutations caused premature differentiation of radial glia resulting in reduced generation of neurons and cortical thinning. These findings highlight the important role of the primary cilium in neocortical expansion and implicate ciliary dysfunction as underlying the pathology of MCPH2 patients.
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Golden, J. A., J. C. Zitz, K. McFadden, and C. L. Cepko. "Cell migration in the developing chick diencephalon." Development 124, no. 18 (September 15, 1997): 3525–33. http://dx.doi.org/10.1242/dev.124.18.3525.
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We previously reported that retrovirally marked clones in the mature chick diencephalon were widely dispersed in the mediolateral, dorsoventral and rostrocaudal planes. The current study was undertaken to define the migration routes that led to the dispersion. Embryos were infected between stages 10 and 14 with a retroviral stock encoding alkaline phosphatase and a library of molecular tags. Embryos were harvested 2.5-5.5 days later and the brains were fixed and serially sectioned. Sibling relationships were determined following PCR amplification and sequencing of the molecular tag. On embryonic day 4, all clones were organized in radial columns spanning the neuroepithelium, which was composed primarily of a ventricular zone at this age. No tangential migration was seen in the ventricular zone. On embryonic day 5, most clones remained radial with many cells located in the ventricular zone; however, a few clones had cells migrating perpendicular to the radial column, in either a rostrocaudal or dorsoventral direction. The tangential migration began just beyond the basal limit of the ventricular zone. On embryonic days 6 and 7, many clones had cells migrating perpendicular to the radial column, which spanned from the ventricular to the pial surface. The migrating cells appeared to be aligned along axes that were perpendicular to the radial column. Using a combination of DiI tracing, immunohistochemistry and electron microscopy, we have determined that axonal tracts are present and are aligned with the migrating cells, suggesting that they support the non-radial cell migration. These data indicate that migration along pathways independent of radial glia occur outside of the ventricular zone in more than 50% of the clones in the chick diencephalon.
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Li, Xiaosu, Guoping Liu, Lin Yang, Zhenmeiyu Li, Zhuangzhi Zhang, Zhejun Xu, Yuqun Cai, et al. "Decoding Cortical Glial Cell Development." Neuroscience Bulletin 37, no. 4 (February 19, 2021): 440–60. http://dx.doi.org/10.1007/s12264-021-00640-9.
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AbstractMouse cortical radial glial cells (RGCs) are primary neural stem cells that give rise to cortical oligodendrocytes, astrocytes, and olfactory bulb (OB) GABAergic interneurons in late embryogenesis. There are fundamental gaps in understanding how these diverse cell subtypes are generated. Here, by combining single-cell RNA-Seq with intersectional lineage analyses, we show that beginning at around E16.5, neocortical RGCs start to generate ASCL1+EGFR+ apical multipotent intermediate progenitors (MIPCs), which then differentiate into basal MIPCs that express ASCL1, EGFR, OLIG2, and MKI67. These basal MIPCs undergo several rounds of divisions to generate most of the cortical oligodendrocytes and astrocytes and a subpopulation of OB interneurons. Finally, single-cell ATAC-Seq supported our model for the genetic logic underlying the specification and differentiation of cortical glial cells and OB interneurons. Taken together, this work reveals the process of cortical radial glial cell lineage progression and the developmental origins of cortical astrocytes and oligodendrocytes.
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Sawada, Kazuhiko. "Tracking of neurons derived from basal radial glia experiencing multiple cell division in the developing neocortex of ferrets." IBRO Reports 6 (September 2019): S84. http://dx.doi.org/10.1016/j.ibror.2019.07.272.
Full textDissertations / Theses on the topic "Basal radial glia cell"
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Pilaz, Louis-Jan. "Role of G1 phase regulators during corticogenesis." Thesis, Lyon 1, 2009. http://www.theses.fr/2009LYO10277.
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Les mécanismes développementaux qui spécifient le nombre et le phénotype laminaire des neurones du cortex cérébral jouent un rôle essentiel dans l’établissement de la cytoarchitecture corticale. Le nombre de neurones dans chaque couche d'une aire donnée est déterminé par le taux de production neuronale, qui dépend étroitement de l'équilibre entre les divisions prolifératives et différenciatives. Des observations clés suggèrent que la durée de la phase G1 (TG1) ferait partie intégrante d'un mécanisme cellulaire régulant le mode de division des précurseurs du cortex. Nous avons testé cette hypothèse par l'accélération expérimentale de la progression dans la phase G1 de précurseurs corticaux de souris in vivo, via la surexpression des cyclines E1 et D1. A E15, la réduction de TG1 promeut la rentrée dans le cycle cellulaire aux dépens de la différenciation neuronale, résultant en une modification de la cytoarchitecture du cortex adulte. Des données de modélisation confirment que les effets induits par la réduction de TG1 sont médiés par des changements du mode de division. Les effets de la surexpression des cyclines E1 et D2 à E13 sont plus modérés qu'à E15, indiquant des différences intrinsèques entre les précurseurs corticaux précoces et tardifs. La mesure des phases du cycle cellulaire des populations de précurseurs corticaux à l’aide de différentes techniques révèle un niveau important d’hétérogénéité et souligne la nécessité de prendre en compte la diversité des précurseurs co‐existant dans les zones germinales du télencéphaleIn the cerebral cortex, area‐specific differences in neuron number and phenotype are distinguishing features both within and across species. The developmental mechanisms that specify the number of neurons and their laminar fate are instrumental in specifying cortical cytoarchitecture. Neuron number in layers and areas correlate with changes in the rate of neuron production, largely determined by the balance between proliferative and differentiative divisions in cortical precursors. Key observations suggest a concerted regulation between the duration of the G1 phase (TG1) and mode of division and have led to the hypothesis that TG1 could be an integral part of a cellular mechanism regulating the mode of division of cortical precursors. To test this hypothesis we experimentally accelerated TG1 in mouse cortical precursors in vivo, via the forced expression of cyclinE1 and cyclinD1. At E15, TG1 reduction promoted cell‐cycle re‐entry at the expense of differentiation and led to cytoarchitectural modifications. Modeling confirms that the TG1‐induced changes in neuron production and laminar fate are mediated via the changes in the mode of division. Forced expression of G1 cyclins was also applied to early cortical precursors. The effects of cyclinD1 and cyclinE1 up‐regulation at E13 were milder than those observed at E15, pointing to intrinsic differences between early and late cortical precursors. The used of various techniques to measure cell‐cycle kinetics in distinct precursor populations underlined the necessity of taking the full diversity of neural precursors co‐existing in the GZ of the telencephalon into account when performing cellcycle kinetics analysis
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Penisson, Maxime. "Mécanismes de LIS1 dans les progéniteurs neuraux contribuant aux malformations de développement du cortex." Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS415.
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Les malformations du développement du cortex sont associées à des troubles de la prolifération des progéniteurs et de la migration neuronale. Les glies radiaires basales (bRGs), un type de progéniteur, sont limités dans les espèces lissencéphaliques mais abondants dans les cerveaux gyrencéphaliques. Le gène LIS1, codant pour un régulateur de la dynéine, est muté dans la lissencéphalie humaine. LIS1 a un rôle dans la division cellulaire et la migration neuronale. Dans cette étude, nous avons généré des cellules bRG-like dans le cerveau embryonnaire murin, pour étudier le rôle de Lis1 dans leur production. Ceci fut réalisé par électroporation in utero du gène hominoïde-spécifique TBC1D3 au jour embryonnaire (E) 14.5. Nous avons confirmé que l’expression de TBC1D3 dans des cerveaux WT induit un grand nombre de cellules bRG-like basales. Puis, nous avons étudié la production des bRGs-like dans des cerveaux murins hétérozygotes pour Lis1. Nos résultats novateurs montrent que la déplétion de Lis1 à partir de E9.5 empêche la production de cellules bRG-like induites par TBC1D3. La déplétion de Lis1 change l’orientation du fuseau mitotique, accroit le nombre de mitoses abventriculaires et altère l’expression de N-Cadhérine. Nous concluons que la perturbation du dosage de Lis1 pourrait perturber le nombre et la position corrects des progéniteurs, contribuant à la pathogenèse de Lis1Human cortical malformations are associated with progenitor proliferation and neuronal migration abnormalities. Basal radial glia (bRGs), a type of progenitor cells, are limited in lissencephalic species (e.g. the mouse) but abundant in gyrencephalic brains. The LIS1 gene coding for a dynein regulator, is mutated in human lissencephaly, associated also in some cases with microcephaly. LIS1 was shown to be important during cell division and neuronal migration. Here, we generated bRG-like cells in the mouse embryonic brain, investigating the role of Lis1 in their formation. This was achieved by in utero electroporation of a hominoid-specific gene TBC1D3 at mouse embryonic day (E) 14.5. We first confirmed that TBC1D3 overexpression in WT brain generates numerous Pax6+ bRG-like cells that are basally localized. Second, we assessed the formation of these cells in heterozygote Lis1 mutant brains. Our novel results show that Lis1 depletion in the forebrain from E9.5 prevented subsequent TBC1D3-induced bRG-like cell amplification. Lis1 depletion changed mitotic spindle orientations at the ventricular surface, increased the proportion of abventricular mitoses, and altered N-Cadherin expression, altering TBC1D3 function. We conclude that perturbation of Lis1/LIS1 dosage is likely to be detrimental for appropriate progenitor number and position, contributing to lissencephaly pathogenesis
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Wong, Fong Kuan. "Generation of basal radial glia in the embryonic mouse dorsal telencephalon." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-149631.
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The human brain, as much as it is “unaccountable” in the eyes of Virginia Woolf, is a marvel. It is the evolutionary increase in brain size, especially in the cerebral cortex, that both allowed Mrs Woolf to create and us to perceive the beautiful imagery that exists in her fictional world. The evolutionary increase in brain size in part reflects the increase in the number of neurons generated during neocortical development. This in turn reflects two principal features of cortical expansion, namely, an increase in the number of neural stem and progenitor cells (from here on referred to as progenitor cells) and their neurogenic potential. Strikingly, in order to cater for this increase in progenitor cells and neurogenic potential, there is a significant expansion and diversification of basal progenitors in the subventricular zone (SVZ).
Basal progenitors can be divided into three types: basal intermediate progenitors (bIPs), basal radial glias (bRGs) and transit-amplifying progenitors (TAPs). bIPs are the most abundant progenitors in the mouse SVZ. These cells are non-polar and are Pax6 and Sox2 negative, but Tbr2 positive. They have limited proliferative capacity as they can divide only once to produce two neurons. bRGs and TAPs, on the other hand, are able to undergo multiple rounds of division and exist in higher abundance in gyrencephalic brains (for bRG, in humans up to 50% versus mouse 5% at mid-neurogenesis). The morphology of bRGs are reported to be dynamic (fluctuating between states of having process(es) to none), whereas TAPs are generally described to be non-polar during mitosis. bRGs are known to express Pax6 and Sox2 but not Tbr2 while TAPs are known to express both Pax6 and Tbr2. The increase in the proportion of these self-renewing basal progenitors (more specifically bRGs) might allow for cortical expansion.
Hence, the main objective of this doctoral work was to generate more bRGs in the mouse dorsal telencephalon, the region that ultimately develops to become the cerebral cortex. To achieve this objective, two approaches were used– (i) a general approach by microinjecting a pool of ferret poly-A+ RNA and (ii) a candidate approach by conditionally expressing the transcription factor Pax6.
In the general approach, the microinjection technique was first established and validated in an organotypic slice culture of the mouse dorsal telencephalon. A pool of ferret poly-A¬+ RNA extracted at P1, the developmental stage corresponding to the peak of bRG production, was then microinjected into the dorsal telencephalon. We hypothesized that at the peak of bRG production, the “instructive” messages on how to generate bRG would be at their peak. Hence, by introducing these “instructive” messages into a apical radial glia (aRG), these cells would thus “know” how to generate bRGs. At 24 h after microinjection, only aRGs, the predominant progenitor residing in the ventricular zone during mid-neurogenesis were recovered. At 48 h after microinjection, however, 75% of cells that translated the ferret poly-A¬+ RNA had a morphology reminiscent of bRG. These cells were located away from the ventricular surface and had a basal but not apical process. We conclude from these experiments that we did indeed generate bRG-like cells in the mouse dorsal telencephalon via microinjection of the ferret poly-A¬+ RNA.
In the candidate approach, this work aimed to conditionally express Pax6, a transcription factor that has been linked to proliferation and neurogenesis in aRG. More specifically, as there is a significant increase in the number of Pax6 positive cells (bRGs) in the SVZ of gyrencephalic animals during mid-neurogenesis, we wanted to recapitulate this phenomenon in the mouse dorsal telencephalon, where Pax6 is normally downregulated. To achieve this, the Tis21–CreERT2 mouse was used. Tis21 is a pan-neurogenic marker that is switched on once aRG switches from a proliferative division (i.e. 1 aRG⇒2aRG) to a neurogenic division (i.e. 1aRG⇒1aRG+1bIP). Consequently, the neurogenic aRGs and its progeny, bIPs would thus be Tis21 positive. By conditionally expressing Pax6 in Tis21 positive aRGs, the ectopic expression of Pax6 was successfully induced in the SVZ of the mouse dorsal telencephalon. Interestingly, conditional expression of Pax6 increased the percentage of proliferating cells in the SVZ. However, instead of producing more bIPs as predicted by the neurogenic division of Tis21 positive aRGs, these cells had the cell morphology, transcription factor expression profile, and division-type of bRGs and/or TAPs. Thus, using the conditional expression of Pax6 we were able to generate more bRG-like progenitors in the mouse dorsal telencephalon.
The fate of these conditionally expressing Pax6 progenitors at a later stage was then investigated. A phenotypic change in the behaviour of neurons generated was observed. Instead of migrating into the cortical plate, cells that were highly expressing Pax6 formed a heterotopia at the SVZ or intermediate zone, suggestive of Pax6 interfering with neuronal migration. Interestingly, of those lowly expressing Pax6 cells that successfully migrated to the CP, a disproportionate majority became upper layer neurons. As the fate of neurons are dependent on their date of birth (i.e early born neurons are normally found in the deep layer while late born neurons are normally found in the upper layer), the increase in the upper layer neurons is consistent with the fact that conditionally expressing Pax6 delayed the birth of these neurons by delaying neurogenesis in order to increase the number of proliferative divisions. Interestingly, this increase in upper layer neurons is consistent with the difference between small- and large-brained species.
In conclusion, through this work more bRGs was successfully generated in the mouse dorsal telencephalon through two distinct but complementary approaches.
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Wong, Fong Kuan [Verfasser], Wieland [Akademischer Betreuer] Huttner, and Frank [Akademischer Betreuer] Buchholz. "Generation of basal radial glia in the embryonic mouse dorsal telencephalon / Fong Kuan Wong. Gutachter: Wieland Huttner ; Frank Buchholz." Dresden : Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://d-nb.info/1068447850/34.
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Da, Fonte Dillon. "Transcriptomic and Proteomic Characterizations of Goldfish (Carassius auratus) Radial Glia Reveal Complex Regulation by the Neuropeptide Secretoneurin." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/35681.
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In the teleost brain, radial glial cells (RGCs) are the main macroglia and are stem- like progenitors that express key steroidogenic enzymes, including the estrogen- synthesizing enzyme, aromatase B (cyp19a1b). As a result, RGCs are integral to neurogenesis and neurosteroidogenesis in the brain, however little is known about the permissive factors and signaling mechanisms that control these functions. The aim of this thesis is to investigate if the secretogranin-derived neuropeptide secretoneurin (SN) can exert regulatory control over goldfish (Carassius auratus) RGCs. Immunohistochemistry revealed a close neuroanatomical relationship between RGCs and soma of SNa- immunoreactive magnocellular and parvocellular neurons in the preoptic nucleus in both goldfish and zebrafish (Danio rerio) models. Both intracerebroventricular injections of SNa into the third brain ventricle and SNa exposures of cultured goldfish RGCs in vitro show that SNa can reduce cyp19a1b expression, thus implicating SNa in the control of neuroestrogen production. RNA-sequencing was used to characterize the in vitro transcriptomic responses elicited by 1000 nM SNa in RGCs. These data revealed that gene networks related to central nervous system function (neurogenesis, glial cell development, synaptic plasticity) and immune function (immune system activation, leukocyte function, macrophage response) were increased by SNa. A dose-response study using quantitative proteomics indicates a low 10 nM dose of SNa increased expression of proteins involved in cell growth, proliferation, and migration whereas higher doses down- regulated proteins involved in these processes, indicating SNa has dose-dependent regulatory effects. Together, through these altered gene and protein networks, this thesis proposes SNa exerts trophic and immunogenic effects in RGCs. These datasets identified a total of 12,180 and 1,363 unique transcripts and proteins, respectively, and demonstrated that RGCs express a diverse receptor and signaling molecule profile. Therefore, RGCs can respond to and synthesize an array of hormones, peptides, cytokines, and growth factors, revealing a multiplicity of new functions critical to neuronal-glial interactions.
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Uzquiano, López Ana. "Progenitor cell mechanisms contributing to cortical malformations : studying the role of the heterotopia gene Eml1/EML1 in radial glia." Electronic Thesis or Diss., Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2019SORUS392.pdf.
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Le cortex cérébral se développe à partir des zones de prolifération des cellules progénitrices dont le comportement anormal peut donner lieu à des malformations corticales. Des mutations dans Eml1/EML1 ont été identifiées chez la souris HeCo, ainsi que dans trois familles présentant une hétérotopie sous-corticale (SH). La SH se caractérise par une position aberrante des neurones dans la substance blanche. Chez la souris HeCo, des anomalies de position des progéniteurs de la glie radiale apicale (aRG) ont été observées aux stades précoces de la corticogenèse. Je me suis concentré sur la caractérisation de l’aRG dans la zone ventriculaire (VZ) afin d’identifier pourquoi certaines cellules quittent cette région et ainsi mieux comprendre les mécanismes qui sous-tendent l’hétérotopie. En combinant la microscopie confocale et électronique (EM), j'ai découvert des anomalies des centrosomes et des cils primaires dans les aRG mutants pour Eml1 : les cils primaires sont plus courts et souvent mal orientés dans des vésicules. La recherche de partenaires interagissant avec Eml1 à l'aide de la spectrométrie de masse (MS), combinée au séquençage d’exome des ADN de patients SH, nous a permis d'identifier : 1) un partenaire ciliaire interagissant avec Eml1, RPGRIP1L ; 2) des mutations du gène RPGRIP1L chez un patient SH. L’analyse ontologique des gènes sur les données de MS a mis en évidence l’appareil de Golgi et le transport des protéines comme catégories enrichies. En effet, j'ai identifié des altérations de l'appareil de Golgi dans les aRG HeCo. L’ensemble de ces données montre que l'axe appareil de Golgi-cil primaire est perturbé quand Eml1/EML1 est muté et conduit à l’identification de nouvelles voies dans un trouble grave du neurodéveloppementCerebral cortical development is a finely regulated process, depending on diverse progenitor cells. Abnormal behavior of the latter can give rise to cortical malformations. Mutations in Eml1/EML1 were identified in the HeCo mouse, as well as in three families presenting severe subcortical heterotopia (SH). SH is characterized by the presence of mislocalized neurons in the white matter. At early stages of corticogenesis, abnormally positioned apical radial glia progenitors (aRG) were found cycling outside the proliferative ventricular zone (VZ) in the HeCo cortical wall. I focused my research on characterizing aRG in the VZ to assess why some cells leave this region and thus to further understand SH mechanisms. Combining confocal and electron microscopy (EM), I uncovered abnormalities of centrosomes and primary cilia in Eml1-mutant aRGs: primary cilia are shorter, and often remain basally oriented within vesicles. Searching for Eml1-interacting partners using mass spectrometry (MS), combined with exome sequencing of SH patient DNAs, allowed us to identify a ciliary Eml1-interacting partner, RPGRIP1L, showing mutations in a SH patient. Gene ontology analyses of MS data pointed to Golgi apparatus and protein transport as enriched categories. Indeed, Golgi abnormalities were identified in HeCo aRGs. Altogether, these data indicate that the Golgi-to-primary cilium axis is perturbed in Eml1mutant conditions, pointing to new intracellular pathways involved in severe neurodevelopmental disorders
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Belmonte, Mateos Carla 1992. "Unveiling the molecular and behavioral properties of hindbrain rhombomere centers." Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2022. http://hdl.handle.net/10803/673433.
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Precise regulation of neurogenesis is achieved by differentially allocating the neurogenic competence along the tissue. In the hindbrain proneural gene expression is stereotypically confined in segment boundary-adjacent regions, hence, being absent in segment centers. This segregation of proneural gene expression therefore hints rhombomere centers as a putative non-neurogenic population.
In this work, we unveil their spatiotemporal molecular profile as well as one of the mechanisms involved in their maintenance as non-committed progenitors. By 4D imaging we shed light for the first time into the in vivo cell behavior this population displays. We propose this population in rhombomere centers is indeed heterogeneous as it harbors cells with different proliferative capacity.La regulació precisa de la neurogènesi s’aconsegueix localitzant la competència neurogènica de manera diferencial al llarg del territori. Al cervell posterior, l’expressió de gens proneurals es restringeix a les zones adjacents a les cèl·lules de les fronteres, i per tant és absent als centres així doncs assenyalant els centres dels rombòmers com una població no neurogènica. En aquest treball, hem revelat el seu perfil molecular espai-temporal així com un dels mecanismes que manté aquestes cèl·lules com a no neurogèniques. Mitjançant imatges 4D hem aportat llum per primera vegada a l’enteniment del seu comportament cel·lular en viu, i proposem que aquesta població dels centres dels rombòmers és de fet heterogènia ja que conté cèl·lules amb diferent capacitat proliferativa.
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Kadoshima, Taisuke. "Self-organization of axial polarity, inside-out layer pattern and species-specific progenitor dynamics in human ES cell-derived neocortex." Kyoto University, 2014. http://hdl.handle.net/2433/188695.
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Than, Trong Emmanuel. "Le rôle de la signalisation Notch3 dans le maintien des cellules souches neurales du télencéphale adulte Neural stem cell quiescence and stemness are molecularly distinct outputs of the Notch3 signaling cascade in the vertebrate adult brain her4-expressing neural stem cells are maintained through population asymmetry and embedded into a hierarchy of progenitors responsible for their life-long expansion Radial Glia and Neural Progenitors in the Adult Zebrafish Central Nervous System." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS541.
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Un certain nombre de régions du cerveau des vertébrés, y compris chez l’homme, continuent d’être le siège de l’ajout de nouveaux neurones à l’âge adulte. Ces nouveaux neurones sont produits à partir de cellules spécialisées, appelées cellules souches neurales (CSN). Celles-ci sont capables de s’auto-renouveler et sont principalement trouvées dans un état d’arrêt transitoire du cycle cellulaire que l’on appelle quiescence. A l’heure actuelle, les mécanismes cellulaires et moléculaires permettant aux CSN de trouver un équilibre entre maintien et différentiation, ainsi que les règles générales gouvernant l’évolution de leur population, ne sont que partiellement compris. A l’échelle moléculaire, plusieurs facteurs et voies de signalisation apparaissent déterminants pour l’homéostasie des CSN. Notamment, la voie de signalisation du récepteur Notch s’avère essentielle pour maintenir à la fois l’état de quiescence et le caractère souche des CSN. Il demeure néanmoins inconnu si la signalisation Notch affecte ces deux propriétés de manière indépendante ou non. A l’échelle cellulaire, la plupart des modèles actuels suggèrent que les CSN se divisent rarement et principalement de manière asymétrique. Cette dernière propriété permettrait aux CSN de se perpétuer tout en donnant naissance à des cellules filles déterminées à se différencier en neurones. Le pallium du poisson-zèbre abrite une population particulièrement importante de CSN, que l’on appelle glies radiaires (GR), et qui possèdent les mêmes caractéristiques fondamentales que leurs homologues chez les mammifères. Notre laboratoire avait précédemment démontré que le récepteur Notch3 était nécessaire au maintien de la quiescence des GR. Le travail présenté dans ce manuscrit se décompose en deux études complémentaires dont les objectifs respectifs étaient: (1) d’améliorer notre compréhension du rôle de la voie de signalisation Notch3 dans l’homéostasie des GR et (2) d’étudier les schémas de divisions adoptés par les GR afin de maintenir leur nombre sur une longue durée. Dans la première étude, nous démontrons que le rôle de la signalisation Notch3 s’étend au-delà du simple contrôle de la quiescence des GR en contribuant également au maintien de leur caractère souche par l’intermédiaire de son gène cible hey1. Un point important de cette découverte est que l’action du facteur Hey1 sur le caractère souche des GR apparaît indépendante du rôle de Notch3 dans le maintien de leur quiescence. Dans la seconde étude, nous avons réalisé une analyse clonale du devenir des GR exprimant le gène her4.1. Ceci nous a permis de mettre en évidence que leurs choix entre différentiation, amplification et auto-renouvellement apparaissent stochastiques, mais équilibrés, ce qui leur permet de maintenir leur population dans le temps. De façon très intéressante, nous avons aussi observé que le nombre total de GR du pallium augmente au cours de la vie, ce qui, au regard du comportement homéostatique de la population de GR exprimant her4.1, nous amène à proposer que la zone neurogénique du pallium est organisée selon une hiérarchie dans laquelle une population inconnue de progéniteurs produit continuellement de nouvelles GR, qui ensuite se maintiennent grâce à un équilibre probabiliste entre leurs différents lignagesNew neurons continue to be added into discrete brain regions of most adult vertebrate species, including humans. Adult born neurons arise from precursor cells, called neural stem cells (NSCs), endowed with self-renewal potential and mostly found in a state of reversible cell cycle arrest, named quiescence. Currently, the molecular, cellular and population rules allowing NSC to balance maintenance and differentiation remain incompletely understood. At the single cell level, several factors and signalling pathways were demonstrated to be essential for NSC homeostasis. Among them, the Notch signalling pathway is critically involved in the control of NSC quiescence and stemness. However, whether these two properties represent molecularly distinct or overlapping outputs of the Notch signalling pathway remains unknown. At the cellular level, current models state that NSCs divide rarely and mostly asymmetrically, allowing both self-renewal and the generation of a more committed progeny that ultimately exits the cell cycle and fulfils neuronal differentiation. The adult zebrafish pallium harbours NSCs, called radial glia (RG), which share with their mammalian counterparts the same basic properties. Previously, our laboratory demonstrated that Notch3 was necessary to maintain RG quiescence. Here, in two different and complementary works, we took advantage of the widespread neurogenic ventricular zone (VZ) of the adult zebrafish pallium to (1) explore further the role of Notch3 signalling in RG homeostasis and (2) investigate the division pattern and dynamics allowing the RG population to be maintained on the long run. In the first study, we demonstrate that the role of Notch3 signalling extends beyond the simple maintenance of RG quiescence and that Notch3 also contributes to RG stemness. By overlapping the transcriptomic profiles of both notch3 mutant RG and adult pallial VZ progenitors, we identified different sets of Notch3 target genes potentially responsible for its pleitropic effect in RG. Notably, we show that the Notch3 signalling contribution to RG stemness critically relies on the transcriptional activation of its canonical target gene hey1 and this, independently of Notch3 action on RG quiescence. In the second study, we performed a quantitative analysis of the fates of individual her4.1(Hes5)-expressing RG. We demonstrate that these cells adopt balanced stochastic fates, which allows their population to reach homeostasis. We also report that the overall RG population of the zebrafish pallium continues to grow during adulthood and that this expansion is very likely driven by a yet undefined upstream population of progenitors. As a consequence, we propose that the adult zebrafish is organised into a hierarchy of progenitors dominated by an unknown population that fuels the ongoing production of an intrinsically homeostatic population of RG which, itself, follows neutral drift dynamics
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Najas, Sales Sònia 1985. "Role of DYRK1A in the development of the cerebral cortex : Implication in Down Syndrome." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/380895.
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In this work we have assessed the possible contribution of the human chromosome-21 gene DYRK1A in the developmental cortical alterations associated with Down Syndrome using the mBACTgDyrk1a mouse, which carries 3 copies of Dyrk1a, and a trisomic model of the syndrome, the Ts65Dn mouse. We show that trisomy of Dyrk1a changes the cell cycle parameters of dorsal telencephalic radial glial (RG) progenitors and the division mode of these progenitors leading to a deficit in glutamatergic neurons that persist until the adulthood. We demonstrate that Dyrk1a is the triplicated gene that causes the deficit in early-born cortical glutamatergic neurons in Ts65Dn mice. Moreover, we provide evidences indicating that DYRK1A-mediated degradation of Cyclin D1 is the underlying mechanism of the cell cycle defects in both, mBACTgDyrk1a and Ts65Dn dorsal RG progenitors. Finally, we show that early neurogenesis is enhanced in the medial ganglionic eminence of mBACTgDyrk1a embryos resulting in an altered proportion of particular cortical GABAergic neuron types. These results indicate that the overexpression of DYRK1A contributes significantly to the formation of the cortical circuitry in Down syndrome.En aquest treball s'ha avaluat la possible contribució del gen DYRK1A, localitzat en el cromosoma humà 21, en les alteracions del desenvolupament de l’escorça cerebral associades a la Síndrome de down (SD) mitjançant l’estudi de dos models murins: el ratolí mBACTgDyrk1a, el qual conté 3 còpies de Dyrk1a, i el ratolí Ts65Dn, un dels models trisòmics de la SD més ben caracteritzats. Els nostres resultats mostren que la trisomia de Dyrk1A altera alguns paràmetres del cicle cel•lular i el tipus de divisió dels progenitors neurals del telencèfal dorsal, donant lloc a un dèficit de neurones glutamatèrgiques que persisteix fins l’edat adulta. Hem demostrat que Dyrk1a és el gen triplicat responsable del dèficit inicial en la generació de neurones glutamatèrgiques corticals observat en el ratolí Ts65Dn. A més a més, hem proporcionat evidències de que la degradació de Ciclina D1 induïda per DYRK1A és el mecanisme molecular subjacent a les alteracions de cicle cel•lular observades en els progenitors neuronals dels embrions mBACTgDyrk1a i Ts65Dn. Per altra banda, hem demostrat que la neurogènesis inicial està incrementada en l’eminència ganglionar medial dels embrions mBACTgDyrk1a, fet que altera la proporció de subtipus específics d’interneurones GABAèrgiques en l’escorça cerebral adulta. En conclusió, els nostres resultats indiquen que la sobreexpressió de DYRK1A contribueix significativament a la formació dels circuits cortical en la SD.
Book chapters on the topic "Basal radial glia cell"
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Gierdalski, Marcin, and Sharon L. Juliano. "Influence of Radial Glia and Cajal-Retzius Cells in Neuronal Migration." In Results and Problems in Cell Differentiation, 75–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-540-46006-0_4.
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Leprince, Pierre, and Grazyna Chanas-Sacré. "Regulation of radial glia phenotype." In Glial cell function, 13–22. Elsevier, 2001. http://dx.doi.org/10.1016/s0079-6123(01)32061-7.
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McGrat, Barbara, Corey McCann, Scott Eisenhuth, and E. S. Anton. "Molecular mechanisms of interactions between radial glia and neurons." In Glial cell function, 197–202. Elsevier, 2001. http://dx.doi.org/10.1016/s0079-6123(01)32076-9.
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Gomes∗, Flávia Carvalho Alcantara, and Stevens Kastrup Rehen. "Role of neuron–glia interactions in nervous system development: highlights on radial glia and astrocytes." In Advances in Molecular and Cell Biology, 97–125. Elsevier, 2003. http://dx.doi.org/10.1016/s1569-2558(03)31004-5.
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V. Pushchina, Evgeniya, Anatoly A. Varaksin, and Dmitry K. Obukhov. "Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain." In Neuroprotection - New Approaches and Prospects. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.90547.
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The H2S-producing systems were studied in trout telencephalon, tectum, and cerebellum at 1 week after eye injury. The results of ELISA analysis have shown a 1.7-fold increase in the CBS expression at 1 week post-injury, as compared to the intact trout. In the ventricular and subventricular regions of trout telencephalon, CBS+ cells, as well as neuroepithelial and glial types, were detected. As a result of injury, the number of CBS+ neuroepithelial cells in the pallial and subpallial periventricular regions of the telencephalon increases. In the tectum, a traumatic damage leads to an increase in the CBS expression in radial glia with a simultaneous decrease in the number of CBS immunopositive neuroepithelial cells detected in intact animals. In the cerebellum, we revealed neuroglial interrelations, in which H2S is probably released from the astrocyte-like cells with subsequent activation of the neuronal NMDA receptors. The organization of the H2S-producing cell complexes suggests that the amount of glutamate produced in the trout cerebellum and its reuptake is controlled with the involvement of astrocyte-like cells, reducing its excitotoxicity. We believe that the increase in the number of H2S-producing cells constitutes a response to oxidative stress, and the overproduction of H2S neutralizes the reactive oxygen species.