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Genes regulated by Mina53 in Mina53-KO NSPCs compared with wild-type NSPCs.

ABSTRACT: In order to investigate the role of Mina53 in the NSPC proliferation and differentiation, we performed RNA-seq using Mina53-KO NSPCs and wild-type NSPCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE275270 | GEO | 2024/11/14

REPOSITORIES: GEO

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Genes enriched with H4R3me2a modification in Mina53-KO NSPCs compared with wild-type NSPCs.

Project description:In order to investigate the role of Mina53 in the NSPC proliferation and differentiation, we performed CUT-TAG using anti-H4R3me2a antibody in Mina53-KO NSPCs and wild-type NSPCs.

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Genes regulated by Mina53 in Mina53-KO NSPCs compared with wild-type NSPCs.

Project description:Genes regulated by Mina53 in Mina53-KO NSPCs compared with wild-type NSPCs.

| PRJNA1150155 | ENA

Genes enriched with H4R3me2a modification in Mina53-KO NSPCs compared with wild-type NSPCs.

Project description:Genes enriched with H4R3me2a modification in Mina53-KO NSPCs compared with wild-type NSPCs.

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miR-153 overexpressing NSPCs derived from mouse ES cells

Project description:Mammalian neural stem/progenitor cells (NSPCs) sequentially generate neurons and glia during central nervous system (CNS) development. Several transcription factors and microRNAs (miRNAs) are involved in the temporal regulation of NSPC differentiation. miRNA-153 (miR-153) as a modulator of NSPC specification. Overexpression (OE) of miR-153 delayed the onset of astrogliogenesis and maintained NSPCs in an undifferentiated state in vitro. miR-153-OE and control NSPCs (tertiary neurospheres (TNs) derived from mouse ES Cells via embryoid body formation) subjected to the gene expression microarray analysis.

2015-08-01 | E-GEOD-70129 | biostudies-arrayexpress

miR-153 overexpressing NSPCs derived from mouse ES cells

2015-08-01 | GSE70129 | GEO

Metabolic control of adult neural stem cell self-renewal by the mitochondrial protease YME1L

Project description:The transition between quiescence and activation in neural stem and progenitor cells (NSPCs) is coupled to reversible changes in energy metabolism with key implications for life-long NSPC self-renewal and neurogenesis. How this metabolic plasticity is ensured between NSPC activity states is unclear. We find that a state-specific rewiring of the mitochondrial proteome by the i-AAA peptidase YME1L is required to preserve NSPC self-renewal. YME1L controls the abundance of numerous mitochondrial substrates in quiescent NSPCs, and its deletion activates a differentiation program characterized by broad metabolic changes causing the irreversible shift away from a fatty acid oxidation-dependent state. Conditional Yme1l deletion in adult NSPCs in vivo results in defective self-renewal and premature differentiation, ultimately leading to NSPC pool depletion. Our results disclose an important role for YME1L in coordinating the switch between metabolic states of NSPCs and suggest that NSPC fate is regulated by compartmentalized changes in protein network dynamics.

2022-02-10 | PXD030995 | Pride

A fatty acid oxidation-dependent metabolic shift regulates adult neural stem cell quiescence

Project description:Adult hippocampal neurogenesis is important for certain forms of cognition and failing neurogenesis has been implicated in neuropsychiatric diseases. The neurogenic capacity of hippocampal neural stem/progenitor cells (NSPCs) depends on a balance between quiescent and proliferative states. However, how this balance is regulated remains poorly understood. Here we show that the rate of fatty acid oxidation (FAO) defines quiescence vs. proliferation in NSPCs. Quiescent NSPCs show high levels of carnitine palmitoyltransferase 1a (Cpt1a)-dependent FAO, which is downregulated in proliferating NSPCs. Pharmacological inhibition and conditional deletion of Cpt1a in vitro and in vivo leads to altered NSPC behavior, showing that Cpt1a-dependent FAO is required for stem cell maintenance and proper neurogenesis. Strikingly, experimental manipulation of malonyl-CoA, the metabolite that regulates levels of FAO, is sufficient to induce exit from quiescence and to enhance NSPC proliferation. Thus, the data presented here identify a shift in FAO metabolism that governs NSPC behavior and suggest an instructive role for fatty acid metabolism in regulating NSPC activity.

2019-11-15 | PXD005598 | Pride

Mina53 regulates the neural stem cell pool by acting as an arginine demethylase

Project description:To investigate the function Mina53 in the regulation of neural stem cells proliferation and differentiation, we collect neural stem cells which Mina53 has been knocked down by shRNA.

2024-05-20 | GSE242238 | GEO

Mina53 regulates the neural stem cell pool by acting as an argnine demethlysae

2024-05-20 | GSE232829 | GEO

The role of nicotinamide phosphoribosyltransferase (Nampt) in hippocampal neural stem/progenitor cells

Project description:Neural stem/progenitor cell (NSPC) proliferation and self-renewal, as well as insult-induced differentiation, decrease markedly with age, but the molecular mechanisms responsible for these declines remain unclear. Here we show that levels of NAD+ and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in mammalian NAD+ biosynthesis, decrease with age in the hippocampus. Ablation of Nampt in adult NSPCs reduced their pool and proliferation in vivo. The decrease in the NSPC pool during aging can be rescued by enhancing hippocampal NAD+ levels. Nampt is the main source of NSPC NAD+ levels and required for G1/S progression of the NSPC cell cycle. Nampt is also critical for oligodendrocytic lineage fate decisions through a mechanism mediated redundantly by Sirt1 and Sirt2. Ablation of Nampt in the adult NSPCs in vivo reduced NSPC-mediated oligodendrogenesis upon injury. These phenotypes recapitulate defects in NSPCs during aging, implicating Nampt-mediated NAD+ biosynthesis as a mediator of these age-associated functional declines. Total RNA obtained from neurospheres derived from postnatal hippocampi subjected to 48 hours in vitro of incubation with Nampt-specific inhibitor FK866 (10 nM, 4 samples) or vehicle (DMSO, 1:1000, 4 samples).

2014-05-08 | E-GEOD-49784 | biostudies-arrayexpress

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