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H3K4 Methylation in β-cells prevents transcriptional downregulation and variance associated with type 2 diabetes [ChIP-seq]

ABSTRACT: H3K4 Methylation in β-cells prevents transcriptional downregulation and variance associated with type 2 diabetes [ChIP-seq]

PROVIDER: PRJNA754033 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15424104_1.fastq.gz	Fastqsanger.gz
	SRR15424104_2.fastq.gz	Fastqsanger.gz
	SRR15424105_1.fastq.gz	Fastqsanger.gz
	SRR15424105_2.fastq.gz	Fastqsanger.gz
	SRR15424106_1.fastq.gz	Fastqsanger.gz

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H3K4 Methylation in β-cells prevents transcriptional downregulation and variance associated with type 2 diabetes.

Project description:H3K4 Methylation in β-cells prevents transcriptional downregulation and variance associated with type 2 diabetes.

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H3K4 Methylation in β-cells prevents transcriptional downregulation and variance associated with type 2 diabetes [RNA-seq]

Project description:H3K4 Methylation in β-cells prevents transcriptional downregulation and variance associated with type 2 diabetes [RNA-seq]

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H3K4 Methylation in β-cells prevents transcriptional downregulation and variance associated with type 2 diabetes [RNA-seq]

Project description:Insufficient insulin release by β-cells is the primary etiology in type 2 diabetes (T2D) and coincides with impaired expression of genes essential to β-cell function, but drivers of gene expression dysregulation are not well resolved. We find that H3K4me3 peak breadth correlates with gene expression dysregulation in T2D. Using an adult β-cell Dpy30-KO mouse model, we show that global reduction of H3K4 methylation causes downregulation of genes also downregulated in T2D. Reduction of H3K4 methylation increases transcriptional entropy and reduces insulin production and glucose-responsiveness. Depletion of H3K4 methylation causes global dilution of epigenetic complexity but does not generally reduce gene expression – instead, genes related to β-cell function and/or in particular chromatin environments are specifically affected. Our data further suggests that promoter-associated H3K4me1 is sufficient to maintain expression in the absence of H3K4me3. These data implicate dysregulation of H3K4 methylation in destabilizing gene expression and contributing to β-cell dysfunction in T2D.

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H3K4 Methylation in β-cells prevents transcriptional downregulation and variance associated with type 2 diabetes [ChIP-seq]

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H3K4 Methylation in β-cells prevents transcriptional downregulation and variance associated with type 2 diabetes.

Project description:This SuperSeries is composed of the SubSeries listed below.

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Downregulation of Human-Specific lncRNA TMEM9B-AS1 in Skeletal Muscle of People with Type 2 Diabetes Impacts Ribosomal Biogenesis

Project description:Long non-coding RNAs (lncRNAs) are important regulators of skeletal muscle physiology, with altered expression noted in several human diseases including type 2 diabetes. Here we report downregulation of TMEM9B-AS1, a previously uncharacterized lncRNA, in skeletal muscle of men with type 2 diabetes. We demonstrate that loss of TMEM9B-AS1 in primary human myotubes leads to reduction in protein synthesis, concomitant with reduced phosphorylation of ribosomal protein S6, downstream of ERK and mTOR pathways. Moreover, we show that TMEM9B-AS1 plays a pivotal role in the regulation of ribosomal biogenesis by facilitating mRNA stabilization of the transcription factor MYC through a direct physical interaction with the RNA-binding protein IGF2BP1. Disrupted ribosomal biogenesis resulting from downregulation of TMEM9B-AS1 links to the decrease in skeletal muscle mass observed in individuals with type 2 diabetes, shedding new light on the molecular mechanisms underlying this metabolic disorder.

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