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Genome-scale CRISPR screening in a single mouse liver

ABSTRACT: Genome-scale CRISPR screening in a single mouse liver

PROVIDER: PRJNA889363 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21859340.fastq.gz	Fastqsanger.gz
	SRR21859341.fastq.gz	Fastqsanger.gz
	SRR21859342.fastq.gz	Fastqsanger.gz
	SRR21859343.fastq.gz	Fastqsanger.gz
	SRR21859344.fastq.gz	Fastqsanger.gz

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Genome-scale CRISPR screening in a single mouse liver

Project description:This paper describes the development and implementation of genome-scale CRISPR screening in the mouse liver. As part of this study, RNA sequencing was performed on livers isolated from mice during development, adulthood, and regeneration to identify the entirety of genes expressed in the liver at each time point.

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In vivo Genome-scale CRISPR-Cas9 knockout screening

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Genome-scale CRISPR screening in a single mouse liver.

Project description:A complete understanding of the genetic determinants underlying mammalian physiology and disease is limited by the capacity for high-throughput genetic dissection in the living organism. Genome-wide CRISPR screening is a powerful method for uncovering the genetic regulation of cellular processes, but the need to stably deliver single guide RNAs to millions of cells has largely restricted its implementation to ex vivo systems. There thus remains a need for accessible high-throughput functional genomics in vivo. Here, we establish genome-wide screening in the liver of a single mouse and use this approach to uncover regulation of hepatocyte fitness. We uncover pathways not identified in cell culture screens, underscoring the power of genetic dissection in the organism. The approach we developed is accessible, scalable, and adaptable to diverse phenotypes and applications. We have hereby established a foundation for high-throughput functional genomics in a living mammal, enabling comprehensive investigation of physiology and disease.

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Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [CRISPR screening]

Project description:Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [CRISPR screening]

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Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage

Project description:Overall data for CRISPR 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

Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [CRISPR screening]

Project description:Aflatoxin B1 (AFB1) is amongst the mycotoxins commonly affecting human and animal health, raising global food safety and control concerns. The mechanisms underlying AFB1 toxicity are poorly understood. Moreover, antidotes against AFB1 are lacking. Genome-wide CRISPR/Cas9 knockout screening in porcine kidney cells identified the transcription factor BTB and CNC homolog 1 (BACH1) as a gene required for AFB1 toxicity. The inhibition of BACH1 expression in porcine kidney cells and human hepatoma cells resulted in increased resistance to AFB1. BACH1 depletion attenuates AFB1-induced oxidative damage via the upregulation of antioxidant genes.

2022-03-25 | GSE199384 | GEO

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Project description:RNA-seq and genome-wide CRISPR activation screening

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Genome-scale CRISPR-Cas9 knockout screening for identification of genes which regulate CD38 expression in RPMI 8226 cells

Project description:We showed that interleukin-6 (IL-6) from bone marrow stromal cells downregulated CD38 expression in multiple myeloma (MM) cells. Then we performed a genome-scale CRISPR-Cas9 knockout screening to identify key molecules mediating IL-6-induced CD38 downregulation. Although IL-6 triggered downregulation of CD38 expression on the majority of RPMI 8226 cells, a small fraction maintained relatively high CD38 expression. We therefore sorted those top 5% cells with CD38-high expression and compared these cells with non-sorted control cells. The gene rank based on p-value identified Janus kinase (JAK) 1 and signal transducer-activator of transcription (STAT) 3 as highly positively enriched genes as potential mediators of IL-6-induced CD38 downregulation. We validated STAT3 and found CD38 expression was regulated by both STAT1 (positively) and STAT3 (negatively), and that inhibition of JAK-STAT3 pathway represents a novel therapeutic option to enhance CD38 expression and anti-CD38 monoclonal antibody-mediated MM cytotoxicity.

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