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WRN knockout effects upon gene expression in SW48 and OVK18

ABSTRACT: WRN knockout effects upon gene expression in SW48 and OVK18

PROVIDER: PRJNA521984 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8568330.fastq.gz	Fastqsanger.gz
	SRR8568321.fastq.gz	Fastqsanger.gz
	SRR8568331.fastq.gz	Fastqsanger.gz
	SRR8568322.fastq.gz	Fastqsanger.gz
	SRR8568332.fastq.gz	Fastqsanger.gz

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WRN knockout effects upon gene expression in SW48 and OVK18

Project description:To determine gene expression changes upon CRISPR/Cas9-mediated WRN knockout in SW48 and OVK18. 72 hours after transduction of sgRNA into Cas9 expressing cells, RNA was harvested and submitted for sequencing.

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Gene expression profiling in the liver of 3-month old mice with a mutant Wrn protein treated with vitamin C compared to the liver of 3-month old untreated mice with a mutant Wrn protein.

Project description:Werner syndrome (WS) is a rare disorder characterized by the premature onset of a number of age-related diseases. The gene responsible for WS is believed to be involved in different aspects of transcription, replication, and/or DNA repair. We generated a mouse model with a deletion in the helicase domain of the murine WRN homologue that recapitulates most of the WS phenotypes including an abnormal hyaluronic acid excretion, higher reactive oxygen species (ROS) levels, increased genomic instability and cancer incidence resulting in a 10-15% decreased life span expectancy. In addition, WS patients and Wrn mutant mice show hallmarks of a metabolic syndrome including premature visceral obesity, hypertriglyceridemia, insulin-resistant diabetes type 2 and associated cardiovascular diseases. In this study, we compared the expression profile of liver tissues from 3 months old Wrn mutant mice treated with 0.4% vitamin C to untreated 3 months old Wrn mutant mice. Microarray analyses were performed on the liver tissues of 3 months old mice. Four independent biological replicates of this experiment (untreated Wrn mutant mice vs vitamin C treated Wrn mutant mice) were carried out on four replicates of each genotype.

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WRN loss accelerates abnormal adipocyte metabolism in Werner Syndrome

Project description:Metabolic dysfunction is one of the main symptoms of Werner syndrome (WS); however, the underlying mechanisms remain unclear. Here, we report that loss of WRN accelerates adipogenesis at an early stage both in vitro (stem cells) and in vivo (zebrafish). Moreover, WRN depletion causes a transient upregulation of late-stage of adipocyte-specific genes at an early stage.

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