Glial cell fate specification modulated by the bHLH gene Hes5 in mouse retina

Development ◽  
2000 ◽  
Vol 127 (12) ◽  
pp. 2515-2522 ◽  
Author(s):  
M. Hojo ◽  
T. Ohtsuka ◽  
N. Hashimoto ◽  
G. Gradwohl ◽  
F. Guillemot ◽  
...  
Keyword(s):  
Glial Cell ◽  
Cell Fate ◽  
Glial Cells ◽  
Expression Patterns ◽  
Cell Number ◽  
Current Data ◽  
Mouse Retina ◽  
Cell Fate Specification ◽  
Bhlh Gene ◽  
Fate Specification

Neurons and glial cells differentiate from common precursors. Whereas the gene glial cells missing (gcm) determines the glial fate in Drosophila, current data about the expression patterns suggest that, in mammals, gcm homologues are unlikely to regulate gliogenesis. Here, we found that, in mouse retina, the bHLH gene Hes5 was specifically expressed by differentiating Muller glial cells and that misexpression of Hes5 with recombinant retrovirus significantly increased the population of glial cells at the expense of neurons. Conversely, Hes5-deficient retina showed 30–40% decrease of Muller glial cell number without affecting cell survival. These results indicate that Hes5 modulates glial cell fate specification in mouse retina.

A glial cell arises from an additional division within the mechanosensory lineage during development of the microchaete on the Drosophila notum

Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4617-4622 ◽  
Author(s):  
G.V. Reddy ◽  
V. Rodrigues
Keyword(s):  
Glial Cell ◽  
Cell Fate ◽  
Cell Lineage ◽  
The Other ◽  
Sensory Cells ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
Low Levels ◽  
Proposed Modification ◽  
Glial Marker

We have used different cell markers to trace the development of the sensory cells of the thoracic microchaete. Our results dictate a revision in the currently accepted model for cell lineage within the mechanosensory bristle. The sensory organ progenitor divides to form two secondary progenitors: PIIa and PIIb. PIIb divides first to give rise to a tertiary progenitor-PIII and a glial cell. This is followed by division of PIIa to form the shaft and socket cells as described before. PIII expresses high levels of Elav and low levels of Prospero and divides to produce neuron and sheath. Its sibling cell expresses low Elav and high Prospero and is recognized by the glial marker, Repo. This cell migrates away from the other cells of the lineage following differentiation. The proposed modification in lineage has important implications for previous studies on sibling cell fate choice and cell fate specification in sensory systems.

scholarly journals Hes5.9 Coordinate FGF and Notch Signaling to Modulate Gastrulation via Regulating Cell Fate Specification and Cell Migration in Xenopus tropicalis

Genes ◽  
2020 ◽  
Vol 11 (11) ◽  
pp. 1363
Author(s):  
Xiao Huang ◽  
Liyue Zhang ◽  
Shanshan Yang ◽  
Yongpu Zhang ◽  
Mingjiang Wu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Notch Signaling ◽  
Signaling Pathways ◽  
Cell Fate ◽  
Expression Patterns ◽  
Marker Genes ◽  
Cell Fate Specification ◽  
Mesodermal Cell ◽  
Cell Fate Decisions ◽  
Fate Specification

Gastrulation drives the establishment of three germ layers and embryonic axes during frog embryonic development. Mesodermal cell fate specification and morphogenetic movements are vital factors coordinating gastrulation, which are regulated by numerous signaling pathways, such as the Wnt (Wingless/Integrated), Notch, and FGF (Fibroblast growth factor) pathways. However, the coordination of the Notch and FGF signaling pathways during gastrulation remains unclear. We identified a novel helix–loop–helix DNA binding domain gene (Hes5.9), which was regulated by the FGF and Notch signaling pathways during gastrulation. Furthermore, gain- and loss-of-function of Hes5.9 led to defective cell migration and disturbed the expression patterns of mesodermal and endodermal marker genes, thus interfering with gastrulation. Collectively, these results suggest that Hes5.9 plays a crucial role in cell fate decisions and cell migration during gastrulation, which is modulated by the FGF and Notch signaling pathways.

Sox proteins: regulators of cell fate specification and differentiation

Development ◽  
2013 ◽  
Vol 140 (20) ◽  
pp. 4129-4144 ◽  
Author(s):  
Y. Kamachi ◽  
H. Kondoh
Keyword(s):  
Cell Fate ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
Sox Proteins

scholarly journals Differential requirement for Gli2 and Gli3 in ventral neural cell fate specification

2003 ◽  
Vol 259 (1) ◽  
pp. 150-161 ◽  
Author(s):  
Jun Motoyama ◽  
Ljiljana Milenkovic ◽  
Mizuho Iwama ◽  
Yayoi Shikata ◽  
Matthew P. Scott ◽  
...  
Keyword(s):  
Cell Fate ◽  
Neural Cell ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
Neural Cell Fate

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.

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