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RNA-seq to compare wild type, db/+ and db/db islets

ABSTRACT: RNA-seq to compare wild type, db/+ and db/db islets

PROVIDER: PRJNA420351 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6329220.fastq.gz	Fastqsanger.gz
	SRR6329221.fastq.gz	Fastqsanger.gz
	SRR6329222.fastq.gz	Fastqsanger.gz
	SRR6329223.fastq.gz	Fastqsanger.gz
	SRR6329224.fastq.gz	Fastqsanger.gz

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RNA-seq to compare wild type, db/+ and db/db islets

Project description:Purpose: RNA seq analysis were to compare and contrast the gene expression profile involved in the dedifferentiation of db/db islets in type 2 diabetes Methods: Islets of wild type, db/+ and db/db were purified using perfusion from 12 week old mice and RNA were isolated. Islated RNA were used in RNA seq to understand the expression pattern Results: Using an optimized data analysis workflow, we mapped about 10 million sequence reads per sample to the mouse genome (build mm9) and identified 16,014 transcripts WT, db/+ and db/db mice islets with TopHat workflow. Hierarchical clustering of differentially expressed genes uncovered there role in type 2 diabetes. Data analysis with TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: We characterised and identified genes involved in dedifferentiation of islets.

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Project description:This program addresses the molecular basis of beta-cell failure associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in pancreatic islets of the db/db mice compared to the control db/+ mice? The db/db mice islets profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the islets of db/db mice compared to the corresponding db/+ controls.

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Diabetic db/db Mice Islets Transcriptomes

Project description:Circular RNAs constitute an extensive fraction of the mammalian transcriptome.In this study, circular RNAs dysregulated in the islets of diabetic db/db mice were identified by high-throughput RNA sequencing. More than 5000 circRNAs were detected using RNA sequencing, indicating that circular transcripts were abundant in islets. Among them, we found that circ-Tulp4 showed significant downregulation in diabetic mouse islet cells. Further experiments indicated that modulating the expression of circ-Tulp4 in β cell lines desensitized β-cells to lipotoxicity.

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Diabetic db/db Mice Islets Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Diabetic db/db Mice Islets Transcriptomes

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Study of the tRNA-derived fragment expression profile in mouse pancreatic islets of pre-diabetic obese db/db mice

Project description:In this study, we discovered cytosolic and mitochondrial fragments resulting from tRNA and mt-tRNA cleavage, which may act as new regulators of cellular and metabolic functions. We analyzed hundreds of these fragments in the pancreatic islets of db/db mice and compared them to heterozygous control db/+ mice. At 16 weeks of age, db/db mice exhibit obesity, insulin resistance, and glucose intolerance. In our analysis, we identified 3858 tRFs in the islets of db/db mice, among which 342 exhibited significant changes (≥ 2 fold; adjusted p value ≤ 0.05) compared to controls. Of these, 199 tRFs showed increased levels, while 170 tRFs showed decreased levels in the pre-diabetic mice. Notably, a striking majority (147 out of 170) of the tRFs with reduced abundance in the islets of db/db mice were derived from the cleavage of tRNAs encoded by the mitochondrial genome. Our findings reveal a significant reshaping of mitochondrial tRFs in pre-diabetic conditions, coinciding with a well-established mitochondrial metabolic defect under these conditions. Specifically, we demonstrated that a fragment (named mt-tRF-LeuTAA) resulting from the cleavage of mt-tRNA-LeuTAA, encoded by the mitochondrial genome and found to be reduced in the islets of db/db mice, acts as a key regulator of mitochondrial OXPHOS functions, mitochondrial membrane potential, the insulin secretory capacity of ß-cells, and the insulin sensitivity of myotube muscle cells.

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