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ABSTRACT: mice islet sequencing

PROVIDER: PRJNA681104 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13171706_1.fastq.gz	Fastqsanger.gz
	SRR13171706_2.fastq.gz	Fastqsanger.gz
	SRR13171707_1.fastq.gz	Fastqsanger.gz
	SRR13171707_2.fastq.gz	Fastqsanger.gz
	SRR13171708.fastq.gz	Fastqsanger.gz

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ARID1A loss in pancreas leads to islet developmental defect and metabolic disturbance ,Islet cell ChIP-Seq HDAC6 arid1a

Project description:ARID1A is a tumor suppressor gene mutated in 7-10% of pancreatic cancer patients. However, its function in pancreas development and endocrine regulation is unclear. We generated mice that lack Arid1a expression in the pancreas. Our results showed that deletion of the Arid1a gene in mice caused a reduction in islet numbers and insulin production, both of which are associated with diabetes mellitus (DM) phenotype.we performed chromatin immunoprecipitation-sequencing analysis (ChIP-seq) to study genome-wide HDAC6 occupancy in the control and Arid1a-depleted islet cells.

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Project description:To get a more complete picture of the transcriptional changes associated with Pdx1 loss in ?-cells, we conducted an mRNA microarray comparing normal islet ?-cells and a-cells to the reprogrammed cells from PKO mice. Islet beta cells are from mice which has a single copy of Pdx1 flox (Pdx1L/+) allele, but is considered normal based on normal islet morphology, gene profiling, and euglycemic status. We chose to use heterozygous mice as control to avoid the litter effect. Islet alpha cells are from normal mice. To enrich for genes directly affected by Pdx1 loss, we chose the early time-point for analysis of PKO mice (5d after TAM administration). Control mRNA profiling was performed on FACS sorted islet YFP+ ?-cells and a-cells obtained from 2 month-old glucagon-Cre; RosaYFP and RIP-CreER; Pdx1fl/+, RosaYFP mice, respectively.

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