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Prosaposin promotes neural stem cell quiescence

ABSTRACT: Prosaposin promotes neural stem cell quiescence

PROVIDER: PRJNA999741 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25453700.fastq.gz	Fastqsanger.gz
	SRR25453701.fastq.gz	Fastqsanger.gz
	SRR25453755.fastq.gz	Fastqsanger.gz
	SRR25453756.fastq.gz	Fastqsanger.gz
	SRR25453757.fastq.gz	Fastqsanger.gz

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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

A lysine demethylase-independent function of Phf2 regulates cohesin-mediated DNA replication for neural stem cell activation

Project description:The activation of quiescent neural stem cells (qNSCs) in the dentate gyrus is required for lifelong neurogenesis. However, the mechanisms that promote the exit of neural stem cells (NSCs) from quiescence remain elusive. We demonstrate that the expression of plant homeodomain finger protein 2 (Phf2) activates the exit of postnatal mouse NSC from shallow quiescence. Loss of Phf2 prevents NSC activation and neurogenesis in postnatal 30 (P30) mice but does not decrease the label-retaining NSC pool, indicating that Phf2 is not required for the exit of NSC from quiescence. NSC-specific deletion of Phf2 modestly compromises embryonic mouse NSC proliferation without increasing apoptosis, indicating that Phf2 is crucial for embryonic development. Moreover, human cortical organoids reveal that Phf2 promotes NPC proliferation via a lysine demethylase-independent manner. Mechanistically, Phf2 directly binds to the cohesion complex via Rad21 and regulates the DNA replication in mouse NSC by associating with the cohesion complex releasing protein Wapl activity. Our study identifies the Phf2-cohesin complex mediated DNA replication for neural stem cell activation in a lysine demethylase-independent manner.

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Intracrine Vascular Endothelial Growth Factor Maintains Hippocampal Neural Stem Cell Quiescence

Project description:Intracrine Vascular Endothelial Growth Factor Maintains Hippocampal Neural Stem Cell Quiescence

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Id4 maintains quiescence of adult hippocampal stem cells

Project description:Quiescence is essential for the long term maintenance of adult stem cells and tissue homeostasis. However, how stem cells maintain quiescence is still poorly understood. Here we show that stem cells in the dentate gyrus of the adult hippocampus actively transcribe the proactivation factor Ascl1 regardless of their activation state. We found that the inhibitor of DNA binding protein Id4 suppresses Ascl1 activity in neural stem cell cultures. Id4 sequesters Ascl1 heterodimerisation partner, promoting the degradation of Ascl1 protein and neural stem cell quiescence. Accordingly, elimination of Id4 from stem cells in the adult hippocampus results in abnormal accumulation of Ascl1 protein and premature stem cell activation. We also found that multiple signalling pathways converge on the regulation of Id4 to control the activity of hippocampal stem cells. Id4 therefore maintains quiescence of adult neural stem cells, in sharp contrast with its role of promoting the proliferation of embryonic neural progenitors.

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Epigenetic maintenance of neural stem cell quiescence in the adult mouse hippocampus via Setd1a

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Human fetal neural stem cell extracellular vesicle proteome

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Histone lysine methyltransferase Pr-set7/SETD8 promotes neural stem cell reactivation

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Retinoid X receptor promotes hematopoietic stem cell fitness and quiescence and preserves hematopoietic homeostasis

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Retinoid X receptor promotes hematopoietic stem cell fitness and quiescence and preserves hematopoietic homesotasis

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LRIG1 is a gatekeeper to exit from quiescence in adult neural stem cells

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