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MRNA-Seq and microRNA-Seq whole-transcriptome analysis of rhesus monkey ESC neural differentiation revealed the potential rosette neural stem cell regulators

ABSTRACT: Rosette neural stem cells (R-NSCs) represent early stage of neural development and possess full neural differentiation and regionalization capacities. R-NSCs are considered as stem cells of neural lineage and have important implications in study of neurogenesis and cell replacement therapy. However, the molecules regulating their functional properties remain largely unknown. Rhesus monkey is ideal model to study human neural degenerative diseases and plays intermediate translational roles as therapeutic strategies evolve from rodent systems to human clinical applications. In this study, we derived R-NSCs from rhesus monkey embryonic stem cells (rESCs) and systematically investigated the unique expressions of mRNAs, microRNAs, and signaling pathways by genome-wide comparison of the mRNA and microRNA profilings of ESCs, R-NSCs at early (R-NSCP1) and late passages (R-NSCP6) and neural progenitor cells (NPCs). Apart from the R-NSCP1 specific protein-coding genes and microRNAs, we identified several pathways including Hedgehog and Wnt highly activated in R-NSCP1. The possible regulatory interactions among the microRNAs, protein-coding genes and signaling pathways were proposed. Besides, many genes with alternative splicing switch were identified at R-NSCP1. These data provided valuable resource to understand the regulation of early neurogenesis and to better manipulate the R-NSCs for cell replacement therapy.

ORGANISM(S): Macaca mulatta

PROVIDER: GSE53260 | GEO | 2014/07/03

SECONDARY ACCESSION(S): PRJNA231461

REPOSITORIES: GEO

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mRNA-Seq and microRNA-Seq whole-transcriptome analysis of rhesus monkey ESC neural differentiation revealed the potential rosette neural stem cell regulators

Project description:Rosette neural stem cells (R-NSCs) represent early stage of neural development and possess full neural differentiation and regionalization capacities. R-NSCs are considered as stem cells of neural lineage and have important implications in study of neurogenesis and cell replacement therapy. However, the molecules regulating their functional properties remain largely unknown. Rhesus monkey is ideal model to study human neural degenerative diseases and plays intermediate translational roles as therapeutic strategies evolve from rodent systems to human clinical applications. In this study, we derived R-NSCs from rhesus monkey embryonic stem cells (rESCs) and systematically investigated the unique expressions of mRNAs, microRNAs, and signaling pathways by genome-wide comparison of the mRNA and microRNA profilings of ESCs, R-NSCs at early (R-NSCP1) and late passages (R-NSCP6) and neural progenitor cells (NPCs). Apart from the R-NSCP1 specific protein-coding genes and microRNAs, we identified several pathways including Hedgehog and Wnt highly activated in R-NSCP1. The possible regulatory interactions among the microRNAs, protein-coding genes and signaling pathways were proposed. Besides, many genes with alternative splicing switch were identified at R-NSCP1. These data provided valuable resource to understand the regulation of early neurogenesis and to better manipulate the R-NSCs for cell replacement therapy. mRNA and miRNA profiles for four stages in rhesus embryonic stem cell neural differentiation, eight samples in all

2014-07-03 | E-GEOD-53260 | biostudies-arrayexpress

Non-coding RNAs and DNA methylation synergistically regulate neural fate determination from rhesus monkey embryonic stem cell

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RNA-binding protein quaking (Qk) promotes switching from neurogenesis to gliogenesis of neural stem cells during brain development [Dif_NSCs]

Project description:During mammalian brain development, neural stem cells (NSCs) initially produce only neurons and subsequently shift to glial production, while it is still unknown what regulates this drastic fate change. Here we discovered RNA-binding protein (RBP) of quaking (Qk) is selectively expressed in NSCs and is essential for switching from neurogenesis to gliogenesis. Using CNS-specific KO mice for Qk, we found that gliogenesis, but not neurogenesis, was specifically disrupted in Qk-/- brains. In glial differentiating condition, Qk-/- NSCs failed to enter gliogenesis but caused ectopic neurogenic gene expression. Pathway analysis of Qk-/- NSCs identified endocytosis as the regulatory functional cluster of Qk which has been shown to facilitate extra-cellular signaling receptors replacement and promote NSC differentiation. Mechanistically, Qk regulates endocytosis pathway genes through stabilizing their mRNAs via Qk binding sequences in 3’UTR. These results uncovered the cell fate determination mechanism of NSCs through mRNA regulation.

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RNA-binding protein quaking (Qk) promotes switching from neurogenesis to gliogenesis of neural stem cells during brain development [P7 cortex]

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Comprehensive proteome of the adult neural stem cell niche identifies key regulators of adult neurogenesis

Project description:Neural stem cells (NSCs) generating new neurons are restricted to few niches in the adult mammalian brain, while the remainder rather promotes gliogenesis. Here we take advantage of the spatial separation of an NSC niche (the subependymal zone) and the region to where the newly generated neurons migrate and integrate (the olfactory bulb). Using state-of-the-art mass spectrometry we present a comprehensive proteomic characterization of these niches compared to a region of the normal brain parenchyma (cerebral cortex) that is not contusive to neurogenesis and new neuron integration. We find unique compositions of regulatory ECM components in the neurogenic niche, with quiescent NSCs as a main source of their local ECM, including the multi-functional enzyme transglutaminase 2 that we identify as crucial for neurogenesis. Atomic force microscopy further corroborates indications from the proteome that neurogenic niches are significantly stiffer than the non-neurogenic parenchyma, highlighting the unique properties of these special niches.

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Palmitoylation of BMPR1a regulates neural stem cell fate

Project description:Neural stem cells (NSCs) generate neurons and glial cells throughout embryonic and postnatal brain development. The role of s-acylation, a reversible post-translational lipid modification of proteins, in regulating fate and activity of NSCs remains largely unknown. We here used an unbiased screening approach to identify proteins that are s-acylated in mouse NSCs.

2019-11-27 | PXD014355 | 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.

2024-03-01 | PXD040515 | JPOST Repository

Rack1 is Essential for Corticogenesis by Preventing P21-Dependent Senescence in Neural Stem Cells

Project description:Normal neurodevelopment relies on intricate signaling pathways that balance neural stem cell (NSC) self-renewal, maturation and survival. Disruptions lead to neurodevelopmental disorders including microcephaly. Here, we implicate the inhibition of NSC senescence as a mechanism underlying neurogenesis and corticogenesis. We report that the receptor for activated C kinase (Rack1), a family member of WD40-repeat (WDR) proteins, is highly enriched in NSCs. Deletion of Rack1 in developing cortical progenitors leads to a microcephaly phenotype. Strikingly, the absence of Rack1 decreases neurogenesis and promotes a cellular senescence phenotype in NSCs. Mechanistically, the senescence-related p21 signaling pathway is dramatically activated in Rack1-null NSCs, and removal of p21 significantly rescues the Rack1-knockout phenotype in vivo. Finally, Rack1 directly interacts with Smad3 to suppress the activation of TGF-β/Smad signaling pathway, which plays a critical role in p21-mediated senescence. Our data implicate Rack1-driven inhibition of p21-induced NSC senescence as a critical mechanism behind normal cortical development.

2021-08-09 | PXD027798 |

Epigenetic and transcriptomic profiling of neural stem cells after midazolam exposure

Project description:Here we show that early-life exposure to midazolam (MDZ), a widely used drug in pediatric anesthesia, persistently alters chromatin accessibility and expression of quiescence-associated genes in neural stem cells (NSCs) in mouse hippocampus. The alterations led to a continuous restriction of NSC proliferation toward adulthood, resulting in reduction of neurogenesis associated with the impairment of hippocampal-dependent memory functions. Moreover, we found that voluntary exercise restored hippocampal neurogenesis accompanied by the normalization of MDZ-perturbed transcriptome and ameliorated declined cognitive ability in MDZ-exposed mice.

2021-08-29 | GSE166322 | GEO

Discovery of novel imprinted genes by transcriptional analysis of parthenogenetic embryonic stem cells

Project description:Parthenogenetic embryonic stem cells (PESCs) may have future utility in cell replacement therapies. We examined genome-wide mRNA expression profiles of monkey PESCs relative to ESCs derived from fertilized embryos. Several known paternally-imprinted genes were in the highly down-regulated group in PESCs compared to ESCs. Allele specific expression analysis of paternally-imprinted genes, i.e., those genes whose expression is down-regulated in PESCs, led to the identification of one novel candidate that was exclusively expressed from a paternal allele. Our findings suggest that PESCs could be used as a model for studying genomic imprinting and in the discovery of novel imprinted genes. Keywords: gene expression The transcriptomes of rhesus monkey embryonic stem cell lines derived from IVF-produced embryos (Oregon Rhesus Macaque Embryonic Stem, ORMES-22) were compared with rhesus monkey parthenogenetic embryonic stem cell lines (heterozygous rhesus Parthenogenetic embryonic stem cell lines, rPESC-2) and homozygous rhesus Parthenogenetic embryonic stem cell lines, ORMES-9). Moreover, the transcriptomes of rPESC-2 line were also compared with ORMES-9. Finally, the adult somatic skin fibroblasts were analyzed. Three biological replicates of each cell line (A, B, C) were analyzed.

2010-07-07 | E-GEOD-17964 | biostudies-arrayexpress

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