scholarly journals Metabolism navigates neural cell fate in development, aging and neurodegeneration

2021 ◽  
Vol 14 (8) ◽  
Author(s):  
Larissa Traxler ◽  
Jessica Lagerwall ◽  
Sophie Eichhorner ◽  
Davide Stefanoni ◽  
Angelo D'Alessandro ◽  
...  
Keyword(s):  
Cell Fate ◽  
Neural Development ◽  
Metabolic Pathways ◽  
Neural Cell ◽  
Adult Brain ◽  
Metabolic States ◽  
Age Dependent ◽  
Phosphorylation Mechanism ◽  
And Function ◽  
Neural Cell Fate

ABSTRACT An uninterrupted energy supply is critical for the optimal functioning of all our organs, and in this regard the human brain is particularly energy dependent. The study of energy metabolic pathways is a major focus within neuroscience research, which is supported by genetic defects in the oxidative phosphorylation mechanism often contributing towards neurodevelopmental disorders and changes in glucose metabolism presenting as a hallmark feature in age-dependent neurodegenerative disorders. However, as recent studies have illuminated roles of cellular metabolism that span far beyond mere energetics, it would be valuable to first comprehend the physiological involvement of metabolic pathways in neural cell fate and function, and to subsequently reconstruct their impact on diseases of the brain. In this Review, we first discuss recent evidence that implies metabolism as a master regulator of cell identity during neural development. Additionally, we examine the cell type-dependent metabolic states present in the adult brain. As metabolic states have been studied extensively as crucial regulators of malignant transformation in cancer, we reveal how knowledge gained from the field of cancer has aided our understanding in how metabolism likewise controls neural fate determination and stability by directly wiring into the cellular epigenetic landscape. We further summarize research pertaining to the interplay between metabolic alterations and neurodevelopmental and psychiatric disorders, and expose how an improved understanding of metabolic cell fate control might assist in the development of new concepts to combat age-dependent neurodegenerative diseases, particularly Alzheimer's disease.

scholarly journals Cadherins in early neural development

2021 ◽  
Author(s):  
Karolina Punovuori ◽  
Mattias Malaguti ◽  
Sally Lowell
Keyword(s):  
Adhesion Molecules ◽  
Cell Fate ◽  
Neural Development ◽  
Ex Vivo ◽  
Directed Differentiation ◽  
Culture Dish ◽  
Cell Identity ◽  
Cell Fate Decisions ◽  
Neural Tissues ◽  
And Function

AbstractDuring early neural development, changes in signalling inform the expression of transcription factors that in turn instruct changes in cell identity. At the same time, switches in adhesion molecule expression result in cellular rearrangements that define the morphology of the emerging neural tube. It is becoming increasingly clear that these two processes influence each other; adhesion molecules do not simply operate downstream of or in parallel with changes in cell identity but rather actively feed into cell fate decisions. Why are differentiation and adhesion so tightly linked? It is now over 60 years since Conrad Waddington noted the remarkable "Constancy of the Wild Type” (Waddington in Nature 183: 1654–1655, 1959) yet we still do not fully understand the mechanisms that make development so reproducible. Conversely, we do not understand why directed differentiation of cells in a dish is sometimes unpredictable and difficult to control. It has long been suggested that cells make decisions as 'local cooperatives' rather than as individuals (Gurdon in Nature 336: 772–774, 1988; Lander in Cell 144: 955–969, 2011). Given that the cadherin family of adhesion molecules can simultaneously influence morphogenesis and signalling, it is tempting to speculate that they may help coordinate cell fate decisions between neighbouring cells in the embryo to ensure fidelity of patterning, and that the uncoupling of these processes in a culture dish might underlie some of the problems with controlling cell fate decisions ex-vivo. Here we review the expression and function of cadherins during early neural development and discuss how and why they might modulate signalling and differentiation as neural tissues are formed.

scholarly journals MicroRNA let-7d regulates the TLX/microRNA-9 cascade to control neural cell fate and neurogenesis

2013 ◽  
Vol 3 (1) ◽  
Author(s):  
Chunnian Zhao ◽  
GuoQiang Sun ◽  
Peng Ye ◽  
Shengxiu Li ◽  
Yanhong Shi
Keyword(s):  
Cell Fate ◽  
Neural Cell ◽  
Neural Cell Fate

scholarly journals Tbx6 is a determinant of cardiac and neural cell fate decisions in multipotent P19CL6 cells

2012 ◽  
Vol 84 (2) ◽  
pp. 176-184 ◽  
Author(s):  
Svetlana Gavrilov ◽  
Thomas G. Nührenberg ◽  
Anthony W. Ashton ◽  
Chang-Fu Peng ◽  
Jennifer C. Moore ◽  
...  
Keyword(s):  
Cell Fate ◽  
Neural Cell ◽  
Cell Fate Decisions ◽  
P19cl6 Cells ◽  
Neural Cell Fate

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

Dysregulation of chromatin organization in pediatric and adult brain tumors: oncoepigenomic contributions to tumorigenesis and cancer stem cell properties

Genome ◽  
2020 ◽  
pp. 1-11
Author(s):  
Seungil Paik ◽  
Francesca Maule ◽  
Marco Gallo
Keyword(s):  
Brain Tumors ◽  
Cell Fate ◽  
Three Dimensional ◽  
Genetic Alterations ◽  
Adult Brain ◽  
Post Translational Modifications ◽  
3D Genome ◽  
Differentiated Cells ◽  
Aberrant Dna Methylation ◽  
And Function

The three-dimensional (3D) organization of the genome is a crucial enabler of cell fate, identity, and function. In this review, we will focus on the emerging role of altered 3D genome organization in the etiology of disease, with a special emphasis on brain cancers. We discuss how different genetic alterations can converge to disrupt the epigenome in childhood and adult brain tumors, by causing aberrant DNA methylation and by affecting the amounts and genomic distribution of histone post-translational modifications. We also highlight examples that illustrate how epigenomic alterations have the potential to affect 3D genome architecture in brain tumors. Finally, we will propose the concept of “epigenomic erosion” to explain the transition from stem-like cells to differentiated cells in hierarchically organized brain cancers.

scholarly journals Genomic DISC1 Disruption in hiPSCs Alters Wnt Signaling and Neural Cell Fate

Cell Reports ◽  
2015 ◽  
Vol 12 (9) ◽  
pp. 1414-1429 ◽  
Author(s):  
Priya Srikanth ◽  
Karam Han ◽  
Dana G. Callahan ◽  
Eugenia Makovkina ◽  
Christina R. Muratore ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Cell Fate ◽  
Neural Cell ◽  
Neural Cell Fate

scholarly journals Epigenetic setting and reprogramming for neural cell fate determination and differentiation

2014 ◽  
Vol 369 (1652) ◽  
pp. 20130511 ◽  
Author(s):  
Takuya Imamura ◽  
Masahiro Uesaka ◽  
Kinichi Nakashima
Keyword(s):  
Cell Fate ◽  
Gene Promoter ◽  
Neural Cell ◽  
Mammalian Brain ◽  
Cell Cycle Regulators ◽  
Promoter Regions ◽  
Cell Fates ◽  
Intergenic Regions ◽  
Variable Combination ◽  
Neural Cell Fate

In the mammalian brain, epigenetic mechanisms are clearly involved in the regulation of self-renewal of neural stem cells and the derivation of their descendants, i.e. neurons, astrocytes and oligodendrocytes, according to the developmental timing and the microenvironment, the ‘niche’. Interestingly, local epigenetic changes occur, concomitantly with genome-wide level changes, at a set of gene promoter regions for either down- or upregulation of the gene. In addition, intergenic regions also sensitize the availability of epigenetic modifiers, which affects gene expression through a relatively long-range chromatinic interaction with the transcription regulatory machineries including non-coding RNA (ncRNA) such as promoter-associated ncRNA and enhancer ncRNA. We show that such an epigenetic landscape in a neural cell is statically but flexibly formed together with a variable combination of generally and locally acting nuclear molecules including master transcription factors and cell-cycle regulators. We also discuss the possibility that revealing the epigenetic regulation by the local DNA–RNA–protein assemblies would promote methodological innovations, e.g. neural cell reprogramming, engineering and transplantation, to manipulate neuronal and glial cell fates for the purpose of medical use of these cells.

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