Single cell RNA-seq analysis of pMN neural progenitors from zebrafish [Reanalysis of GSE155988 data set]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA725224 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14326880_1.fastq.gz | Fastqsanger.gz | |||
| SRR14326880_2.fastq.gz | Fastqsanger.gz | |||
| SRR14326881_1.fastq.gz | Fastqsanger.gz | |||
| SRR14326881_2.fastq.gz | Fastqsanger.gz | |||
| SRR14326882_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:The goal of this study was to identify distinct cell populations that arise from ventral spinal cord pMN progenitors. To do so, we sorted fluorescently marked pMN cells obtained from Tg(olig2:EGFP) zebrafish embryos at 24, 36 and 48 hours post fertilization and performed 10X Chromium single cell RNA-seq.
2021-04-27 | GSE173350 | GEO
Project description:The goal of this study was to identify distinct cell populations that arise from ventral spinal cord pMN progenitors. To do so, we sorted fluorescently marked pMN cells obtained from Tg(olig2:EGFP) zebrafish embryos at 24, 36 and 48 hours post fertilization and performed 10X Chromium single cell RNA-seq.
2020-08-11 | GSE155988 | GEO
Project description:Single cell RNA-seq analysis of pMN neural progenitors from zebrafish
| PRJNA656271 | ENA
Project description:Echinoderm microtubule (MT)-associated protein-like 1 (Eml1) is mutated in the HeCo mouse, which exhibits subcortical band heterotopia (SBH), a developmental malformation of the cerebral cortex. EML1 mutations are also found in human patients affected by severe ribbon-like heterotopia, associated with epilepsy and intellectual disability (1). Neural progenitors in the ventricular zone (VZ) of the developing cerebral cortex undergo precisely regulated divisions, and mitotic perturbations contribute to pathological mechanisms (2). Eml1 is expressed in the mouse VZ and ectopic progenitors are present in the mutant developing cortex, when Eml1 is absent, at early stages of development (1). Thus, Eml1 is likely to play a role in neural progenitors during cortical development. We performed cell and molecular biology assays aiming to elucidate the function of Eml1 in neural progenitors, and explored the VZ of the HeCo mutant in order to find morphological perturbations that might explain the initiation of SBH formation (3). As part of this study, we searched for Eml1 molecular partners by pull-downs from mouse cortical extracts at embryonic day E13.5 and mass spectrometry (MS) analyses in order to identify the molecular pathways in which the protein is involved (3). Eml1 is formed by an N-terminal region that contains a dimerization domain and a C-terminal region that forms a ‘tandem atypical propeller in EMLs’ (TAPE) domain. The isolated N-terminal domain strongly binds MTs, while the C-terminal domain preferentially binds tubulin, and its beta-propeller structure is thought also to mediate the interaction with other molecules (4,5). We focused for this study on the N-terminal part of the protein (amino acids 1-178). Future study will validate or elucidate new interactions by using the C-terminal domain and/or the full-length protein. The results obtained from the N terminal MS data, integrated with other experimental findings, allow us to insert Eml1 in a network of proteins that are likely to regulate the assembly and function of the mitotic spindle in neural progenitors (3). More precisely, we showed that the protein regulates MT dynamics and its loss leads to perturbations in metaphase spindle length, which in turn impact progenitor morphology and behavior (3). References 1. Kielar, M., et al. Mutations in Eml1 lead to ectopic progenitors and neuronal heterotopia in mouse and human. Nat. Neurosci. 17, 923–933 (2014). 2. Bizzotto, S., & Francis, F. Morphological and functional aspects of progenitors perturbed in cortical malformations. Front Cell Neurosci. 9, 30; 10.3389/fncel00030 (2015). 3. Bizzotto, S., et al. Eml1 loss impairs apical progenitor spindle length and soma shape in the developing cerebral cortex. 4. Richards, M. W., et al. Crystal structure of EML1 reveals the basis for Hsp90 dependence of oncogenic EML4-ALK by disruption of an atypical β-propeller domain. Proc. Natl. Acad. Sci. U.S.A. 111, 5195–5200 (2014). 5. Richards, M. W., et al. Microtubule association of EML proteins and the EML4-ALK variant 3 oncoprotein require an N-terminal trimerization domain. Biochem. J. 467, 529–536 (2015).
2017-12-19 | PXD006837 | Pride
Project description:The pMN domain is a restricted domain in the ventral spinal cords, defined by the expression of olig2 gene. The fate determination of pMN progenitors is highly temporally and spatially regulated, with motor neurons and oligodendrocyte progenitor cells (OPCs) developing sequentially. Insight into the heterogeneity and molecular programs of pMN progenitors is currently lacking. With the zebrafish model, we identified multiple states of neural progenitors using single-cell sequencing: proliferating progenitors, common progenitors for both motor neurons and OPCs, and restricted precursors for either motor neurons or OPCs. We found specific molecular programs for neural progenitor fate transition, and manipulations of representative genes in the motor neuron or OPC lineage confirmed their critical role in cell fate determination. Deciphering progenitor heterogeneity and molecular mechanisms for these transitions will elucidate the formation of complex neuron-glia networks in the central nervous system during development, and understand the basis of neurodevelopmental disorders.
2022-08-20 | GSE179096 | GEO
Project description:pmn progenitors and their offspring in spinal cords are isolated for sc-RNAseq
2022-08-20 | GSE186163 | GEO
Project description:Next Generation Sequencing Facilities Quantitative analysis of hiPSC derived neural stem cells, early neural progenitors, neural progenitors and neural progenitors after exposure to Idebenone and Bezafibrate Transcriptomes
| PRJNA686679 | ENA
Project description:The mechanisms of neural differentiation of human induced pluripotent stem cells (hiPSCs) have been widely investigated, however the genes that play key regulatory role, especially involved in mitochondrial function are still unidentified. In this report transcriptome analysis of hiPSC differentiating into neural stem cells (NSC), early neural progenitors (eNP) and neural progenitors (NP) were performed. Gene Ontology and Network Analysis was implemented considering especially mitochondrial genes at all developmental stages and upon stimulation by idebenon (IDB) and bezafibrate (BZ) at NP stage. The genes strongly up-regulated during the process of differentiation in all tested stages belong mainly to: WNT; Cadherin and Gonadotropin-releasing hormone receptor signaling pathways. The interaction network shows that the transcription factors including HOXD3, ASCL1, HES5, and ZEB1 are possible key players in this process. Mitochondrial unfolded protein response (UPRmt), ROS defense, and pyruvate metabolism were the strongest up-regulated mitochondrial processes in all analyzed stages of neural differentiation. IDB and BZ treatment at NP stage induced different set of nuclear encoded mitochondrial genes involved in respiratory electron transport chain and fatty acid metabolic process respectively. Thus PARP agonist-mediated stimulation of mitochondrial genes influence the process of neural differentiation despite of mitochondrial biogenesis, but through the specific receptor pathways.
2021-12-21 | GSE163556 | GEO
Project description:Schizophrenia is a complex and severe neuropsychiatric disorder, with a wide range of debilitating symptoms. Several aspects of its multifactorial complexity are still unknown, and some are accepted to be an early developmental deficiency with a more specifically neurodevelopmental origin. Understanding timepoints of disturbances during neural cell differentiation processes could lead to an insight into the development of the disorder. In this context, human brain organoids and neural cells differentiated from patient-derived induced pluripotent stem cells are of great interest as a model to study the developmental origins of the disease. Here we evaluated the differential expression of proteins of schizophrenia patient-derived neural progenitors, early neurons, and brain organoids. Using bottom-up shotgun proteomics with a label-free approach for quantitative analysis. Multiple dysregulated proteins were found in pathways related to synapses, in line with postmortem tissue studies of schizophrenia patients. However, organoids and immature neurons exhibit impairments in pathways never before found in patient-derived induced pluripotent stem cell studies, such as spliceosomes and amino acid metabolism. In conclusion, here we provide comprehensive, large-scale, protein-level data that may uncover underlying mechanisms of the developmental origins of schizophrenia.
2023-03-11 | PXD026593 | Pride
Project description:Decoding heterogeneity of pluripotent stem cell (PSC)-derived neural progeny is fundamental for revealing the origin of diverse progenitors, for defining their lineages, and for identifying fate determinants driving transition through distinct potencies. Here we prospectively isolated consecutively appearing PSC-derived primary progenitors based on their Notch activation state. We first isolate early neuroepithelial cells and show their broad Notch-dependent developmental and proliferative potential. Neuroepithelial cells further yield successive Notch-dependent functional primary progenitors, from early and mid neurogenic radial glia and their derived basal progenitors, to gliogenic radial glia and adult-like neural progenitors, together recapitulating hallmarks of neural stem cell (NSC) ontogeny. Gene expression profiling reveals dynamic stage specific transcriptional patterns that may link development of distinct progenitor identities through Notch activation. Our observations provide a platform for characterization and manipulation of distinct progenitor cell types amenable for developing streamlined neural lineage specification paradigms for modeling development in health and disease. Human embryonic stem cells (hESCs) H9 were differentiated into 5 distinct populations of neural precursor cells (NPCs) over a time course of 200 days. Each neural precursor populations was then sorted for HES5 expression based on a GFP-HES5 reporter. Both the HES5 positive and HES5 negative populations were then subjected to microarray profiling in singlicate, as well as the hESCs using GeneChipPrimeView Human Gene Expression Array
2015-02-18 | E-GEOD-65369 | biostudies-arrayexpress