The growing role of the Hippo-NDR kinase signalling in neuronal development and disease

2011 ◽  
Vol 150 (2) ◽  
pp. 133-141 ◽  
Author(s):  
K. Emoto
Keyword(s):  
Neuronal Development ◽  
Ndr Kinase

scholarly journals Tcf4 Is Involved in Subset Specification of Mesodiencephalic Dopaminergic Neurons

Biomedicines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 317
Author(s):  
Simone Mesman ◽  
Iris Wever ◽  
Marten P. Smidt
Keyword(s):  
Neuronal Differentiation ◽  
Dopaminergic Neurons ◽  
Neuronal Development ◽  
Neuronal Population ◽  
Minor Role ◽  
Initial Increase ◽  
E Box ◽  
A Minor ◽  
Bhlh Factor

During development, mesodiencephalic dopaminergic (mdDA) neurons form into different molecular subsets. Knowledge of which factors contribute to the specification of these subsets is currently insufficient. In this study, we examined the role of Tcf4, a member of the E-box protein family, in mdDA neuronal development and subset specification. We show that Tcf4 is expressed throughout development, but is no longer detected in adult midbrain. Deletion of Tcf4 results in an initial increase in TH-expressing neurons at E11.5, but this normalizes at later embryonic stages. However, the caudal subset marker Nxph3 and rostral subset marker Ahd2 are affected at E14.5, indicating that Tcf4 is involved in correct differentiation of mdDA neuronal subsets. At P0, expression of these markers partially recovers, whereas expression of Th transcript and TH protein appears to be affected in lateral parts of the mdDA neuronal population. The initial increase in TH-expressing cells and delay in subset specification could be due to the increase in expression of the bHLH factor Ascl1, known for its role in mdDA neuronal differentiation, upon loss of Tcf4. Taken together, our data identified a minor role for Tcf4 in mdDA neuronal development and subset specification.

scholarly journals Dissecting the role of redox signaling in neuronal development

2016 ◽  
Vol 137 (4) ◽  
pp. 506-517 ◽  
Author(s):  
Daniel A. Bórquez ◽  
Pamela J. Urrutia ◽  
Carlos Wilson ◽  
Brigitte van Zundert ◽  
Marco Tulio Núñez ◽  
...  
Keyword(s):  
Neuronal Development ◽  
Redox Signaling

scholarly journals Functions of Sleep

2021 ◽  
pp. 177-182
Author(s):  
E Miletínová ◽  
J Bušková
Keyword(s):  
Neuronal Development ◽  
Well Being ◽  
Main Function ◽  
Complex Issue ◽  
Complex Process ◽  
Scientific Papers ◽  
System Functioning ◽  
Function Of Sleep ◽  
The Individual

Sleep is essential component of life. Even though the research in this field develops constantly, there are still many aspects of this rather complex process that remains to be fully clarified. One of these aspects, reason why we actually sleep, is perhaps the most crucial. In this mini review we aim to address this question and discuss potential functions of sleep. Many recent scientific papers are currently available that covers similar topic. We tried to summarize these recent findings. There are certainly many ways how to approach this rather complex issue. Our article will specifically focus on role of sleep in neuronal development, synaptic plasticity, memory consolidation or mental health in general. Its role in immune system functioning will also be mentioned. Moreover, we will also consider more general functions of sleep, such as well-being of the organisms or securing survival of the individual. In conclusion, we will highlight possible main function of sleep.

scholarly journals The role of Purα in neuronal development, the relationship between Purα and epilepsy in the current researches

2017 ◽  
Vol 8 ◽  
pp. 01056 ◽  
Author(s):  
Shanshan Guo ◽  
Bingying Zhang ◽  
Chengmin Yuan ◽  
Ping Li ◽  
Tao Sun ◽  
...  
Keyword(s):  
Neuronal Development ◽  
The Relationship

scholarly journals The Role of Synaptic GTPase-Activating Protein in Neuronal Development and Synaptic Plasticity

2003 ◽  
Vol 23 (4) ◽  
pp. 1119-1124 ◽  
Author(s):  
Jee Hae Kim ◽  
Hey-Kyoung Lee ◽  
Kogo Takamiya ◽  
Richard L. Huganir
Keyword(s):  
Synaptic Plasticity ◽  
Neuronal Development ◽  
Gtpase Activating Protein

Neurotrophic factors, neuronal selectionism, and neuronal proliferation

1997 ◽  
Vol 20 (4) ◽  
pp. 561-562 ◽  
Author(s):  
T. Elliott ◽  
N. R. Shadbolt
Keyword(s):  
Neurotrophic Factors ◽  
Neuronal Development ◽  
Neuronal Proliferation ◽  
Synaptic Remodelling

Quartz & Sejnowski (Q&S) disregard evidence that suggests that their view of dendrites is inadequate and they ignore recent results concerning the role of neurotrophic factors in synaptic remodelling. They misrepresent neuronal selectionism and thus erect a straw-man argument. Finally, the results discussed in section 4.2 require neuronal proliferation, but this does not occur during the period of neuronal development of relevance here.

scholarly journals Aberrant Oligodendrogenesis in Down Syndrome: Shift in Gliogenesis?

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1591 ◽  
Author(s):  
Laura Reiche ◽  
Patrick Küry ◽  
Peter Göttle
Keyword(s):  
Down Syndrome ◽  
White Matter ◽  
Cell Fate ◽  
Neuronal Development ◽  
Demyelinating Diseases ◽  
Therapeutic Interventions ◽  
Cell Lineages ◽  
Cns Malformations ◽  
Current Experience

Down syndrome (DS), or trisomy 21, is the most prevalent chromosomal anomaly accounting for cognitive impairment and intellectual disability (ID). Neuropathological changes of DS brains are characterized by a reduction in the number of neurons and oligodendrocytes, accompanied by hypomyelination and astrogliosis. Recent studies mainly focused on neuronal development in DS, but underestimated the role of glial cells as pathogenic players. Aberrant or impaired differentiation within the oligodendroglial lineage and altered white matter functionality are thought to contribute to central nervous system (CNS) malformations. Given that white matter, comprised of oligodendrocytes and their myelin sheaths, is vital for higher brain function, gathering knowledge about pathways and modulators challenging oligodendrogenesis and cell lineages within DS is essential. This review article discusses to what degree DS-related effects on oligodendroglial cells have been described and presents collected evidence regarding induced cell-fate switches, thereby resulting in an enhanced generation of astrocytes. Moreover, alterations in white matter formation observed in mouse and human post-mortem brains are described. Finally, the rationale for a better understanding of pathways and modulators responsible for the glial cell imbalance as a possible source for future therapeutic interventions is given based on current experience on pro-oligodendroglial treatment approaches developed for demyelinating diseases, such as multiple sclerosis.

scholarly journals The structure and global distribution of the endoplasmic reticulum network are actively regulated by lysosomes

2020 ◽  
Vol 6 (51) ◽  
pp. eabc7209
Author(s):  
Meng Lu ◽  
Francesca W. van Tartwijk ◽  
Julie Qiaojin Lin ◽  
Wilco Nijenhuis ◽  
Pierre Parutto ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Nutritional Status ◽  
Neuronal Development ◽  
Critical Role ◽  
Causal Link ◽  
Global Distribution ◽  
Growth Defects ◽  
Cellular Environment ◽  
Axonal Extension

The endoplasmic reticulum (ER) comprises morphologically and functionally distinct domains: sheets and interconnected tubules. These domains undergo dynamic reshaping in response to changes in the cellular environment. However, the mechanisms behind this rapid remodeling are largely unknown. Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status: The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection. We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology. Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly. Dysfunction in this mechanism during axonal extension may lead to axonal growth defects. Our results demonstrate a critical role of lysosome-regulated ER dynamics and reshaping in nutrient responses and neuronal development.

scholarly journals Structural basis of tubulin tyrosination by tubulin tyrosine ligase

2013 ◽  
Vol 200 (3) ◽  
pp. 259-270 ◽  
Author(s):  
Andrea E. Prota ◽  
Maria M. Magiera ◽  
Marijn Kuijpers ◽  
Katja Bargsten ◽  
Daniel Frey ◽  
...  
Keyword(s):  
Neuronal Development ◽  
Structural Basis ◽  
Tubulin Dimer ◽  
Cellular Assays ◽  
Molecular Mechanism Of Action ◽  
Tubulin Tyrosine Ligase ◽  
Modified Forms ◽  
Tubulin Structure ◽  
Β Tubulin

Tubulin tyrosine ligase (TTL) catalyzes the post-translational retyrosination of detyrosinated α-tubulin. Despite the indispensable role of TTL in cell and organism development, its molecular mechanism of action is poorly understood. By solving crystal structures of TTL in complex with tubulin, we here demonstrate that TTL binds to the α and β subunits of tubulin and recognizes the curved conformation of the dimer. Biochemical and cellular assays revealed that specific tubulin dimer recognition controls the activity of the enzyme, and as a consequence, neuronal development. The TTL–tubulin structure further illustrates how the enzyme binds the functionally crucial C-terminal tail sequence of α-tubulin and how this interaction catalyzes the tyrosination reaction. It also reveals how TTL discriminates between α- and β-tubulin, and between different post-translationally modified forms of α-tubulin. Together, our data suggest that TTL has specifically evolved to recognize and modify tubulin, thus highlighting a fundamental role of the evolutionary conserved tubulin tyrosination cycle in regulating the microtubule cytoskeleton.

scholarly journals Role of endogenous nicotinic signaling in guiding neuronal development

2007 ◽  
Vol 74 (8) ◽  
pp. 1112-1119 ◽  
Author(s):  
Zhaoping Liu ◽  
Jingming Zhang ◽  
Darwin K. Berg
Keyword(s):  
Neuronal Development
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