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A genetic screen identifies Etl4-deficiency capable of stabilizing the haploidy in embryonic stem cells

ABSTRACT: A genetic screen identifies Etl4-deficiency capable of stabilizing the haploidy in embryonic stem cells

PROVIDER: PRJNA631518 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11746574_1.fastq.gz	Fastqsanger.gz
	SRR11746574_2.fastq.gz	Fastqsanger.gz
	SRR11746575_1.fastq.gz	Fastqsanger.gz
	SRR11746575_2.fastq.gz	Fastqsanger.gz
	SRR11746576_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

A genetic screen identifies Etl4-deficiency capable of stabilizing the haploidy in embryonic stem cells

Project description:We performed a genome-wild loss-of-function screening and revealed several gene mutations could significantly reduce the rate of self-diploidization in haESCs. We further demonstrated that CRISPR/Cas9 mediated Etl4 knockout stabilizes the haploid state in different haploid cell lines. More interestingly, Etl4 deficiency could increase the mitochondrial oxidative phosphorylation (OXPHOS) capacity and decrease glycolysis in haESCs. Collectively, our study identifies Etl4 as a novel haploidy-related factor and suggests that the changes of energy metabolism is associated with self-diploidization.

2021-01-11 | GSE150215 | GEO

A Genetic Screen Identifies Etl4-Deficiency Capable of Stabilizing the Haploidy in Embryonic Stem Cells.

Project description:Mammalian haploid embryonic stem cells (haESCs) hold great promise for functional genetic studies and forward screening. However, all established haploid cells are prone to spontaneous diploidization during long-term culture, rendering application challenging. Here, we report a genome-wide loss-of-function screening that identified gene mutations that could significantly reduce the rate of self-diploidization in haESCs. We further demonstrated that CRISPR/Cas9-mediated Etl4 knockout (KO) stabilizes the haploid state in different haESC lines. More interestingly, Etl4 deficiency increases mitochondrial oxidative phosphorylation (OXPHOS) capacity and decreases glycolysis in haESCs. Mimicking this effect by regulating the energy metabolism with drugs decreased the rate of self-diploidization. Collectively, our study identified Etl4 as a novel haploidy-related factor linked to an energy metabolism transition occurring during self-diploidization of haESCs.

| S-EPMC7815943 | biostudies-literature

A genetic deficiency screen in vivo reveals rescue mechanisms of mitochondrial dysfunction

Project description:The mitochondrial network forms a central hub in cellular metabolism, adapting to a vast array of environmental and cellular signals to maintain cellular homeostasis. Derangements to this network can lead to mitochondrial diseases but are also increasingly recognised to be a contributing factor in common disorders including heart failure, neurodegeneration, cancer, or the natural ageing process. Despite its central importance, little is known how the cell responds to a mitochondrial dysfunction, contributing to our lack of affective treatment strategies. Here we performed an unbiased genetic deficiency screen in the fruit fly to identify mechanisms that can rescue a lethal mitochondrial dysfunction. After screening ~40% of the fly genome, we identified 10 genes from four distinct cellular pathways that rescued the mitochondrial dysfunction upon heterozygous deletion, resulting in viable adult flies. The data presented here includes proteomic analysis of larvae of control, mutant, and rescued lines.

2024-12-01 | PXD041418 | Pride

A Sleeping Beauty Forward Genetic Screen Identifies Genes Promoting Osteosarcoma Development and Metastasis

Project description:A Sleeping Beauty (SB) transposon forward genetic screen was performed to identify the genes that promote osteosarcoma (OS) development and metastasis. Mutagenesis induced OS in wild type mice and accelerated it on a Trp53 deficient background. Analysis of tumors demonstrated that Trp53 deficiency is correlated with genomic instability, which was virtually absent in tumors induced by SB mutagenesis alone. Metastases developed in a subset of animals and in nearly all cases were clonal related to primary tumors. Over 200 candidate genes were identified, many of which are altered in human cancers including OS. Signaling pathways enriched for candidate genes were also identified and a subset of these pathways and genes were functionally validated and represent new targets for OS treatment. Bisulphite converted DNA from the 21 diagnosis osteosarcoma patients and 3 hOB cell line replicates were hybridised to the Illumina Infinium 450K Human Methylation Beadchip.

2015-04-07 | E-GEOD-58770 | biostudies-arrayexpress

A Sleeping Beauty Forward Genetic Screen Identifies Genes Promoting Osteosarcoma Development and Metastasis

2015-04-07 | GSE58770 | GEO

An in vivo CRISPR screen identifies stepwise genetic dependencies of metastatic progression

Project description:In vivo genome-wide loss-of-function CRISPR screen identifies critical genes required for individual steps of the metastatic cascade in human CTC-derived xenografts, suggesting novel drivers and vulnerabilities of breast cancer metastasis.

2022-01-27 | GSE138813 | GEO

A functional screen identifies specific microRNAs capable of inhibiting human melanoma cell viability.

Project description:Malignant melanoma is an aggressive form of skin cancer with poor prognosis. Despite improvements in awareness and prevention of this disease, its incidence is rapidly increasing. MicroRNAs (miRNAs) are a class of small RNA molecules that regulate cellular processes by repressing messenger RNAs (mRNAs) with partially complementary target sites. Several miRNAs have already been shown to attenuate cancer phenotypes, by limiting proliferation, invasiveness, tumor angiogenesis, and stemness. Here, we employed a genome-scale lentiviral human miRNA expression library to systematically survey which miRNAs are able to decrease A375 melanoma cell viability. We highlight the strongest inhibitors of melanoma cell proliferation, including the miR-15/16, miR-141/200a and miR-96/182 families of miRNAs and miR-203. Ectopic expression of these miRNAs resulted in long-term inhibition of melanoma cell expansion, both in vitro and in vivo. We show specifically miR-16, miR-497, miR-96 and miR-182 are efficient effectors when introduced as synthetic miRNAs in several melanoma cell lines. Our study provides a comprehensive interrogation of miRNAs that interfere with melanoma cell proliferation and viability, and offers a selection of miRNAs that are especially promising candidates for application in melanoma therapy.

| S-EPMC3425484 | biostudies-literature

A Chemical Screen Identifies Compounds Capable of Selecting for Haploidy in Mammalian Cells.

Project description:The recent availability of somatic haploid cell lines has provided a unique tool for genetic studies in mammals. However, the percentage of haploid cells rapidly decreases in these cell lines, which we recently showed is due to their overgrowth by diploid cells present in the cultures. Based on this property, we have now performed a phenotypic chemical screen in human haploid HAP1 cells aiming to identify compounds that facilitate the maintenance of haploid cells. Our top hit was 10-Deacetyl-baccatin-III (DAB), a chemical precursor in the synthesis of Taxol, which selects for haploid cells in HAP1 and mouse haploid embryonic stem cultures. Interestingly, DAB also enriches for diploid cells in mixed cultures of diploid and tetraploid cells, including in the colon cancer cell line DLD-1, revealing a general strategy for selecting cells with lower ploidy in mixed populations of mammalian cells.

| S-EPMC6656781 | biostudies-literature

Genome-wide CRISPR-Cas9 screen reveals selective vulnerability of ARID1A deficiency Hepatocellular Carcinoma

Project description:Genome-wide CRISPR-Cas9 screen reveals selective vulnerability of ARID1A deficiency Hepatocellular Carcinoma

| PRJNA948439 | ENA

A chemical screen identifies PRMT5 as a therapeutic vulnerability for paclitaxel-resistant triple-negative breast cancer

Project description:Paclitaxel -resistant triple negative breast cancer (TNBC) remains one of the most challenging breast cancers to treat. Using an epigenetic chemical probe screen, we uncover an acquired vulnerability of paclitaxel-resistant TNBC cells to protein arginine methyltransferases (PRMTs) inhibition. Analysis of cell lines and in-house clinical samples demonstrates that resistant cells evade paclitaxel killing through stabilizing mitotic chromatin assembly. Genetic or pharmacologic inhibition of PRMT5 alters RNA splicing, particularly intron retention of Aurora kinases B (AURKB), leading to a decrease in protein expression, and finally results in selective mitosis catastrophe in paclitaxel-resistant cells. These findings are fully recapitulated in a patient derived xenograft (PDX) model generated from a paclitaxel-resistant TNBC patient, providing the rationale for targeting PRMTs in paclitaxel-resistant TNBC.

2024-06-21 | GSE264630 | GEO

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