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Pooled CRISPR screening with single-cell transcriptome read-out

ABSTRACT: Pooled CRISPR screening with single-cell transcriptome read-out

OTHER RELATED OMICS DATASETS IN: GSE92872

PROVIDER: PRJNA358686 | ENA |

REPOSITORIES: ENA

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Pooled CRISPR screening with single-cell transcriptome read-out

Project description:We combined CRISPR genome editing with single-cell RNA sequencing to assess complex phenotypes in pooled cellular screens. Our method for CRISPR droplet sequencing (CROP-seq) comprises four key components: a gRNA vector that makes individual gRNAs detectable in single-cell transcriptomes, a high-throughput assay for single-cell RNA-seq, a computational pipeline for assigning single-cell transcriptomes to gRNAs, and a bioinformatic method for analyzing and interpreting gRNA-induced transcriptional profiles. CROP-seq allowed us to link gRNA expression to the associated transcriptome responses in thousands of single cells using a straightforward and broadly applicable screening workflow. Additional information are available from the CROP-seq website http://crop-seq.computational-epigenetics.org

2017-01-18 | GSE92872 | GEO

Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation

Project description:Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation

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Optimized CRISPR-Cas12a platform for combinatorial drop-out genetic screening (RNA-seq)

Project description:Optimized CRISPR-Cas12a platform for combinatorial drop-out genetic screening (RNA-seq)

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CRISPR Screening in Glioblastoma

Project description:This is an in vitro genome-wide CRISPR/cas9 screen in human glioblastoma stem cells, screening for genes essential for survival of these cells. These cells express cas9 and have been transfected with a guide RNA library causing gene knockouts. We will analyse the sequencing data for depletion of guide RNAs. In this particular study, we will do RNA sequencing to correlate CRISPR with expression levels in specific cancer cell subpopulations. 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/

2016-03-22 | E-ERAD-448 | biostudies-arrayexpress

Pooled CRISPR screens in human intestinal organoids [CRISPR screens]

Project description:Pooled CRISPR screens in human intestinal organoids [CRISPR screens]

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Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [Amplicon-seq]

Project description:Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [Amplicon-seq]

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Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [RNA-seq]

Project description:Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [RNA-seq]

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Increasing the performance of pooled CRISPR-Cas9 drop-out screening.

Project description: Not available

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CRISPR-GEMM pooled mutagenic screening identifies KMT2D as a major modulator of immune checkpoint blockade (ATAC-Seq)

Project description:Immune checkpoint blockade (ICB) has shown remarkable clinical efficacy across multiple cancer types. However, only a fraction of patients respond to ICB. Here, we performed pooled mutagenic screening with CRISPR-mediated genetically engineered mouse models (CRISPR-GEMMs) in ICB settings, and identified KMT2D as a major modulator of ICB response across multiple cancer types. Kmt2d encodes a histone H3K4 methyltransferase and is among the most frequently mutated genes in cancer patients. Kmt2d loss led to increased DNA damage and mutation burden, chromatin remodeling, intron retention, and activation of transposable elements. Additionally, Kmt2d-deficient cells exhibit increased protein turnover and IFN-γ-stimulated antigen presentation. In turn, Kmt2d-mutant tumors in both mouse and human are characterized by increased immune infiltration. These data demonstrate that KMT2D deficiency sensitizes tumors to ICB by augmenting tumor immunogenicity, highlighting the power of CRISPR-GEMMs for interrogating complex molecular landscapes in immunotherapeutic contexts that preserve the native tumor microenvironment.

2020-11-18 | GSE151226 | GEO

CRISPR-GEMM pooled mutagenic screening identifies KMT2D as a major modulator of immune checkpoint blockade (RNA-Seq)

2020-11-18 | GSE151225 | GEO

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