scholarly journals gcm2 Promotes Glial Cell Differentiation and Is Required with glial cells missing for Macrophage Development in Drosophila

2002 ◽  
Vol 248 (2) ◽  
pp. 369-383 ◽  
Author(s):  
Teresa B Alfonso ◽  
Bradley W Jones
Keyword(s):  
Cell Differentiation ◽  
Glial Cell ◽  
Glial Cells

loco encodes an RGS protein required for Drosophila glial differentiation

Development ◽  
1999 ◽  
Vol 126 (8) ◽  
pp. 1781-1791 ◽  
Author(s):  
S. Granderath ◽  
A. Stollewerk ◽  
S. Greig ◽  
C.S. Goodman ◽  
C.J. O'Kane ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
G Protein ◽  
Glial Cell ◽  
Glial Cells ◽  
Cell Development ◽  
Rgs Proteins ◽  
Glial Differentiation ◽  
G Protein Signalling ◽  
Rgs Domain ◽  
Longitudinal Axon

In Drosophila, glial cell development depends on the gene glial cells missing (gcm). gcm activates the expression of other transcription factors such as pointed and repo, which control subsequent glial differentiation. In order to better understand glial cell differentiation, we have screened for genes whose expression in glial cells depends on the activity of pointed. Using an enhancer trap approach, we have identified loco as such a gene. loco is expressed in most lateral CNS glial cells throughout development. Embryos lacking loco function have an normal overall morphology, but fail to hatch. Ultrastructural analysis of homozygous mutant loco embryos reveals a severe glial cell differentiation defect. Mutant glial cells fail to properly ensheath longitudinal axon tracts and do not form the normal glial-glial cell contacts, resulting in a disruption of the blood-brain barrier. Hypomorphic loco alleles were isolated following an EMS mutagenesis. Rare escapers eclose which show impaired locomotor capabilities. loco encodes the first two known Drosophila members of the family of Regulators of G-protein signalling (RGS) proteins, known to interact with the alpha subunits of G-proteins. loco specifically interacts with the Drosophila alphai-subunit. Strikingly, the interaction is not confined to the RGS domain. This interaction and the coexpression of LOCO and Galphai suggests a function of G-protein signalling for glial cell development.

Expression of a novel Muller glia specific antigen during development and after optic nerve lesion

Development ◽  
1991 ◽  
Vol 111 (3) ◽  
pp. 789-799 ◽  
Author(s):  
B. Schlosshauer ◽  
D. Grauer ◽  
D. Dutting ◽  
J. Vanselow
Keyword(s):  
Monoclonal Antibodies ◽  
Cell Differentiation ◽  
Optic Nerve ◽  
Glial Cell ◽  
Glial Cells ◽  
Ganglion Cells ◽  
Müller Cell ◽  
Cell Type ◽  
Muller Cell

To generate monoclonal antibodies, immunogen fractions were purified from embryonic chick retinae by temperature-induced detergent-phase separation employing Triton X-114. Under reducing conditions, the monoclonal antibody (mAb) 2M6 identifies a protein doublet at 40 and 46 × 10(3) Mr, which appears to form disulfide-coupled multimers. The 2M6 antigen is regulated developmentally during retinal histogenesis and its expression correlates with Muller glial cell differentiation. Isolated glial endfeet and retinal glial cells in vitro were found to be 2M6-positive, identified with the aid of the general glia marker mAb R5. mAb 2M6 does not bind to any other glial cell type in the CNS as judged from immunohistochemical data. Cell-type specificity was further substantiated by employing retinal explant and single cell cultures on laminin in conjunction with two novel neuron-specific monoclonal antibodies. MAb 2M6 does not bind either to neurites or to neuronal cell bodies. Incubation of retinal cells in vitro with bromodeoxyuridine (BrdU) and subsequent immunodouble labelling with mAb 2M6 and anti-BrdU reveal that mitotic Muller cells can also express the 2M6 antigen. To investigate whether Muller cell differentiation depends on interactions with earlier differentiating ganglion cells, transections of early embryonic optic nerves in vivo were performed. This operation eliminates ganglion cells. Muller cell development and 2M6 antigen expression were not affected, suggesting a ganglion-cell-independent differentiation process. If, however, the optic nerve of juvenile chicken was crushed to induce a transient degeneration/regeneration process in the retina, a significant increase of 2M6 immunoreactivity became evident. These data are in line with the hypothesis that Muller glial cells, in contrast to other distinct glial cell types, might facilitate neural regeneration.

scholarly journals Estrogen receptor β controls proliferation of enteric glia and differentiation of neurons in the myenteric plexus after damage

2018 ◽  
Vol 115 (22) ◽  
pp. 5798-5803 ◽  
Author(s):  
F. D’Errico ◽  
G. Goverse ◽  
Y. Dai ◽  
W. Wu ◽  
M. Stakenborg ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Cell Differentiation ◽  
Glial Cell ◽  
Glial Cells ◽  
Myenteric Plexus ◽  
Neuronal Damage ◽  
Estrogen Receptor Β ◽  
Enteric Glial Cells ◽  
Cell Medium

Injury to the enteric nervous system (ENS) can cause several gastrointestinal (GI) disorders including achalasia, irritable bowel syndrome, and gastroparesis. Recently, a subpopulation of enteric glial cells with neuronal stem/progenitor properties (ENSCs) has been identified in the adult ENS. ENSCs have the ability of reconstituting the enteric neuronal pool after damage of the myenteric plexus. Since the estrogen receptor β (ERβ) is expressed in enteric glial cells and neurons, we investigated whether a selective ERβ agonist, LY3201, can influence neuronal and glial cell differentiation. Myenteric ganglia from the murine muscularis externa were isolated and cultured in either glial cell medium or neuronal medium. In glial cell medium, the number of glial progenitor cells (Sox10+) was increased by fourfold in the presence of LY3201. In the neuronal medium supplemented with an antimitotic agent to block glial cell proliferation, LY3201 elicited a 2.7-fold increase in the number of neurons (neurofilament+ or HuC/D+). In addition, the effect of LY3201 was evaluated in vivo in two murine models of enteric neuronal damage and loss, namely, high-fat diet and topical application of the cationic detergent benzalkonium chloride (BAC) on the intestinal serosa, respectively. In both models, treatment with LY3201 significantly increased the recovery of neurons after damage. Thus, LY3201 was able to stimulate glial-to-neuron cell differentiation in vitro and promoted neurogenesis in the damaged myenteric plexus in vivo. Overall, our study suggests that selective ERβ agonists may represent a therapeutic tool to treat patients suffering from GI disorders, caused by excessive neuronal/glial cell damage.

Glial development in the Drosophila CNS requires concomitant activation of glial and repression of neuronal differentiation genes

Development ◽  
1997 ◽  
Vol 124 (12) ◽  
pp. 2307-2316 ◽  
Author(s):  
K. Giesen ◽  
T. Hummel ◽  
A. Stollewerk ◽  
S. Harrison ◽  
A. Travers ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Neuronal Differentiation ◽  
Glial Cell ◽  
Glial Cells ◽  
Neuronal Development ◽  
Egf Receptor ◽  
Dual Process ◽  
Glial Development ◽  
Receptor Signalling ◽  
Cns Midline

Two classes of glial cells are found in the embryonic Drosophila CNS, midline glial cells and lateral glial cells. Midline glial development is triggered by EGF-receptor signalling, whereas lateral glial development is controlled by the gcm gene. Subsequent glial cell differentiation depends partly on the pointed gene. Here we describe a novel component required for all CNS glia development. The tramtrack gene encodes two zinc-finger proteins, one of which, ttkp69, is expressed in all non-neuronal CNS cells. We show that ttkp69 is downstream of gcm and can repress neuronal differentiation. Double mutant analysis and coexpression experiments indicate that glial cell differentiation may depend on a dual process, requiring the activation of glial differentiation by pointed and the concomitant repression of neuronal development by tramtrack.

scholarly journals The principal neurons of the medial nucleus of the trapezoid body and NG2+ glial cells receive coordinated excitatory synaptic input

2009 ◽  
Vol 134 (2) ◽  
pp. 115-127 ◽  
Author(s):  
Jochen Müller ◽  
Daniel Reyes-Haro ◽  
Tatjyana Pivneva ◽  
Christiane Nolte ◽  
Roland Schaette ◽  
...  
Keyword(s):  
Glial Cell ◽  
Glial Cells ◽  
Synaptic Input ◽  
Medial Nucleus ◽  
Synaptic Structure ◽  
Excitatory Synaptic Input ◽  
Cell Processes ◽  
To Receive ◽  
Trapezoid Body ◽  
Axosomatic Synapse

Glial cell processes are part of the synaptic structure and sense spillover of transmitter, while some glial cells can even receive direct synaptic input. Here, we report that a defined type of glial cell in the medial nucleus of the trapezoid body (MNTB) receives excitatory glutamatergic synaptic input from the calyx of Held (CoH). This giant glutamatergic terminal forms an axosomatic synapse with a single principal neuron located in the MNTB. The NG2 glia, as postsynaptic principal neurons, establish synapse-like structures with the CoH terminal. In contrast to the principal neurons, which are known to receive excitatory as well as inhibitory inputs, the NG2 glia receive mostly, if not exclusively, α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor–mediated evoked and spontaneous synaptic input. Simultaneous recordings from neurons and NG2 glia indicate that they partially receive synchronized spontaneous input. This shows that an NG2+ glial cell and a postsynaptic neuron share presynaptic terminals.

scholarly journals Far beyond the motor neuron: the role of glial cells in amyotrophic lateral sclerosis

2016 ◽  
Vol 74 (10) ◽  
pp. 849-854
Author(s):  
Paulo Victor Sgobbi de Souza ◽  
Wladimir Bocca Vieira de Rezende Pinto ◽  
Flávio Moura Rezende Filho ◽  
Acary Souza Bulle Oliveira
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Motor Neuron ◽  
Motor Neuron Disease ◽  
Glial Cell ◽  
Glial Cells ◽  
Motor Neurons ◽  
Cell Interaction ◽  
Cell Functions ◽  
Glial Cell Interactions ◽  
Lateral Sclerosis

ABSTRACT Motor neuron disease is one of the major groups of neurodegenerative diseases, mainly represented by amyotrophic lateral sclerosis. Despite wide genetic and biochemical data regarding its pathophysiological mechanisms, motor neuron disease develops under a complex network of mechanisms not restricted to the unique functions of the alpha motor neurons but which actually involve diverse functions of glial cell interaction. This review aims to expose some of the leading roles of glial cells in the physiological mechanisms of neuron-glial cell interactions and the mechanisms related to motor neuron survival linked to glial cell functions.

scholarly journals Glial Purinergic Signaling in Neurodegeneration

2021 ◽  
Vol 12 ◽  
Author(s):  
Marie J. Pietrowski ◽  
Amr Ahmed Gabr ◽  
Stanislav Kozlov ◽  
David Blum ◽  
Annett Halle ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Glial Cell ◽  
Glial Cells ◽  
Purinergic Signaling ◽  
Expression Patterns ◽  
Specific Expression ◽  
Cell Functions ◽  
Signaling Components ◽  
Therapeutical Options

Purinergic signaling regulates neuronal and glial cell functions in the healthy CNS. In neurodegenerative diseases, purinergic signaling becomes dysregulated and can affect disease-associated phenotypes of glial cells. In this review, we discuss how cell-specific expression patterns of purinergic signaling components change in neurodegeneration and how dysregulated glial purinergic signaling and crosstalk may contribute to disease pathophysiology, thus bearing promising potential for the development of new therapeutical options for neurodegenerative diseases.

scholarly journals Sufu regulation of Hedgehog signaling in P19 cells is required for proper glial cell differentiation

2021 ◽  
Author(s):  
Danielle M. Spice ◽  
Joshua Dierolf ◽  
Gregory M. Kelly
Keyword(s):  
Retinoic Acid ◽  
Cell Differentiation ◽  
Glial Cell ◽  
Neural Differentiation ◽  
Hedgehog Signaling ◽  
Target Genes ◽  
Cell Model ◽  
Ectopic Expression ◽  
Negative Regulator ◽  
Embryonal Carcinoma Cell

AbstractHedgehog signaling is essential for vertebrate development, however, less is known about the negative regulators that influence this pathway during the differentiation of cell fates. Using the mouse P19 embryonal carcinoma cell model, Suppressor of Fused (SUFU), a negative regulator of the Hedgehog pathway, was investigated during retinoic acid-induced neural differentiation. We found Hedgehog signaling was activated in the early phase of neural differentiation and became inactive during terminal differentiation of neurons and astrocytes. SUFU, which regulates signaling at the level of GLI, remained relatively unchanged during the differentiation process, however SUFU loss through CRISPIR-Cas9 gene editing resulted in decreased cell proliferation and ectopic expression of Hedgehog target genes. Interestingly, SUFU-deficient cells were unable to differentiate in the absence of retinoic acid, but when differentiated in its presence they showed delayed and decreased astrocyte differentiation; neuron differentiation did not appear to be affected. Retinoic acid-induced differentiation also caused ectopic activation of Hh target genes in SUFU-deficient cells and while the absence of the GLI3 transcriptional inhibitor suggested the pathway was active, no full-length GLI3 was detected even though the message encoding Gli3 was present. Thus, the study would indicate the proper timing and proportion of glial cell differentiation requires SUFU, and its normal regulation of GLI3 to maintain Hh signaling in an inactive state.

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.

Sheaths of the Motor Axons of the Crab Carcinus

1964 ◽  
Vol s3-105 (70) ◽  
pp. 175-181
Author(s):  
G. A. HORRIDGE ◽  
R. A. CHAPMAN
Keyword(s):  
Cell Membrane ◽  
Glial Cell ◽  
Cross Section ◽  
Glial Cells ◽  
Fibrous Material ◽  
Motor Axons ◽  
Cell Cytoplasm ◽  
Fibrous Sheath ◽  
Outer Sheath ◽  
Sheath Structure

In crab leg nerves, the largest axons, which are the motor axons usually isolated for physiological experiments, have a sheath structure which is different from that in medium sized and smaller axons of the same nerve or of any other described nerves. Axons with a diameter over 20 µ have (a) an outer sheath, about 5µ thick, of wellspaced layers of alternating glial cell cytoplasm and extracellular fibrous material, formed from fewer cells than there are layers, and (b) an inner sheath of elongated cells which creep along the axon longitudinally and interdigitate where they meet, as seen 2 or 3 times round the outside of the membranes of axons in cross-section. Therefore, possible channels between inner glial cells are elongated and few. On these structural grounds, together with physiological evidence, they seem unlikely to be preferred pathways of diffusion of ions in crab axons. Smaller axons have simple sheaths; some occur in groups within a fibrous sheath; the thinnest axons frequently occur in bundles and have no glial cell membrane in contact with them.

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