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CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [CRISPR]

ABSTRACT: CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [CRISPR]

PROVIDER: PRJNA480848 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7515410.fastq.gz	Fastqsanger.gz
	SRR7515420.fastq.gz	Fastqsanger.gz
	SRR7515411.fastq.gz	Fastqsanger.gz
	SRR7515421.fastq.gz	Fastqsanger.gz
	SRR7515412.fastq.gz	Fastqsanger.gz

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CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [CRISPR]

Project description:The coordination of developmental potential and proliferation in stem and progenitor cells is essential for mammalian development and tissue homeostasis. To better understand this coordination in human neural progenitor cells (hNPCs), we performed CRISPR-Cas9 screens and identified genes that limit their expansion. These screens revealed that knockout of growth-limiting genes, including CREBBP, NF2, PTPN14, TAOK1, or TP53, caused increased hNPC expansion via skipping of a transient G0-like state, accompanied by transcriptional reprogramming of G1 subpopulations. Hallmarks of the G0-like state included expression of genes associated with quiescent neural stem cells and neural development and molecular features found in quiescent cells (e.g., hypo-phosphorylated Rb, CDK2low activity, and p27high). Further, G0-skip genes act through both distinct and convergent downstream effectors, including cell cycle, Hippo-YAP, and novel targets. The results suggest that hNPC expansion is constrained by a transient G0-like state, regulated by multiple pathways, that facilitates retention of neurodevelopmental identity.

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CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [scRNA-seq]

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CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [Bulk RNA-seq]

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CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors

Project description:CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors

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CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [scRNA-seq]

Project description:CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [scRNA-seq]

| PRJNA480847 | ENA

CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [Bulk RNA-seq]

Project description:CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [Bulk RNA-seq]

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CRISPR Cas9 screens for drug resistance in AML cell lines

Project description:Acute myeloid leukaemia (AML) continues to have a very high mortality and its treatment hasnot changed for more than 20 years.Here, we propose to apply genomic-wide screens to directly identify therapeutic vulnerabilitiesof AML using AML cells lines with pre-defined somatic mutations. Our studies will be basedon genome-wide CRISPR/CAs9 gRNA screens and will be used to identify drivers of drugresistance to standard chemotherapies.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/

2015-02-03 | E-ERAD-335 | biostudies-arrayexpress

Genome-wide CRISPR-Cas9 screens reveal loss of redundancy between PKMYT1 and WEE1 in Glioblastoma stem-like cells

Project description:To identify new therapeutic targets for Glioblastoma (GBM), we performed genome-wide CRISPR-Cas9 "knockout" (KO) screens in patient-derived GBM stem-like cells (GSCs) and human neural stem/progenitors (NSCs), non-neoplastic stem cell controls, for genes required for their in vitro growth. Surprisingly, the vast majority GSC-lethal hits were found outside of molecular networks commonly altered in GBM and GSCs (e.g., oncogenic drivers). In vitro and in vivo validation of GSC-specific targets revealed several strong hits, including the wee1-like kinase, PKMYT1/Myt1. Mechanistic studies demonstrated that PKMYT1 acts redundantly with WEE1 to inhibit Cyclin B-CDK1 activity via CDK1-Tyr15 phosphorylation and to promote timely completion of mitosis in NSCs. However, in GSCs, this redundancy is lost, likely as a result of oncogenic signaling, causing GBM-specific lethality. A whole-genome CRISPR-Cas9 knockout screens targeting over 18,000 genes using the all-in-one LV-sgRNA:Cas9 platform system were performed using a âshot gunâ approach by transducing 2 GBM patient-derived isolates and 2 human neural stem cell isolates with the pool library (2 biological replicates), and cultures were outgrown for ~3 weeks. The end time point of each screen was compared to day 0 in order to determine which sgRNAs were overrepresented or underrepresented in the population.

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2025-10-29 | GSE268588 | GEO

Genome-scale CRISPR-Cas9 knockout screens for enterovirus D68 and rhinovirus C15

Project description:H1-HeLa cells were stably transduced with lentiCas9-Blast (Addgene, Plasmid #52962) and subsequently selected using blasticidin to generate constitutively expressing Cas9 H1-HeLa cells. A single Cas9-expressing H1-HeLa clone was then transduced with lentivirus without a selection marker to stably express CDHR3 C529Y (H1-HeLa+CDHR3). A single CDHR3-expressing H1-HeLa clone was then chosen based on RT-qPCR of CHDR3 expression and RV-C15 RNA levels for mutagenesis. 300 million of the H1-HeLa cells constitutively expressing CDHR3 and Cas9 were transduced with the lentiGuide-Puro from the GeCKO v2 library at a MOI of 0.3. Cells were selected using puromycin and heterogeneous H1-HeLa knockout cell populations were subsequently pooled together. The CRISPR genetic screens were started 10 days post transduction. >1000-fold coverage of mutagenized cells (libraries A and B) was infected with either RV-C15 (MOI=1 PFU/cell) or EV-D68 Missouri (MOI=1 PFU/cell). RV-C15 infection was repeated for an additional round at 6 days post-infection. As soon as appearance of visibly viable colonies was observed, populations of virus-resistant cells were pooled and harvested. Uninfected starting populations of mutagenized cells were used as the unselected reference. Total genomic DNA from both virus-resistant and uninfected cells was respectively extracted using QIAamp DNA Mini Kit (Qiagen). The inserted guide RNA sequences were retrieved from the genomic DNA by PCR amplification. The PCR products were then purified and subjected to NextSeq platform (Illumina) next-generation sequencing.

2019-07-10 | E-MTAB-8125 | biostudies-arrayexpress

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