Mash1 regulates neurogenesis in the ventral telencephalon

Development ◽  
1999 ◽  
Vol 126 (3) ◽  
pp. 525-534 ◽  
Author(s):  
S. Casarosa ◽  
C. Fode ◽  
F. Guillemot
Keyword(s):  
Nervous System ◽  
Notch Signaling ◽  
Subventricular Zone ◽  
Ventricular Zone ◽  
Ganglionic Eminence ◽  
Ventral Telencephalon ◽  
Neuronal Populations ◽  
Neuronal Precursors ◽  
Important Regulator ◽  
The Central Nervous System

Previous studies have shown that mice mutant for the gene Mash1 display severe neuronal losses in the olfactory epithelium and ganglia of the autonomic nervous system, demonstrating a role for Mash1 in development of neuronal lineages in the peripheral nervous system. Here, we have begun to analyse Mash1 function in the central nervous system, focusing our studies on the ventral telencephalon where it is expressed at high levels during neurogenesis. Mash1 mutant mice present a severe loss of progenitors, particularly of neuronal precursors in the subventricular zone of the medial ganglionic eminence. Discrete neuronal populations of the basal ganglia and cerebral cortex are subsequently missing. An analysis of candidate effectors of Mash1 function revealed that the Notch ligands Dll1 and Dll3, and the target of Notch signaling Hes5, fail to be expressed in Mash1 mutant ventral telencephalon. In the lateral ganglionic eminence, loss of Notch signaling activity correlates with premature expression of a number of subventricular zone markers by ventricular zone cells. Therefore, Mash1 is an important regulator of neurogenesis in the ventral telencephalon, where it is required both to specify neuronal precursors and to control the timing of their production.

A role for Gsh1 in the developing striatum and olfactory bulb of Gsh2 mutant mice

Development ◽  
2001 ◽  
Vol 128 (23) ◽  
pp. 4769-4780 ◽  
Author(s):  
Håkan Toresson ◽  
Kenneth Campbell
Keyword(s):  
Olfactory Bulb ◽  
Subventricular Zone ◽  
Ventricular Zone ◽  
Cell Number ◽  
Mutant Mice ◽  
Ganglionic Eminence ◽  
Ventral Telencephalon ◽  
Molecular Identity ◽  
Lateral Ganglionic Eminence

We have examined the role of the two closely related homeobox genes Gsh1 and Gsh2, in the development of the striatum and the olfactory bulb. These two genes are expressed in a partially overlapping pattern by ventricular zone progenitors of the ventral telencephalon. Gsh2 is expressed in both of the ganglionic eminences while Gsh1 is largely confined to the medial ganglionic eminence. Previous studies have shown that Gsh2–/– embryos suffer from an early misspecification of precursors in the lateral ganglionic eminence (LGE) leading to disruptions in striatal and olfactory bulb development. This molecular misspecification is present only in early precursor cells while at later stages the molecular identity of these cells appears to be normalized. Concomitant with this normalization, Gsh1 expression is notably expanded in the Gsh2–/– LGE. While no obvious defects in striatal or olfactory bulb development were detected in Gsh1–/– embryos, Gsh1/2 double homozygous mutants displayed more severe disruptions than were observed in the Gsh2 mutant alone. Accordingly, the molecular identity of LGE precursors in the double mutant is considerably more perturbed than in Gsh2 single mutants. These findings, therefore, demonstrate an important role for Gsh1 in the development of the striatum and olfactory bulb of Gsh2 mutant mice. In addition, our data indicate a role for Gsh genes in controlling the size of the LGE precursor pools, since decreasing copies of Gsh2 and Gsh1 alleles results in a notable decrease in precursor cell number, particularly in the subventricular zone.

scholarly journals Regulation of Notch Signaling by a Novel Mechanism Involving Suppressor of Hairless Stability and Carboxyl Terminus-Truncated Notch

2003 ◽  
Vol 23 (16) ◽  
pp. 5581-5593 ◽  
Author(s):  
Cedric S. Wesley ◽  
Lee-Peng Mok
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Drosophila Melanogaster ◽  
Notch Signaling ◽  
Full Length ◽  
Carboxyl Terminus ◽  
Animal Development ◽  
Suppressor Of Hairless ◽  
The Central Nervous System ◽  
Different Tissues

ABSTRACT Different amounts of Suppressor of Hairless (SuH)-dependent Notch (N) signaling is often used during animal development to produce two different tissues from a population of equipotent cells. During Drosophila melanogaster embryogenesis, cells with high amounts of this signaling differentiate the larval epidermis whereas cells with low amounts, or none, differentiate the central nervous system (CNS). The mechanism by which SuH-dependent N signaling is increased or decreased in these different cells is obscure. The developing epidermis is known to get enriched for the full-length N (NFull) and the developing CNS for the carboxyl terminus-truncated N (NΔCterm). Results described here indicate that this differential accumulation of N receptors is part of a mechanism that would promote SuH-dependent N signaling in the developing epidermis but suppress it in the developing CNS. This mechanism involves SuH-dependent stability of NFull, NFull-dependent accumulation of SuH, stage specific stability of SuH, and NΔCterm-dependent loss of SuH and NFull.

scholarly journals Mimicking Neural Stem Cell Niche by Biocompatible Substrates

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Citlalli Regalado-Santiago ◽  
Enrique Juárez-Aguilar ◽  
Juan David Olivares-Hernández ◽  
Elisa Tamariz
Keyword(s):  
Subventricular Zone ◽  
Current Knowledge ◽  
Ventricular Zone ◽  
Neurogenic Niche ◽  
Extracellular Matrix Components ◽  
The Central Nervous System ◽  
Cell Niche ◽  
Extracellular Environment

Neural stem cells (NSCs) participate in the maintenance, repair, and regeneration of the central nervous system. During development, the primary NSCs are distributed along the ventricular zone of the neural tube, while, in adults, NSCs are mainly restricted to the subependymal layer of the subventricular zone of the lateral ventricles and the subgranular zone of the dentate gyrus in the hippocampus. The circumscribed areas where the NSCs are located contain the secreted proteins and extracellular matrix components that conform their niche. The interplay among the niche elements and NSCs determines the balance between stemness and differentiation, quiescence, and proliferation. The understanding of niche characteristics and how they regulate NSCs activity is critical to buildingin vitromodels that include the relevant components of thein vivoniche and to developing neuroregenerative approaches that consider the extracellular environment of NSCs. This review aims to examine both the current knowledge on neurogenic niche and how it is being used to develop biocompatible substrates for thein vitroandin vivomimicking of extracellular NSCs conditions.

PCDHB14- and GABRB1-like nervous system developmental genes are altered during early neuronal differentiation of NCCIT cells treated with ethanol

2015 ◽  
Vol 34 (10) ◽  
pp. 1017-1027 ◽  
Author(s):  
D Halder ◽  
C Mandal ◽  
BH Lee ◽  
JS Lee ◽  
MR Choi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nervous System ◽  
Neuronal Differentiation ◽  
Pathway Analysis ◽  
Synapse Formation ◽  
Fetal Alcohol Spectrum Disorders ◽  
Fetal Alcohol ◽  
Neuronal Precursors ◽  
The Central Nervous System ◽  
Fetal Alcohol Spectrum

Ethanol (EtOH) exposure during embryonic development causes dysfunction of the central nervous system (CNS). Here, we examined the effects of chronic EtOH on gene expression during early stages of neuronal differentiation. Human embryonic carcinoma (NCCIT) cells were differentiated into neuronal precursors/lineages in the presence or absence of EtOH and folic acid. Gene expression profiling and pathway analysis demonstrated that EtOH deregulates many genes and pathways that are involved in early brain development. EtOH exposure downregulated several important genes, such as PCDHB14, GABRB1, CTNND2, NAV3, RALDH1, and OPN5, which are involved in CNS development, synapse assembly, synaptic transmission, and neurotransmitter receptor activity. GeneGo pathway analysis revealed that the deregulated genes mapped to disease pathways that were relevant to fetal alcohol spectrum disorders (FASD, such as neurotic disorders, epilepsy, and alcohol-related disorders). In conclusion, these findings suggest that the impairment of the neurological system or suboptimal synapse formation resulting from EtOH exposure could underlie the neurodevelopmental disorders in individuals with FASD.

scholarly journals Chromatin remodeling in oligodendrogenesis

2021 ◽  
Vol 25 (5) ◽  
pp. 573-579
Author(s):  
E. V. Antontseva ◽  
N. P. Bondar
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chromatin Remodeling ◽  
Local Density ◽  
Ventricular Zone ◽  
Electrical Signal ◽  
Structural Function ◽  
Electrical Insulator ◽  
Chromatin Remodeling Complexes ◽  
The Central Nervous System

Oligodendrocytes are one type of glial cells responsible for myelination and providing trophic support for axons in the central nervous system of vertebrates. Thanks to myelin, the speed of electrical-signal conduction increases several hundred-fold because myelin serves as a kind of electrical insulator of nerve f ibers and allows for quick saltatory conduction of action potentials through Ranvier nodes, which are devoid of myelin. Given that different parts of the central nervous system are myelinated at different stages of development and most regions contain both myelinated and unmyelinated axons, it is obvious that very precise mechanisms must exist to control the myelination of individual axons. As they go through the stages of specification and differentiation – from multipotent neuronal cells in the ventricular zone of the neural tube to mature myelinating oligodendrocytes as well as during migration along blood vessels to their destination – cells undergo dramatic changes in the pattern of gene expression. These changes require precisely spatially and temporally coordinated interactions of various transcription factors and epigenetic events that determine the regulatory landscape of chromatin. Chromatin remodeling substantially affects transcriptional activity of genes. The main component of chromatin is the nucleosome, which, in addition to the structural function, performs a regulatory one and serves as a general repressor of genes. Changes in the type, position, and local density of nucleosomes require the action of specialized ATP-dependent chromatin-remodeling complexes, which use the energy of ATP hydrolysis for their activity. Mutations in the genes encoding proteins of the remodeling complexes are often accompanied by serious disorders at early stages of embryogenesis and are frequently identified in various cancers. According to the domain arrangement of the ATP-hydrolyzing subunit, most of the identified ATP-dependent chromatin-remodeling complexes are classified into four subfamilies: SWI/SNF, CHD, INO80/SWR, and ISWI. In this review, we discuss the roles of these subunits of the different subfamilies at different stages of oligodendrogenesis.

Notch Signaling in the Central Nervous System with Special Reference to its Expression in Microglia

2013 ◽  
Vol 12 (6) ◽  
pp. 807-814 ◽  
Author(s):  
Linli Yao ◽  
Qiong Cao ◽  
Chunyun Wu ◽  
Charanjit Kaur ◽  
Aijun Hao ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Special Reference ◽  
Notch Signaling ◽  
The Central Nervous System

Developmental models of brain dysfunctions induced by targeted cellular ablations with methylazoxymethanol

1997 ◽  
Vol 77 (1) ◽  
pp. 199-215 ◽  
Author(s):  
F. Cattabeni ◽  
M. Di Luca
Keyword(s):  
Nervous System ◽  
Long Term Potentiation ◽  
Developmental Models ◽  
Neuronal Populations ◽  
Term Potentiation ◽  
Brain Malformations ◽  
Time Table ◽  
Dependent Protein ◽  
The Central Nervous System ◽  
Molecular Substrates

Abnormal brain development represents one of the major causes of neurological disorders in humans, and determining the factors responsible for generating specific brain malformations represents a formidable task for developmental neurobiology. The knowledge of the precise neurogenetic time table and the use of toxins, like methylazoxymethanol, able to interfere with neuroepithelial cells entering their last mitotic cycle, have allowed for targeted neuronal ablations in specific brain areas of the central nervous system (CNS) when administered at different gestational or postnatal days in various animal species. Of particular relevance are the studies in which ablations of neuronal populations of cortex, hippocampus, and cerebellum have been made. The results obtained show that these early ablations induce a number of neuroanatomic, neurochemical, and electrophysiological changes that give us the possibility to unravel the biochemical strategies utilized by surviving neurons to adapt to the perturbated environment. Most striking are the findings that target deprivation does not affect the survival of afferent neurons in the CNS (except for neurons of the lateral geniculate nucleus), in sharp contrast to the notion of target dependence for peripheral nervous system neurons. Animals showing selective ablations in the Ammon's horn of the hippocampus allow us to understand the complex biochemical pathways leading to changes in activity-dependent synaptic plasticity, and the data underscore the fundamental role of diverse Ca(2+)-dependent protein kinases, and their substrates, in modulating pre- and postsynaptic events during induction and maintenance of long-term potentiation (LTP). Because LTP represents a useful model to study molecular substrates of learning and memory, this animal model might be of relevance in understanding cognitive brain dysfunctions.

scholarly journals Notch signaling is a critical initiator of roof plate formation as revealed by the use of RNA profiling of the dorsal neural tube

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Shai Ofek ◽  
Sophie Wiszniak ◽  
Sarah Kagan ◽  
Markus Tondl ◽  
Quenten Schwarz ◽  
...  
Keyword(s):  
Nervous System ◽  
Notch Signaling ◽  
Neural Tube ◽  
Cell Types ◽  
Molecular Heterogeneity ◽  
Specific Cell ◽  
Rna Profiling ◽  
Dorsal Neural Tube ◽  
Roof Plate ◽  
The Central Nervous System

AbstractBackgroundThe dorsal domain of the neural tube is an excellent model to investigate the generation of complexity during embryonic development. It is a highly dynamic and multifaceted region being first transiently populated by prospective neural crest (NC) cells that sequentially emigrate to generate most of the peripheral nervous system. Subsequently, it becomes the definitive roof plate (RP) of the central nervous system. The RP, in turn, constitutes a patterning center for dorsal interneuron development. The factors underlying establishment of the definitive RP and its segregation from NC and dorsal interneurons are currently unknown.ResultsWe performed a transcriptome analysis at trunk levels of quail embryos comparing the dorsal neural tube at premigratory NC and RP stages. This unraveled molecular heterogeneity between NC and RP stages, and within the RP itself. By implementing these genes, we asked whether Notch signaling is involved in RP development. First, we observed that Notch is active at the RP-interneuron interface. Furthermore, gain and loss of Notch function in quail and mouse embryos, respectively, revealed no effect on early NC behavior. Constitutive Notch activation caused a local downregulation of RP markers with a concomitant development of dI1 interneurons, as well as an ectopic upregulation of RP markers in the interneuron domain. Reciprocally, in mice lacking Notch activity, both the RP and dI1 interneurons failed to form and this was associated with expansion of the dI2 population.ConclusionsCollectively, our results offer a new resource for defining specific cell types, and provide evidence that Notch is required to establish the definitive RP, and to determine the choice between RP and interneuron fates, but not the segregation of RP from NC.

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