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Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors

ABSTRACT: Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors

PROVIDER: PRJNA353643 | ENA |

REPOSITORIES: ENA

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Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors

Project description:This SuperSeries is composed of the SubSeries listed below.

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Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors [genotype]

Project description:We have generated human induced Pluripotent Stem cells (hiPSc) using Sendai virus-mediated delivery of reprogramming factors. hiPSc lines have been screened using SNP array to assess chromosomal stability (alongside the fibroblast lines from which they derived), and validation of the pluripotency of the hiPSc lines is provided by Pluritest assessment of transcriptome datasets, prior to differentiation and downstream assays. Excess α-synuclein compromises phagocytosis in iPSC-derived macrophages.

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Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors [gene expression]

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Brain transcriptomic analysis in Parkinson's disease patients stratified by Braak Lewy body stage / Sex differences in Parkinson's disease brain transcriptome

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Project description:Genome-wide association studies (GWAS) have uncovered thousands of single nucleotide polymorphisms (SNPs) that are associated with Parkinson's disease (PD) risk. The functions of most of these SNPs, including the cell type they influence, and how they affect PD etiology remain largely unknown. To identify functional SNPs, we aligned PD risk SNPs within active regulatory regions of DNA in microglia, a cell type implicated in PD development. Out of 6,749 ‘SNPs of interest’ from the most recent PD GWAS metanalysis, 73 were located in open regulatory chromatin as determined by both ATAC-seq and H3K27ac ChIP-seq. We identified an active enhancer in microglia in intron two of SNCA that overlaps two PD risk SNPs, rs2737004 and rs2619356. In iPSC-derived microglia, CRISPR/Cas9 deletion of the open chromatin encompassing these SNPs caused reduced expression of multiple genes including SNCA and the adjacent gene MMRN1. Loss of the enhancer also led to upregulation of genes involved in glucose metabolism, a process that is known to be altered in PD patients. Our work expands the role of SNCA in Parkinson’s Disease and provides a connection between PD-associated genetic variants and underlying biology that points to a risk mechanism in microglia.

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Parkinson's Disease Risk Enhancers in Microglia [ATAC-seq]

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Transcriptome datasets of neural progenitors and neurons differentiated from induced pluripotent stem cells of healthy donors and Parkinson's disease patients with mutations in PARK2 gene

Project description:Parkinson's disease (PD) is a complex systemic disease caused by neurodegenerative processes in the brain, in which the death of dopaminergic neurons (DN) of the substantia nigra is primarily noted. 50% of cases of familial PD are associated with mutations in the PARK2 gene. Induced pluripotent stem cells (iPSCs) and their neuronal derivatives are powerful tool for disease modeling. Here, we presented the transcriptome profiles for neural progenitors (NP) and neurons, presumably DN, differentiated from iPSC lines of healthy donors and PARK2 mutations-associated PD patients generated on an NextSeq 500 System (Illumina). A comparative transcriptome analysis of neuronal derivatives of healthy donors and patients with PD will allow determining the contribution of mutations of the PARK2 gene to PD pathogenesis upon neuronal differentiation.

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