Notch signaling represses the glial fate in fly PNS

Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1381-1390 ◽  
Author(s):  
V. Van De Bor ◽  
A. Giangrande
Keyword(s):  
Nervous System ◽  
Notch Signaling ◽  
Glial Cell ◽  
Glial Cells ◽  
Genetic Switch ◽  
Organ Type ◽  
A Cell ◽  
Glial Fate ◽  
Glial Precursor

By using gain-of-function mutations it has been proposed that vertebrate Notch promotes the glial fate. We show in vivo that glial cells are produced at the expense of neurons in the peripheral nervous system of flies lacking Notch and that constitutively activated Notch produces the opposite phenotype. Notch acts as a genetic switch between neuronal and glial fates by negatively regulating glial cell deficient/glial cells missing, the gene required in the glial precursor to induce gliogenesis. Moreover, Notch represses neurogenesis or gliogenesis, depending on the sensory organ type. Numb, which is asymmetrically localized in the multipotent cell that produces the glial precursor, induces glial cells at the expense of neurons. Thus, a cell-autonomous mechanism inhibits Notch signaling.

Glide directs glial fate commitment and cell fate switch between neurones and glia

Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 131-139 ◽  
Author(s):  
S. Vincent ◽  
J.L. Vonesch ◽  
A. Giangrande
Keyword(s):  
Nervous System ◽  
Drosophila Melanogaster ◽  
Peripheral Nervous System ◽  
Glial Cell ◽  
Cell Fate ◽  
Glial Cells ◽  
Neuronal Development ◽  
Precursor Cells ◽  
A Cell ◽  
Glial Fate

Glial cells constitute the second component of the nervous system and are important during neuronal development. In this paper we describe a gene, glial cell deficient, (glide), that is necessary for glial cell fate commitment in Drosophila melanogaster. Mutations at the glide locus prevent glial cell determination in the embryonic central and peripheral nervous system. Moreover, we show that the absence of glial cells is the consequence of a cell fate switch from glia to neurones. This suggests the existence of a multipotent precursor cells in the nervous system. glide mutants also display defects in axonal navigation, which confirms and extends previous results indicating a role for glial cells in these processes.

Some fly sensory organs are gliogenic and require glide/gcm in a precursor that divides symmetrically and produces glial cells

Development ◽  
2000 ◽  
Vol 127 (17) ◽  
pp. 3735-3743 ◽  
Author(s):  
V. Van De Bor ◽  
R. Walther ◽  
A. Giangrande
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Peripheral Nervous System ◽  
Glial Cell ◽  
Glial Cells ◽  
Sensory Organ ◽  
Asymmetric Distribution ◽  
Sensory Organs ◽  
The Central Nervous System ◽  
Glial Precursor

In flies, the choice between neuronal and glial fates depends on the asymmetric division of multipotent precursors, the neuroglioblast of the central nervous system and the IIb precursor of the sensory organ lineage. In the central nervous system, the choice between the two fates requires asymmetric distribution of the glial cell deficient/glial cell missing (glide/gcm) RNA in the neuroglioblast. Preferential accumulation of the transcript in one of the daughter cells results in the activation of the glial fate in that cell, which becomes a glial precursor. Here we show that glide/gcm is necessary to induce glial differentiation in the peripheral nervous system. We also present evidence that glide/gcm RNA is not necessary to induce the fate choice in the peripheral multipotent precursor. Indeed, glide/gcm RNA and protein are first detected in one daughter of IIb but not in IIb itself. Thus, glide/gcm is required in both central and peripheral glial cells, but its regulation is context dependent. Strikingly, we have found that only subsets of sensory organs are gliogenic and express glide/gcm. The ability to produce glial cells depends on fixed, lineage related, cues and not on stochastic decisions. Finally, we show that after glide/gcm expression has ceased, the IIb daughter migrates and divides symmetrically to produce several mature glial cells. Thus, the glide/gcm-expressing cell, also called the fifth cell of the sensory organ, is indeed a glial precursor. This is the first reported case of symmetric division in the sensory organ lineage. These data indicate that the organization of the fly peripheral nervous system is more complex than previously thought.

scholarly journals Insights Into Central Nervous System Glial Cell Formation and Function From Zebrafish

2021 ◽  
Vol 9 ◽  
Author(s):  
Sarah A. Neely ◽  
David A. Lyons
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Cell ◽  
Glial Cells ◽  
Large Body ◽  
Cell Types ◽  
Cell Interactions ◽  
Glial Cell Interactions ◽  
And Function

The term glia describes a heterogenous collection of distinct cell types that make up a large proportion of our nervous system. Although once considered the glue of the nervous system, the study of glial cells has evolved significantly in recent years, with a large body of literature now highlighting their complex and diverse roles in development and throughout life. This progress is due, in part, to advances in animal models in which the molecular and cellular mechanisms of glial cell development and function as well as neuron-glial cell interactions can be directly studied in vivo in real time, in intact neural circuits. In this review we highlight the instrumental role that zebrafish have played as a vertebrate model system for the study of glial cells, and discuss how the experimental advantages of the zebrafish lend themselves to investigate glial cell interactions and diversity. We focus in particular on recent studies that have provided insight into the formation and function of the major glial cell types in the central nervous system in zebrafish.

Cell proliferation in the repairing adult insect central nervous system: incorporation of the thymidine analogue 5-bromo-2-deoxyuridine in vivo

1990 ◽  
Vol 95 (4) ◽  
pp. 599-604
Author(s):  
P.J. Smith ◽  
E.A. Howes ◽  
J.E. Treherne
Keyword(s):  
Central Nervous System ◽  
Cell Proliferation ◽  
Nervous System ◽  
Blood Brain Barrier ◽  
Glial Cells ◽  
Past Research ◽  
Thymidine Analogue ◽  
Adult Insect ◽  
Insect Central Nervous System

Uptake of the thymidine analogue 5-bromo-2-deoxyuridine into non-neuronal cells of the insect central nervous system has been examined following a controlled lesioning of the glial elements. The pattern of BUdR labelling along the penultimate abdominal connective was examined over a period of 17 days. Cell proliferation occurred in and immediately around the site of damage in both perineurial and subperineurial glial cells but at different times post-lesion for the two regions. Proliferation in the perineurial zone was maximal at 6–8 days post-lesion but continued for at least 17 days. Subperineurial proliferation was less dramatic and peaked between days 8–11 post-lesion. In both areas division appears to be confined to the reactive glial cells. These results are discussed in the context of past research on this system, particularly with regard to the restoration of the blood-brain barrier.

scholarly journals Actomyosin dynamics, Bmp and Notch signaling pathways drive apical extrusion of proepicardial cells

2018 ◽  
Author(s):  
Laura Andrés-Delgado ◽  
Alexander Ernst ◽  
María Galardi-Castilla ◽  
David Bazaga ◽  
Marina Peralta ◽  
...  
Keyword(s):  
Cell Viability ◽  
Notch Signaling ◽  
Heart Development ◽  
Zebrafish Model ◽  
Pharmacological Agents ◽  
Apical Extrusion ◽  
A Cell ◽  
Cell Extrusion ◽  
Unique Mechanism

ABSTRACTThe epicardium, the outer mesothelial layer enclosing the myocardium, plays key roles in heart development and regeneration. During embryogenesis it arises from the proepicardium (PE), a cell cluster that appears in the dorsal pericardium close to the venous pole of the heart. Little is known about how the PE emerges from the pericardial mesothelium. Using the zebrafish model and a combination of genetic tools, pharmacological agents and quantitative in vivo imaging we reveal that a coordinated collective movement of the dorsal pericardium drives PE formation. We found that PE cells are apically extruded in response to actomyosin activity. Our results reveal that the coordinated action of Notch/Bmp pathways is critically needed for apical extrusion of PE cells. More generally, by comparison to cell extrusion for the elimination of unfit cells from epithelia, our results describe a unique mechanism where extruded cell viability is maintained.

scholarly journals Dpp and Hedgehog promote the glial response to neuronal apoptosis in the developing Drosophila visual system

PLoS Biology ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. e3001367
Author(s):  
Sergio B. Velarde ◽  
Alvaro Quevedo ◽  
Carlos Estella ◽  
Antonio Baonza
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Glial Cell ◽  
Glial Cells ◽  
Neuronal Apoptosis ◽  
Morphological Changes ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Jnk Pathway ◽  
Glial Cell Proliferation

Damage in the nervous system induces a stereotypical response that is mediated by glial cells. Here, we use the eye disc of Drosophila melanogaster as a model to explore the mechanisms involved in promoting glial cell response after neuronal cell death induction. We demonstrate that these cells rapidly respond to neuronal apoptosis by increasing in number and undergoing morphological changes, which will ultimately grant them phagocytic abilities. We found that this glial response is controlled by the activity of Decapentaplegic (Dpp) and Hedgehog (Hh) signalling pathways. These pathways are activated after cell death induction, and their functions are necessary to induce glial cell proliferation and migration to the eye discs. The latter of these 2 processes depend on the function of the c-Jun N-terminal kinase (JNK) pathway, which is activated by Dpp signalling. We also present evidence that a similar mechanism controls glial response upon apoptosis induction in the leg discs, suggesting that our results uncover a mechanism that might be involved in controlling glial cells response to neuronal cell death in different regions of the peripheral nervous system (PNS).

Demyelination-remyelination in the Central Nervous System: Ligand-dependent Participation of the Notch Signaling Pathway

2019 ◽  
Vol 171 (1) ◽  
pp. 172-192 ◽  
Author(s):  
Patricia A Mathieu ◽  
María F Almeira Gubiani ◽  
Débora Rodríguez ◽  
Laura I Gómez Pinto ◽  
María de Luján Calcagno ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Notch Signaling ◽  
Progenitor Cells ◽  
Central Nervous System Disease ◽  
Notch Signaling Pathway ◽  
Signaling Activation

Abstract Multiple sclerosis (MS) is an immune-mediated central nervous system disease mostly affecting young people. Multiple sclerosis and other neurodegenerative and white matter disorders involve oligodendrocyte (OL) damage and demyelination. Therefore, elucidating the signaling pathways involved in the remyelination process through the maturation of OL progenitor cells (OPCs) may contribute to the development of new therapeutic approaches. In this context, this paper further characterizes toxic cuprizone (CPZ)-induced demyelination and spontaneous remyelination in rats and investigates the role of ligand-dependent Notch signaling activation along demyelination/remyelination both in vivo and in vitro. Toxic treatment generated an inflammatory response characterized by both microgliosis and astrogliosis. Interestingly, early demyelination revealed an increase in the proportion of Jagged1+/GFAP+ cells, which correlated with an increase in Jagged1 transcript and concomitant Jagged1-driven Notch signaling activation, particularly in NG2+ OPCs, in both the corpus callosum (CC) and subventricular zone (SVZ). The onset of remyelination then exhibited an increase in the proportion of F3/contactin+/NG2+ cells, which correlated with an increase in F3/contactin transcript during ongoing remyelination in the CC. Moreover, neurosphere cultures revealed that neural progenitor cells present in the brain SVZ of CPZ-treated rats recapitulate in vitro the mechanisms underlying the response to toxic injury observed in vivo, compensating for mature OL loss. Altogether, the present results offer strong evidence of cell-type and ligand-specific Notch signaling activation and its time- and area-dependent participation in toxic demyelination and spontaneous remyelination.

The appearance of neural and glial cell markers during early development of the nervous system in the amphibian embryo

Development ◽  
1989 ◽  
Vol 107 (1) ◽  
pp. 43-54 ◽  
Author(s):  
N.J. Messenger ◽  
A.E. Warner
Keyword(s):  
Nervous System ◽  
Glial Cell ◽  
Glial Cells ◽  
Cell Type ◽  
Neurofilament Protein ◽  
Amphibian Embryo ◽  
Specific Antibodies ◽  
Cell Type Specific ◽  
Radial Glial ◽  
The Brain

Cell-type-specific antibodies have been used to follow the appearance of neurones and glia in the developing nervous system of the amphibian embryo. Differentiated neurones were recognized with antibodies against neurofilament protein while glial cells were identified with antibodies against glial fibrillary acidic protein (GFAP). The appearance of neurones containing the neurotransmitters 5-hydroxytryptamine and dopamine has been charted also. In Xenopus, neurofilament protein in developing neurones was observed occasionally at NF stage 21 and was present reliably in the neural tube and in caudal regions of the brain at stage 23. Antibodies to the low molecular weight fragment of the neurofilament triplet recognized early neurones most reliably. Radial glial cells, identified with GFAP antibody, were identified from stage 23 onwards in the neural tube and caudal regions of the brain. In the developing spinal cord, GFAP staining was apparent throughout the cytoplasm of each radial glial cell. In the brain, the peripheral region only of each glial cell contained GFAP. By stage 36, immunohistochemically recognizable neurones and glia were present throughout the nervous system. In the axolotl, by stage 36 the pattern of neural and glial staining was identical to that observed in Xenopus. GFAP staining of glial cells was obvious at stage 23, although neuronal staining was clearly absent. This implies that glial cells differentiate before neurones. 5-HT-containing cell bodies were first observed in caudal regions of the developing brain on either side of the midline at stage 26. An extensive network of 5-HT neurones appeared gradually, with a substantial subset crossing to the opposite side of the brain through the developing optic chiasma. 5,7-dihydroxytryptamine prevented the appearance of 5-HT. Depletion of 5-HT had little effect on development or swimming behaviour. Dopamine-containing neurones in the brain first differentiated at stage 35–36 and gradually increased in number up to stage 45–47, the latest stage examined. The functional role of 5-HT- or dopamine-containing neurones remains to be elucidated. We conclude that cell-type-specific antibodies can be used to identify neurones and glial cells at early times during neural development and may be useful tools in circumstances where functional identification is difficult.

scholarly journals GAP-43 is expressed by nonmyelin-forming Schwann cells of the peripheral nervous system.

1992 ◽  
Vol 116 (6) ◽  
pp. 1455-1464 ◽  
Author(s):  
R Curtis ◽  
H J Stewart ◽  
S M Hall ◽  
G P Wilkin ◽  
R Mirsky ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Peripheral Nervous System ◽  
Schwann Cells ◽  
Glial Cells ◽  
Distal Stump ◽  
Metabolic Labeling ◽  
General Role

Recently it has been demonstrated that the growth-associated protein GAP-43 is not confined to neurons but is also expressed by certain central nervous system glial cells in tissue culture and in vivo. This study has extended these observations to the major class of glial cells in the peripheral nervous system, Schwann cells. Using immunohistochemical techniques, we show that GAP-43 immunoreactivity is present in Schwann cell precursors and in mature non-myelin-forming Schwann cells both in vitro and in vivo. This immunoreactivity is shown by Western blotting to be a membrane-associated protein that comigrates with purified central nervous system GAP-43. Furthermore, metabolic labeling experiments demonstrate definitively that Schwann cells in culture can synthesize GAP-43. Mature myelin-forming Schwann cells do not express GAP-43 but when Schwann cells are removed from axonal contact in vivo by nerve transection GAP-43 expression is upregulated in nearly all Schwann cells of the distal stump by 4 wk after denervation. In contrast, in cultured Schwann cells GAP-43 is not rapidly upregulated in cells that have been making myelin in vivo. Thus the regulation of GAP-43 appears to be complex and different from that of other proteins associated with nonmyelin-forming Schwann cells such as N-CAM, glial fibrillary acidic protein, A5E3, and nerve growth factor receptor, which are rapidly upregulated in myelin-forming cells after loss of axonal contact. These observations suggest that GAP-43 may play a more general role in the nervous system than previously supposed.

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