Relevant bibliographies by topics / Glia Progenitors

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Glia Progenitors'

Author: Grafiati
Published: 6 June 2025
Last updated: 8 June 2025

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Journal articles on the topic "Glia Progenitors"

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Pose-Méndez, Sol, Michel Rehbock, Alexandra Wolf-Asseburg, and Reinhard W. Köster. "In Vivo Monitoring of Fabp7 Expression in Transgenic Zebrafish." Cells 13, no. 13 (July 2, 2024): 1138. http://dx.doi.org/10.3390/cells13131138.

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In zebrafish, like in mammals, radial glial cells (RGCs) can act as neural progenitors during development and regeneration in adults. However, the heterogeneity of glia subpopulations entails the need for different specific markers of zebrafish glia. Currently, fluorescent protein expression mediated by a regulatory element from the glial fibrillary acidic protein (gfap) gene is used as a prominent glia reporter. We now expand this tool by demonstrating that a regulatory element from the mouse Fatty acid binding protein 7 (Fabp7) gene drives reliable expression in fabp7-expressing zebrafish glial cells. By using three different Fabp7 regulatory element-mediated fluorescent protein reporter strains, we reveal in double transgenic zebrafish that progenitor cells expressing fluorescent proteins driven by the Fabp7 regulatory element give rise to radial glia, oligodendrocyte progenitors, and some neuronal precursors. Furthermore, Bergmann glia represent the almost only glial population of the zebrafish cerebellum (besides a few oligodendrocytes), and the radial glia also remain in the mature cerebellum. Fabp7 regulatory element-mediated reporter protein expression in Bergmann glia progenitors suggests their origin from the ventral cerebellar proliferation zone, the ventricular zone, but not from the dorsally positioned upper rhombic lip. These new Fabp7 reporters will be valuable for functional studies during development and regeneration.
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Morrow, Theresa, Mi-Ryoung Song, and Anirvan Ghosh. "Sequential specification of neurons and glia by developmentally regulated extracellular factors." Development 128, no. 18 (September 15, 2001): 3585–94. http://dx.doi.org/10.1242/dev.128.18.3585.

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Cortical progenitor cells give rise to neurons during embryonic development and to glia after birth. While lineage studies indicate that multipotent progenitor cells are capable of generating both neurons and glia, the role of extracellular signals in regulating the sequential differentiation of these cells is poorly understood. To investigate how factors in the developing cortex might influence cell fate, we developed a cortical slice overlay assay in which cortical progenitor cells are cultured over cortical slices from different developmental stages. We find that embryonic cortical progenitors cultured over embryonic cortical slices differentiate into neurons and those cultured over postnatal cortical slices differentiate into glia, suggesting that the fate of embryonic progenitors can be influenced by developmentally regulated signals. In contrast, postnatal progenitor cells differentiate into glial cells when cultured over either embryonic or postnatal cortical slices. Clonal analysis indicates that the postnatal cortex produces a diffusible factor that induces progenitor cells to adopt glial fates at the expense of neuronal fates. The effects of the postnatal cortical signals on glial cell differentiation are mimicked by FGF2 and CNTF, which induce glial fate specification and terminal glial differentiation respectively. These observations indicate that cell fate specification and terminal differentiation can be independently regulated and suggest that the sequential generation of neurons and glia in the cortex is regulated by a developmental increase in gliogenic signals.
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Ojalvo-Sanz, Ana Cristina, and Laura López-Mascaraque. "Gliogenic Potential of Single Pallial Radial Glial Cells in Lower Cortical Layers." Cells 10, no. 11 (November 19, 2021): 3237. http://dx.doi.org/10.3390/cells10113237.

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During embryonic development, progenitor cells are progressively restricted in their potential to generate different neural cells. A specific progenitor cell type, the radial glial cells, divides symmetrically and then asymmetrically to produce neurons, astrocytes, oligodendrocytes, and NG2-glia in the cerebral cortex. However, the potential of individual progenitors to form glial lineages remains poorly understood. To further investigate the cell progeny of single pallial GFAP-expressing progenitors, we used the in vivo genetic lineage-tracing method, the UbC-(GFAP-PB)-StarTrack. After targeting those progenitors in embryonic mice brains, we tracked their adult glial progeny in lower cortical layers. Clonal analyses revealed the presence of clones containing sibling cells of either a glial cell type (uniform clones) or two different glial cell types (mixed clones). Further, the clonal size and rostro-caudal cell dispersion of sibling cells differed depending on the cell type. We concluded that pallial E14 neural progenitors are a heterogeneous cell population with respect to which glial cell type they produce, as well as the clonal size of their cell progeny.
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Barriola, Sonsoles, Fernando Pérez-Cerdá, Carlos Matute, Ana Bribián, and Laura López-Mascaraque. "A Clonal NG2-Glia Cell Response in a Mouse Model of Multiple Sclerosis." Cells 9, no. 5 (May 21, 2020): 1279. http://dx.doi.org/10.3390/cells9051279.

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NG2-glia, also known as oligodendrocyte precursor cells (OPCs), have the potential to generate new mature oligodendrocytes and thus, to contribute to tissue repair in demyelinating diseases like multiple sclerosis (MS). Once activated in response to brain damage, NG2-glial cells proliferate, and they acquire a reactive phenotype and a heterogeneous appearance. Here, we set out to investigate the distribution and phenotypic diversity of NG2-glia relative to their ontogenic origin, and whether there is a clonal NG2-glial response to lesion in an experimental autoimmune encephalomyelitis (EAE) murine model of MS. As such, we performed in utero electroporation of the genomic lineage tracer, StarTrack, to follow the fate of NG2-glia derived from single progenitors and to evaluate their response to brain damage after EAE induction. We then analyzed the dispersion of the NG2-glia derived clonally from single pallial progenitors in the brain of EAE mice. In addition, we examined several morphological parameters to assess the degree of NG2-glia reactivity in clonally-related cells. Our results reveal the heterogeneity of these progenitors and their cell progeny in a scenario of autoimmune demyelination, revealing the ontogenic phenomena at play in these processes.
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Dimou, Leda, and Magdalena Götz. "Glial Cells as Progenitors and Stem Cells: New Roles in the Healthy and Diseased Brain." Physiological Reviews 94, no. 3 (July 2014): 709–37. http://dx.doi.org/10.1152/physrev.00036.2013.

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The diverse functions of glial cells prompt the question to which extent specific subtypes may be devoted to a specific function. We discuss this by reviewing one of the most recently discovered roles of glial cells, their function as neural stem cells (NSCs) and progenitor cells. First we give an overview of glial stem and progenitor cells during development; these are the radial glial cells that act as NSCs and other glial progenitors, highlighting the distinction between the lineage of cells in vivo and their potential when exposed to a different environment, e.g., in vitro. We then proceed to the adult stage and discuss the glial cells that continue to act as NSCs across vertebrates and others that are more lineage-restricted, such as the adult NG2-glia, the most frequent progenitor type in the adult mammalian brain, that remain within the oligodendrocyte lineage. Upon certain injury conditions, a distinct subset of quiescent astrocytes reactivates proliferation and a larger potential, clearly demonstrating the concept of heterogeneity with distinct subtypes of, e.g., astrocytes or NG2-glia performing rather different roles after brain injury. These new insights not only highlight the importance of glial cells for brain repair but also their great potential in various aspects of regeneration.
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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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Gray, G. E., and J. R. Sanes. "Lineage of radial glia in the chicken optic tectum." Development 114, no. 1 (January 1, 1992): 271–83. http://dx.doi.org/10.1242/dev.114.1.271.

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In many parts of the central nervous system, the elongated processes of radial glial cells are believed to guide immature neurons from the ventricular zone to their sites of differentiation. To study the clonal relationships of radial glia to other neural cell types, we used a recombinant retrovirus to label precursor cells in the chick optic tectum with a heritable marker, the E. coli lacZ gene. The progeny of the infected cells were detected at later stages of development with a histochemical stain for the lacZ gene product. Radial glia were identified in a substantial fraction of clones, and these were studied further. Our main results are the following. (a) Clones containing radial glia frequently contained neurons and/or astrocytes, but usually not other radial glia. Thus, radial glia derive from a multipotential progenitor rather than from a committed radial glial precursor. (b) Production of radial glia continues until at least embryonic day (E) 8, after the peak of neuronal birth is over (approximately E5) and after radial migration of immature neurons has begun (E6-7). Radial glial and neuronal lineages do not appear to diverge during this interval, and radial glia are among the last cells that their progenitors produce. (c) As they migrate, many cells are closely apposed to the apical process of their sibling radial glia. Thus, radial glia may frequently guide the migration of their clonal relatives. (d) The population of labelled radial glia declines between E15 and E19-20 (just before hatching), concurrent with a sharp increase in the number of labelled astrocytes. This result suggests that some tectal radial glia transform into astrocytes, as occurs in mammalian cerebral cortex, although others persist after hatching. To reconcile the observations that many radial glia are present early, that radial glia are among the last offspring of a multipotential stem cell, and that most clones contain only a single radial glial cell, we suggest that the stem cell is, or becomes, a radial glial cell.
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Hui, Subhra Prakash, Tapas Chandra Nag, and Sukla Ghosh. "Neural cells and their progenitors in regenerating zebrafish spinal cord." International Journal of Developmental Biology 64, no. 4-5-6 (2020): 353–66. http://dx.doi.org/10.1387/ijdb.190130sg.

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The zebrafish (Danio rerio), among all amniotes is emerging as a powerful model to study vertebrate organogenesis and regeneration. In contrast to mammals, the adult zebrafish is capable of regenerating damaged axonal tracts; it can replace neurons and glia lost after spinal cord injury (SCI) and functionally recover. In the present paper, we report ultrastructural and cell biological analyses of regeneration processes after SCI. We have focused on event specific analyses of spinal cord regeneration involving different neuronal and glial cell progenitors, such as radial glia, oligodendrocyte progenitors (OPC), and Schwann cells. While comparing the different events, we frequently refer to previous ultrastructural analyses of central nervous system (CNS) injury in higher vertebrates. Our data show (a) the cellular events following injury, such as cell death and proliferation; (b) demyelination and remyelination followed by target innervation and regeneration of synaptic junctions and c) the existence of different progenitors and their roles during regeneration. The present ultrastructural analysis corroborates the cellular basis of regeneration in the zebrafish spinal cord and confirms the presence of both neuronal and different glial progenitors.
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Pawolski, Verena, and Mirko H. H. Schmidt. "Neuron–Glia Interaction in the Developing and Adult Enteric Nervous System." Cells 10, no. 1 (December 31, 2020): 47. http://dx.doi.org/10.3390/cells10010047.

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The enteric nervous system (ENS) constitutes the largest part of the peripheral nervous system. In recent years, ENS development and its neurogenetic capacity in homeostasis and allostasishave gained increasing attention. Developmentally, the neural precursors of the ENS are mainly derived from vagal and sacral neural crest cell portions. Furthermore, Schwann cell precursors, as well as endodermal pancreatic progenitors, participate in ENS formation. Neural precursors enherite three subpopulations: a bipotent neuron-glia, a neuronal-fated and a glial-fated subpopulation. Typically, enteric neural precursors migrate along the entire bowel to the anal end, chemoattracted by glial cell-derived neurotrophic factor (GDNF) and endothelin 3 (EDN3) molecules. During migration, a fraction undergoes differentiation into neurons and glial cells. Differentiation is regulated by bone morphogenetic proteins (BMP), Hedgehog and Notch signalling. The fully formed adult ENS may react to injury and damage with neurogenesis and gliogenesis. Nevertheless, the origin of differentiating cells is currently under debate. Putative candidates are an embryonic-like enteric neural progenitor population, Schwann cell precursors and transdifferentiating glial cells. These cells can be isolated and propagated in culture as adult ENS progenitors and may be used for cell transplantation therapies for treating enteric aganglionosis in Chagas and Hirschsprung’s diseases.
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Nagashima, Mikiko, and Peter F. Hitchcock. "Inflammation Regulates the Multi-Step Process of Retinal Regeneration in Zebrafish." Cells 10, no. 4 (April 1, 2021): 783. http://dx.doi.org/10.3390/cells10040783.

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The ability to regenerate tissues varies between species and between tissues within a species. Mammals have a limited ability to regenerate tissues, whereas zebrafish possess the ability to regenerate almost all tissues and organs, including fin, heart, kidney, brain, and retina. In the zebrafish brain, injury and cell death activate complex signaling networks that stimulate radial glia to reprogram into neural stem-like cells that repair the injury. In the retina, a popular model for investigating neuronal regeneration, Müller glia, radial glia unique to the retina, reprogram into stem-like cells and undergo a single asymmetric division to generate multi-potent retinal progenitors. Müller glia-derived progenitors then divide rapidly, numerically matching the magnitude of the cell death, and differentiate into the ablated neurons. Emerging evidence reveals that inflammation plays an essential role in this multi-step process of retinal regeneration. This review summarizes the current knowledge of the inflammatory events during retinal regeneration and highlights the mechanisms whereby inflammatory molecules regulate the quiescence and division of Müller glia, the proliferation of Müller glia-derived progenitors and the survival of regenerated neurons.
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Dissertations / Theses on the topic "Glia Progenitors"

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Murdoch, Barbara. "Identification, regulation and lineage tracing of embryonic olfactory progenitors." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/994.

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Neurogenesis occurs in exclusive regions in the adult nervous system, the subventricular zone and dentate gyrus in the brain, and olfactory epithelium (OE) in the periphery. Cell replacement after death or injury, occurs to varying degrees in neural tissue, and is thought to be dependent upon the biological responses of stem and/or progenitor cells. Despite the progress made to identify adult OE and central nervous system (CNS) progenitors and lineage trace their progeny, our spatial and temporal understanding of embryonic OE neuroglial progenitors has been stalled by the paucity of identifiable genes able to distinguish individual candidate progenitors. In the developing CNS, radial glia serve as both neural progenitors and scaffolding for migrating neuroblasts and are identified by the expression of a select group of antigens, including nestin. Here, I show that the embryonic OE contains a novel radial glial-like progenitor (RGLP) that is not detected in adult OE. RGLPs express the radial glial antigens nestin, GLAST and RC2, but not brain lipid binding protein (BLBP), which, distinct from CNS radial glia, is instead found in olfactory ensheathing cells, a result confirmed using lineage tracing with BLBP-cre mice. Nestin-cre-mediated lineage tracing with three different reporters reveals that only a subpopulation of nestin-expressing RGLPs activate the “CNS-specific” nestin regulatory elements, and produce spatially restricted neurons in the OE and vomeronasal organ. The dorsal-medial restriction of transgene-activating cells is also seen in the embryonic OE of Nestin-GFP transgenic mice, where GFP is found in a subpopulation of GFP+ Mash1+ neuronal progenitors, despite the fact that endogenous nestin expression is found in RGLPs throughout the OE. In vitro, embryonic OE progenitors produce three biologically distinct colony subtypes, that when generated from Nestin-cre/ZEG mice, produce GFP+ neurons, recapitulating their in vivo phenotype, and are enriched for the most neurogenic colony subtype. Neurogenesis in vitro is driven by the proliferation of nestin+ progenitors in response to FGF2. I thus provide evidence for a novel neurogenic precursor, the RGLP of the OE, that can be regulated by FGF2, and provide the first evidence for intrinsic differences in the origin and spatiotemporal potential of distinct progenitors during OE development.
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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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BOZZO, MATTEO. "Glial cells of the developing amphioxus: a molecular study." Doctoral thesis, Università degli studi di Genova, 2021. http://hdl.handle.net/11567/1043680.

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Glial cells play important roles in the development and homeostasis of metazoan nervous systems. However, while their involvement in the development and function in the central nervous system (CNS) of vertebrates is increasingly well understood, much less is known about invertebrate glia and the evolutionary history of glial cells more generally. An investigation into amphioxus glia is therefore timely, as this organism is the best living proxy for the last common ancestor of all chordates, and hence provides a window on the role of glial cells development and function at the transition between invertebrates and vertebrates. We report here our findings on amphioxus glia as characterized by molecular probes correlated with anatomical data at the TEM level. The results show amphioxus glial lineages express genes typical of vertebrate astroglia and radial glia and segregate early in development, forming what appears to be a spatially separated cell proliferation zone positioned laterally, between the dorsal and ventral zones of neural cell proliferation. Our study provides strong evidence for the presence of vertebrate-type glial cells in amphioxus while highlighting the role played by segregated progenitor cell pools in CNS development. There are implications also for our understanding of glial cells in a broader evolutionary context and insights into patterns of precursor cell deployment in the chordate nerve cord.
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Badsha, Farhath. "A comparative study of neocortical development between humans and great apes." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-224196.

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The neocortex is the most recently evolved part of the mammalian brain which is involved in a repertoire of higher order brain functions, including those that separate humans from other animals. Humans have evolved an expanded neocortex over the course of evolution through a massive increase in neuron number (compared to our close relatives-­‐‑ the chimpanzees) in spite of sharing similar gestation time frames. So what do humans do differently compared to chimpanzees within the same time frame during their development? This dissertation addresses this question by comparing the developmental progression of neurogenesis between humans and chimpanzees using cerebral organoids as the model system. The usage of cerebral organoids, has enabled us to compare the development of both the human neocortex, and the chimpanzee neocortex from the very initiation of the neural phase of embryogenesis until very long periods of time. The results obtained so far suggest that the genetic programs underlying the development of the chimpanzee neocortex and the human neocortex are not very different, but rather the difference lies in the timing of the developmental progression. These results show that the chimpanzee neocortex spends lesser time in its proliferation phase, and allots lesser time to the generation of its neurons than the human neocortex. In more scientific terms, the neurogenic phase of the neocortex is shorter in chimpanzees than it is in humans. This conclusion is supported by (1) an earlier onset of gliogenesis in chimpanzees compared to humans which is indicative of a declining neurogenic phase, (2) an earlier increase in the chimpanzee neurogenic progenitors during development, compared to humans, (3) a higher number of stem cell– like progenitors in human cortices compared to chimpanzees, (4) a decline in neurogenic areas within the chimpanzee cerebral organoids over time compared to human cerebral organoids.
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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.
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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 lignages
New 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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Smith, Maria Civita. "MAPPING ASTROCYTE DEVELOPMENT IN THE DORSAL CORTEX OF THE MOUSE BRAIN." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1373039738.

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Chapman, Heather M. "Gsx genes control the neuronal to glial fate switch in telencephalic progenitors." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1394725163.

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Beligala, Dilshan Harshajith. "Stem-like cells and glial progenitors in the adult mouse suprachiasmatic nucleus." Bowling Green State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1566319291491512.

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Bizzotto, Sara. "Eml1 in radial glial progenitors during cortical development : the neurodevelopmental role of a protein mutated in subcortical heterotopia in mouse and human." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066118.

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Le développement du cortex cérébral résulte de processus de prolifération, neurogenèse, migration et différenciation cellulaire qui sont contrôlés génétiquement. Les malformations corticales qui résultent d'anomalies de ces processus sont associées à l'épilepsie et la déficience intellectuelle. Nous avons étudié la souris mutante HeCo (heterotopic cortex), qui présente une hétérotopie sous-cortical bilatérale (neurones présents dans la substance blanche) et nous avons identifié la présence d'une mutation sur le gène Eml1 (Echinoderm Microtubule-associated protein-Like 1). De plus, des mutations du gène EML1 ont été identifiées chez des patients atteints d'une forme sévère et rare d'hétérotopie. Dans le cerveau embryonnaire des souris HeCo, des progéniteurs ont été identifiés en dehors de la zone de prolifération, ce qui représente une nouvelle cause de cette malformation. Nous avons étudié la fonction d'Eml1 dans les progéniteurs de la glie radiaire, qui sont clés au cours de la corticogenèse. Nous avons montré qu'Eml1 se localise dans le fuseau mitotique où elle est susceptible de réguler la dynamique des microtubules. Nos données suggèrent qu'Eml1 peut jouer un rôle dans la régulation de la longueur du fuseau puisque celle-ci est perturbée dans les cellules de la glie radiaire chez la souris HeCo. Ceci pourrait représenter la cause primaire de leur ectopie. Nous avons analysé le nombre et la taille des cellules en métaphase dans la partie apicale de la zone ventriculaire où ont lieu les mitoses. Nous proposons ici de nouveaux mécanismes qui régissent l'organisation des progéniteurs dans la zone ventriculaire au cours du développement cortical normal et pathologique
The cerebral cortex develops through genetically regulated processes of cellular proliferation, neurogenesis, migration and differentiation. Cortical malformations represent a spectrum of heterogeneous disorders due to abnormalities in these steps, and associated with epilepsy and intellectual disability. We studied the HeCo (heterotopic cortex) mutant mouse, which exhibits bilateral subcortical band heterotopia (SBH), characterized by many aberrantly positioned neurons in the white matter. We found that Eml1 (Echinoderm Microtubule-associated protein-Like 1) is mutated in these mice. Screening of EML1 in heterotopia patients identified mutations giving rise to a severe and rare form of atypical heterotopia. In HeCo embryonic brains, progenitors were identified outside the normal proliferative ventricular zone (VZ), representing a novel cause of this disorder. We studied Eml1 function in radial glial progenitors (RGCs), which are important during corticogenesis generating other subtypes of progenitors and post-mitotic neurons, and serving as guides for migrating neurons. We showed that Eml1 localizes to the mitotic spindle where it might regulate microtubule dynamics. My data suggest a role in the establishment of the steady state metaphase spindle length. Indeed, HeCo RGCs in the VZ showed a perturbed spindle length during corticogenesis, and this may represent one of the primary mechanisms leading to abnormal progenitor behavior. I also analyzed cell number and metaphase cell size at the apical side of the VZ, where mitosis occurs. I thus propose new mechanisms governing normal and pathological VZ progenitor organization and function during cortical development
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Books on the topic "Glia Progenitors"

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Leone, Dino. Tamoxifen-inducible glia-specific cre mice for somatic mutagenesis in oligodendrocytes and schwann cells and [beta]1-integrin regulates neural progenitor maintenance through modulation of growth factor signaling. 2003.

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Book chapters on the topic "Glia Progenitors"

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Eugenín-von Bernhardi, Jaime, and Leda Dimou. "NG2-glia, More Than Progenitor Cells." In Advances in Experimental Medicine and Biology, 27–45. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40764-7_2.

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Bosch, E. Peter, José G. Assouline, and Ramon Lim. "In Vitro Effects of Glia Maturation Factor on Bipotential Glial Progenitor Cells." In Model Systems of Development and Aging of the Nervous System, 125–37. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2037-1_10.

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Scolding, Neil. "The adult human oligodendrocyte progenitor." In Molecular Signaling and Regulation in Glial Cells, 288–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60669-4_25.

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Franklin, Robin J. M. "The biology of the transplanted oligodendrocyte progenitor." In Molecular Signaling and Regulation in Glial Cells, 367–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60669-4_32.

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Balasubramanian, Swarnalatha, Elizabeth M. Powell, and Jennie B. Leach. "Culturing Neurons, Glia, and Progenitor Cells in Three-Dimensional Hydrogels." In Extracellular Matrix, 91–99. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2083-9_9.

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Ader, Marius, Volker Enzmann, and Mike Francke. "Potential of Müller Glia and Stem/Progenitor Cells to Regenerate Retinal Tissue." In Stem Cell Biology and Regenerative Medicine, 161–75. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0787-8_8.

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Espinosa, A., D. Espejo, and J. de Vellis. "Transplantation of Oligodendrocyte Progenitors and CG4 Cells into the Dveloping Rat Brain: Differences and Similarities." In Molecular Signaling and Regulation in Glial Cells, 329–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60669-4_29.

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Nishikawa, Masashi, Koh-ichi Nagata, and Hidenori Tabata. "Live Imaging of Migrating Neurons and Glial Progenitors Visualized by in Utero Electroporation." In Methods in Molecular Biology, 201–9. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-3810-1_17.

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Nelson, Craig M., and David R. Hyde. "Müller Glia as a Source of Neuronal Progenitor Cells to Regenerate the Damaged Zebrafish Retina." In Retinal Degenerative Diseases, 425–30. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0631-0_54.

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Small, R. "Differentiation of a Migratory Bipotential Glial Progenitor Cell in the Developing Rat Optic Nerve." In Neural Development and Regeneration, 677–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73148-8_71.

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Conference papers on the topic "Glia Progenitors"

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Sudina, A. K., D. V. Goldshtein, D. N. Silachev, and D. I. Salikhova. "GLIAL PROGENITOR CELL TRANSPLANTATION ENHANCES RECOVERY OF SENSORIMOTOR DEFICITS IN RATS AFTER TRAUMATIC BRAIN INJURY." In XI МЕЖДУНАРОДНАЯ КОНФЕРЕНЦИЯ МОЛОДЫХ УЧЕНЫХ: БИОИНФОРМАТИКОВ, БИОТЕХНОЛОГОВ, БИОФИЗИКОВ, ВИРУСОЛОГОВ, МОЛЕКУЛЯРНЫХ БИОЛОГОВ И СПЕЦИАЛИСТОВ ФУНДАМЕНТАЛЬНОЙ МЕДИЦИНЫ. IPC NSU, 2024. https://doi.org/10.25205/978-5-4437-1691-6-105.

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The search for new methods of therapy of traumatic brain injury is one of the important tasks of modern biomedicine. In this work, the therapeutic effect of glial progenitor cells obtained from induced pluripotent stem cells was investigated in an experimental model of traumatic brain injury.
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Grinchevskaia, L. R., D. I. Salikhova, T. K. Fatkhudinov, and D. V. Goldshtein. "THE ROLE OF GLIAL PROGENITOR CELLS IN ANGIOGENESIS." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY, 205–9. LLC Institute Information Technologies, 2024. http://dx.doi.org/10.47501/978-5-6044060-4-5.205-209.

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Diseases associated with impaired blood supply to organs and tissues are one of the common causes of mortality in the world. Despite their high frequency of occurrence, the effectiveness of existing therapies remains insufficient, so it is important to search for new ways of therapy of ischemic tissues.
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