ATAC-seq of human lymphoblastoid cells (LCL)
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ABSTRACT:
PROVIDER: PRJEB17990 | ENA |
REPOSITORIES: ENA
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Project description:We generated these data to compare two modifications of the original ATAC-seq protocol. One was the cleavage of mtDNA using CRISPR/Cas9 and 100 gRNAs targeting mtDNA. The other was the removal of detergent from the cell lysis step. There are 27 sample pairs, untreated and treated with anti-mt CRISPR/Cas9 grouped by sample pair number. Refer to Supplemental File 1 of the article describing this data set for more information on the samples.
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Project description:Impact of regulatory variation across human iPSCs and differentiated cells [ATAC-seq LCL]
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Project description:Although genome-wide association study is an important tool for linking genetic variation to common complex diseases, it remains difficult to identify the causal variants underlying susceptibility loci. Recent work demonstrated mapping chromatin accessibility across different individuals can be a powerful method for interpreting genetic variant function, existing assays to measure chromatin landscapes (e.g., DNaseI-seq) are labor intensive and require very large numbers of cells preventing their application in real-world settings. This project aims to assess the ability of a novel assay for chromatin accessibility, ATAC-seq, to detect chromatin structure variation among individuals. We will apply ATAC-seq in 24 GBR HapMap lymphoblastoid cell lines (LCLs), which are a model system for studying the function of human genetic variation. We will also employ a novel approach to molecular quantitative trait locus identification which utilizes both population quantitative trait locus and allele-specific signatures, and gives increased mapping power in small sample sizes.This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
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Project description:Genome wide DNA methylation profiling of control and neurodevelopmental disorder lymphoblastoid cell lines (LCL). The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in LCLs. Samples included 19 control, 18 Rett syndrome, 17 autism and 6 generalized epilepsy LCL samples. Six technical replicates were also included in the analysis.
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Project description:ATAC-seq in 24 GBR lymphoblastoid cell lines
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Project description:Glycosylation of proteins is an important post-translational modification that comprises two major stages: synthesis and attachment of glycans in the endoplasmic reticulum (ER), and glycan remodeling in the ER and Golgi apparatus (GA). Genetic disorders impairing a step of this process give rise to a group of pathologies named congenital disorders of glycosylation (CDG). The most common CDG type is PMM2-CDG, caused by mutations on PMM2 (phosphomannomutase 2) genes. PMM2-CDG clinical presentation vary among affected individuals. CDG condition is considered a form of chronic ER stress. Inhibition of glycosylation results in the accumulation of misfolded proteins in the ER, which induces a complex protective reaction known as the unfolded protein response (UPR), which includes translational repression, transcriptional activation of ER chaperones, and ER-associated degradation of unfolded proteins. In search for CDG biomarkers, EBV-transformed CDG B-lymphoblastoid cell lines (B-LCL) were used as cellular models due to two main advantages: first, B-LCL are secretory cells that are forced to continuously synthetize proteins such as immunoglobulins, cytokines or other cell to cell communication molecules, so their ER is chronically stressed; second, as immune system cells, they express common genes and share common regulatory mechanisms with nervous system cells such as neurons (affected cell in most CDG patients). In this work we generated a collection of 7 EBV-transformed PMM2-CDG B-LCL by culture of patients' purified blood B lymphocytes with supernatants of the marmoset EBV-leukocyte cell line B95-8, and compared their transcriptome with that of 7 EBV-transformed healthy B-LCL. Our analysis revealed 348 significantly up-regulated and 106 down-regulated protein-coding genes compared to non-CDG cell lines, which included response to stress, transcription factors, glycosylation, motility and cell junction, development and cell (neuron) differentiation and synapse genes. Gene Set Enrichment Analysis (GSEA) identified biological consequences associated to gene expression changes in PMM2-CDG cells related to the unfolded protein response (UPR), RNA metabolism and the endoplasmic reticulum, Golgi apparatus and mitochondria components. Dysregulated important genes were MAN1A1, MGAT2, CHST4, LARGE, ADAM23, SEMA4D, UNC13C, AUTS2, CA2, SMN1, EXOSC2 expressed not only in the immune system but in other tissues including the nervous system that were compatible with CDG pathophysiology. Our results confirm PMM2-CDG EBV-transformed B-LCL as a suitable cell model that expands both our knowledge and tools to study CDG pathology at the cellular level, useful for functional characteristics and potential therapeutic drugs testing.
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