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EZH2 KO RNA-seq in HSC-5 cells

ABSTRACT: EZH2 KO RNA-seq in HSC-5 cells

PROVIDER: PRJNA837250 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19170883.fastq.gz	Fastqsanger.gz
	SRR19170884.fastq.gz	Fastqsanger.gz
	SRR19170885.fastq.gz	Fastqsanger.gz
	SRR19170886.fastq.gz	Fastqsanger.gz
	SRR19170887.fastq.gz	Fastqsanger.gz

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EZH2 KO RNA-seq in HSC-5 cells

Project description:CRISPR was used to deplete EZH2 in HSC-5 cells. RNA-seq was then carried out to identify changes in the transcriptome following EZH2 loss in these cells. Critically, we identified TP63 to be downregulated in the EZH2-depleted cells, and also RUNX3 to be significantly upregulated.

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ATAC-seq in WT, p53-ko, Ezh2-ko primary macrophages

Project description:Assess chromatin accessibility in WT, p53-ko, Ezh2-ko primary macrophages using ATAC-seq.

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CHIP-seq in WT, p53-ko, Ezh2-ko primary macrophages

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Full proteome analysis of WT and Ezh2-KO K562 cells

Project description:Chemotherapy resistance is the main impediment in the treatment of acute myeloid leukaemia (AML). Despite rapid advances, the various mechanisms that lead to resistance development remain to be defined in detail. Here we report that loss-of-function mutations (LOF) in the histone methyltransferase EZH2 have the potential to confer resistance against the chemotherapeutic agent cytarabine. We identify seven distinct EZH2 mutations leading to loss of H3K27 trimethylation via multiple mechanisms. Analysis of matched diagnosis and relapse samples reveal a heterogenous regulation of EZH2 and a loss of EZH2 in 50% of patients. We confirm that loss of EZH2 induces resistance against cytarabine in the cell lines HEK293T and K562 as well as in a patient-derived xenograft (PDX) model. Proteomics and transcriptomics analysis reveal that resistance is conferred by upregulation of multiple direct and indirect EZH2 target genes that are involved in apoptosis evasion, augmentation of proliferation and alteration of transmembrane transporter function. Our data indicates, that loss of EZH2 results in upregulation of its target genes, providing the cell with a selective growth advantage, which mediates chemotherapy resistance.

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Project description:Polycomb-mediated gene repression plays an important role in adult stem cell maintenance. We knocked out (using the inducible AhCre-LoxP system) Polycomb genes Eed and Ezh2 in the intestine for 6 weeks, after which crypts - the small intestinal stem cell zone - were harvested and RNA sequenced. We found Wnt, Notch and cell cycle pathways to be affected in Eed knockout (KO) but not Ezh2 KO crypts. Direct targets of Eed were determined by comparing this data with ChIP-sequencing. Small intestinal crypt mRNA profiles of 6 weeks-induced 12 weeks old Eed KO, Ezh2 KO and WT mice (all triplicates) as well as 10 days-induced Eed KO and WT organoids (duplicates) were generated by RNA sequencing over two runs and using IlluminaHiseq2000 and Hiseq2500.

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Project description:CHIP-seq and ATAC-seq in WT, p53-ko, Ezh2-ko primary macrophages

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