MicroRNA-934 is a novel regulator orchestrating neurogenesis during early human neural development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA490191 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7815410.fastq.gz | Fastqsanger.gz | |||
| SRR7815411.fastq.gz | Fastqsanger.gz | |||
| SRR7815412.fastq.gz | Fastqsanger.gz | |||
| SRR7815413_1.fastq.gz | Fastqsanger.gz | |||
| SRR7815413_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
Similar Datasets
Project description:To identify miR-934 effects on mRNA and microRNA expression regulation.
2020-06-06 | GSE119760 | GEO
Project description:To identify microRNAs (miRNAs) with a key role in the molecular mechanisms controlling human neurogenesis, we performed deep sequencing of small and long RNA transcripts at distinct stages of directed neuronal differentiation of human embryonic and induced pluripotent stem cells.
2020-06-06 | GSE101548 | GEO
Project description:MicroRNA-934 is a novel regulator orchestrating neurogenesis during early human neural development
| PRJNA394766 | ENA
Project description:Neural stem cells residing in the hippocampal neurogenic niche sustain life-long neurogenesis in the adult brain. Adult hippocampal neurogenesis (AHN) is functionally linked to mnemonic and cognitive plasticity in humans and rodents. In Alzheimer’s disease (AD), the process of generating new neurons at the hippocampal neurogenic niche is impeded, yet the mechanisms involved are unknown. Here we identify miR-132, one of the most consistently downregulated microRNAs in AD, as a potent regulator of AHN, exerting cell-autonomous pro-neurogenic effects in the adult neural stem cells and their progeny. Using distinct AD mouse models, cultured human primary and established neural stem cells, and human patient material, we demonstrate that AHN is directly impacted by AD pathology. miR-132 replacement in adult mouse AD hippocampus restores AHN and relevant memory deficits. Our findings corroborate the significance of AHN in AD and reveal the possible therapeutic significance of targeting miR-132 in neurodegeneration.
2021-06-21 | GSE172402 | GEO
Project description:Intrinsic and extrinsic inhibition of axonal and neuronal regeneration obstruct spinal cord (SC) repair in mammals. In contrast, adult zebrafish achieve functional recovery after SC damage. While studies of innate SC regeneration have focused on axon regrowth as a primary repair mechanism, how local neurogenesis impacts functional recovery is unknown. We uncovered dynamic expression of myostatin b (mstnb) in a niche of dorsal ependymal progenitors after complete SC transection in zebrafish. Genetic loss-of-function in mstnb impaired functional recovery, although glial and axonal bridging across the lesion were unaffected. Using a series of transgenic reporter lines, we quantified the numbers of stem, progenitor, and neuronal cells in the absence of mstnb. We found neural stem cell proliferation was reduced, while newborn neurons were increased in mstnb null tissues, suggesting mstnb is a negative regulator of neurogenesis. Molecularly, neuron differentiation genes were upregulated, while the neural stem cell maintenance gene fgf1b was downregulated in mstnb mutants. Finally, we show that human FGF1 treatment rescued neuronal gene expression in mstnb mutants. These studies uncover unanticipated neurogenic functions for mstnb in adult zebrafish, and establish the importance of local neurogenesis for functional SC repair.
2022-10-20 | GSE183644 | GEO
Project description:Important hallmark of neurogenesis is activation of quiescent neural stem cells (NSC) in dentate gyrus. Precise mechanisms of NSC activation are not fully clear. In the current study we interrogate the role of homeodomain finger protein 2 (Phf2) in this process. Here we performed mouse transcriptome RNA-seq profiling of epigenetic regulator Phf2 in neural stem cells without and with knock-down in order to uncover mechanistic components/pathways affecting protein translational capacity in activated NSC.
2023-05-30 | GSE159311 | GEO
Project description:While the transcriptional network of human embryonic stem cells (hESCs) has been extensively studied, relatively little is known about how post-transcriptional modulations determine hESC function. RNA-binding proteins play central roles in RNA regulation, including translation and turnover. Here we show that the RNA-binding protein CSDE1 is highly expressed in hESCs to maintain their undifferentiated state and prevent default neural fate. Notably, loss of CSDE1 accelerates neural differentiation and potentiates neurogenesis. Conversely, ectopic expression of CSDE1 impairs neural differentiation. We find that CSDE1 post-transcriptionally modulates core components of multiple regulatory nodes of hESC identity, neuroectoderm commitment and neurogenesis. Among these key pro-neural/neuronal factors, CSDE1 binds fatty acid binding protein 7 (FABP7) and vimentin (VIM) mRNAs as well as transcripts involved in neuron projection development regulating their stability and translation. Thus, our results uncover CSDE1 as a central post-transcriptional regulator of hESC identity and neurogenesis.
2018-05-16 | PXD007270 | Pride
Project description:Neural development is tightly controlled at multiple levels to orchestrate appropriate choices of cell fate and differentiation. While more attention has been paid to the roles of neural-restricted factors, broadly-expressed factors can have compelling impacts on tissue-specific development. Here, we describe in vivo genetic analysis of Ars2, which has mostly been studied as a general RNA processing factor in yeast and cultured cells. Ars2 protein exhibits a dynamic expression pattern during neural lineage progression, and conditional knockout analyses demonstrated that Ars2 is required for proliferation of embryonic neural stem cells (NSCs). In addition, Ars2 null neural stem cells can still transition into post-mitotic neurons, but fail to undergo terminal differentiation. Ars2 is similarly required for neurogenesis in the adult brain. We next generated Ars2 ChIP-seq data to broaden evidence for a distinct role for Ars2 as a transcriptional regulator in neural development. Notably, Ars2 preferentially occupies DNA enhancers in NSCs, and broadly colocalizes with the NSC regulator SOX2, but exhibits markedly reduced association with chromatin following differentiation. Finally, we demonstrate a continuous requirement for Ars2 during adult neurogenesis, since adult-specific deletion of Ars2 compromises hippocampal neurogenesis and results in specific behavioral defects. Together, we provide evidence for Ars2 as an essential neural regulator that interacts dynamically with DNA and controls neural lineage development.
2020-01-13 | GSE134106 | GEO
Project description:The development of autonomic nerve fibres in the tumour microenvironment is a pivotal event that regulates prostate cancer initiation and dissemination, but how nerves emerge in tumours is presently unknown. Here we show that Doublecortine-expressing (DCX+) neural precursors from the central nervous system (CNS) infiltrate prostate tumours and differentiate into neo-neurons that contribute to tumour development. In human primary prostate tumours and transgenic mouse cancer tissues, the density of DCX+ neural progenitors is strongly associated with tumour aggressiveness, invasion and recurrence. We found that DCX+ neural precursors egress from the subventricular zone, a neurogenic area of the CNS, and circulate in the blood to reach the tumour where they initiate neurogenesis. Hence, the DCX+ cells in prostate tumour can differentiate into neurons ex vivo and build up a tumour-associated neural network in vivo. Selective genetic depletion of DCX+ cells in mice significantly inhibits the early phases of prostate cancer development, whereas orthotopic transplantation of DCX+ cells purified from prostate tumour or brain tissues promotes tumour growth and cancer cell dissemination. These results unveil a unique crosstalk between the CNS and the tumour that drives a process of neurogenesis necessary for prostate cancer development, and indicate a novel neural element of the tumour microenvironment as a potential target for cancer treatment.
2019-05-16 | E-MTAB-7727 | biostudies-arrayexpress
Project description:We compared hESCs with their neuronal counterpart to quantify differences in the expression of cold-shock domain containing proteins. While the transcriptional network of human embryonic stem cells (hESCs) has been extensively studied, relatively little is known about how post-transcriptional modulations determine hESC function. RNA-binding proteins play central roles in RNA regulation, including translation and turnover. Here we show that the RNA-binding protein CSDE1 is highly expressed in hESCs to maintain their undifferentiated state and prevent default neural fate. Notably, loss of CSDE1 accelerates neural differentiation and potentiates neurogenesis. Conversely, ectopic expression of CSDE1 impairs neural differentiation. We find that CSDE1 post-transcriptionally modulates core components of multiple regulatory nodes of hESC identity, neuroectoderm commitment and neurogenesis. Among these key pro-neural/neuronal factors, CSDE1 binds fatty acid binding protein 7 (FABP7) and vimentin (VIM) mRNAs as well as transcripts involved in neuron projection development regulating their stability and translation. Thus, our results uncover CSDE1 as a central post-transcriptional regulator of hESC identity and neurogenesis.
2018-05-16 | PXD007738 | Pride