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ABSTRACT: mice islet

PROVIDER: PRJNA577480 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10276357.fastq.gz	Fastqsanger.gz
	SRR10276358.fastq.gz	Fastqsanger.gz
	SRR10276359.fastq.gz	Fastqsanger.gz
	SRR10276360.fastq.gz	Fastqsanger.gz
	SRR10276361.fastq.gz	Fastqsanger.gz

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Project description:To get a more complete picture of the transcriptional changes associated with Pdx1 loss in β-cells, we conducted an mRNA microarray comparing normal islet β-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.

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Project description:We knocked out the critical autophagy enzyme, ATG7, in the β-cells of mice (ATG7Δβ-cell) then monitored blood glucose to assess the phenotype induced by this KO model. We found that all ATG7Δβ-cell mice developed diabetes between 11-15 weeks of age. We isolated islets from ATG7Δβ-cell and littermate control mice several weeks prior to diabetes development (7-10 weeks of age) and performed bulk islet proteomics. The purpose of this experiment was to understand the islet biological process pathways altered by dysfunctional β-cell autophagy in the ATG7Δβ-cell model.

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Global epigenomic analysis of primary human pancreatic islets provides insights into type 2 diabetes susceptibility loci

Project description:Identifying cis-regulatory elements is important to understand how human pancreatic islets modulate gene expression in physiologic or pathophysiologic (e.g., diabetic) conditions. We conducted genome-wide analysis of DNase I hypersensitive sites, histone H3 lysine methylation marks (K4me1, K4me3, K79me2), and CCCTC factor (CTCF) binding in human islets. This identified ~18,000 putative promoters (several hundred novel and islet-active). Surprisingly, active promoter marks were absent at genes encoding islet-specific hormones, suggesting a distinct regulatory mechanism. Of 34,039 distal (non-promoter) regulatory elements, 47% are islet-unique and 22% are CTCF-bound. These findings present a global snapshot of the human islet epigenome and should provide functional context for non-coding variants emerging from genetic studies of T2D and other pancreatic islet disorders. Three different islet samples were tested for DNase I hypersensitivity by DNase-Seq. Five different primary pancreatic islet samples were evaluated for several chromatin modifications (H3K4me3, H3K4me1, H3K79me2) by ChIP-seq. One islet sample was evaluated for CTCF binding via ChIP-seq, All ChIP-seq samples have both non-specific IP (GFP) and input DNA controls.

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