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Transcriptional profiling for CRISPR activation of a myeloma-preferential dependency

ABSTRACT: Transcriptional profiling for CRISPR activation of a myeloma-preferential dependency

PROVIDER: PRJNA777245 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16695367.fastq.gz	Fastqsanger.gz
	SRR16695368.fastq.gz	Fastqsanger.gz
	SRR16695369.fastq.gz	Fastqsanger.gz
	SRR16695370.fastq.gz	Fastqsanger.gz
	SRR16695371.fastq.gz	Fastqsanger.gz

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Transcriptional profiling for CRISPR activation of a myeloma-preferential dependency

Project description:Clinical progress in multiple myeloma (MM), an incurable plasma cell (PC) neoplasia, has been driven by therapies which have limited applications beyond MM/PC neoplasias and do not target specific oncogenic mutations in MM. Instead, these agents target pathways critical for PC biology yet largely dispensable for malignant or normal cells of most other lineages. We systematically characterized the lineage-preferential molecular dependencies of MM through genome-scale CRISPR gene editing studies in MM vs. hundreds of non-MM lines. This identified a collection of genes whose disruption has more pronounced or recurrent impact on the MM cell fitness compared to other malignancies. These genes, some known, others not previously linked to MM, encode transcription factors, chromatin modifiers, endoplasmic reticulum components, metabolic regulators or signaling molecules. The current dataset describes the transcriptional profiling of a MM cell line with CRISPR activation for the myeloma-preferential dependency, POU2AF1. The transcriptional profile of CRISPR activation of an additional gene (PANK1), which does not serve as a MM-preferential dependency in CRISPR gene editing studies, is also described.

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MYC dependency in GLS1 and NAMPT is a therapeutic vulnerability in multiple myeloma

Project description:MYC dependency in GLS1 and NAMPT is a therapeutic vulnerability in multiple myeloma

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Multiplexed activation of endogenous genes by CRISPR-on, an RNA-guided transcriptional activator system

Project description:Technologies allowing for specific regulation of endogenous genes are valuable for the study of gene functions and have great potential in therapeutics. We created the CRISPR-on system, a two-component transcriptional activator consisting of a nuclease-dead Cas9 (dCas9) protein fused with a transcriptional activation domain and single guide RNAs (sgRNAs) with complementary sequence to gene promoters. We demonstrate that CRISPR-on can efficiently activate exogenous reporter genes in both human and mouse cells in a tunable manner. In addition, we show that robust reporter gene activation in vivo can be achieved by injecting the system components into mouse zygotes. Furthermore we show that CRISPR-on can activate the endogenous IL1RN, SOX2, and OCT4 genes. The most efficient gene activation was achieved by clusters of 3 to 4 sgRNAs binding to the proximal promoters suggesting their synergistic action in gene induction. Significantly, when sgRNAs targeting multiple genes were simultaneously introduced into cells, robust multiplexed endogenous gene activation was achieved. Genome-wide expression profiling demonstrated high specificity of the system. We used microarray to assay the gene expression changes after transfection of dCas9VP160 with the different sgRNAs

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