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Mitochondrial GpC and CpG DNA hypermethylation cause metabolic stress induced mitophagy and cholestophagy [RNA-seq]

ABSTRACT: Mitochondrial GpC and CpG DNA hypermethylation cause metabolic stress induced mitophagy and cholestophagy [RNA-seq]

PROVIDER: PRJNA1008586 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25743608_1.fastq.gz	Fastqsanger.gz
	SRR25743608_2.fastq.gz	Fastqsanger.gz
	SRR25743609_1.fastq.gz	Fastqsanger.gz
	SRR25743609_2.fastq.gz	Fastqsanger.gz
	SRR25743610_1.fastq.gz	Fastqsanger.gz

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Mitochondrial GpC and CpG DNA hypermethylation cause metabolic stress induced mitophagy and cholestophagy

Project description:Mitochondrial GpC and CpG DNA hypermethylation cause metabolic stress induced mitophagy and cholestophagy

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Mitochondrial GpC and CpG DNA hypermethylation cause metabolic stress induced mitophagy and cholestophagy

Project description:Metabolic dysfunction associated steatotic liver disease (MASLD) is characterized by a constant accumulation of lipids in the liver. This lipotoxicity in the liver is associated with dysregulation of the first step in lipid catabolism called beta oxidation in the mitochondrial matrix, eventually leading to mitochondrial dysfunction. To evaluate possible involvement of mitochondrial DNA methylation in this lipid metabolic dysfunction we investigated the functional metabolic effects of mitochondrial overexpression of CpG (MSssI) and GpC (MCviPI) DNA methyltransferases in relation to gene expression and (mito)epigenetic signatures. Overall, the results show that mitochondrial GpC and to a lesser extent CpG methylation increase bile acid metabolic gene expression, inducing cholestasis by mito-nuclear epigenetic reprogramming. Moreover, increased expression of metabolic nuclear receptors in both MSssI and MCviPI cells promote mitochondrial swelling and induce basal overactivation of mitochondrial respiration which favours lipid accumulation and metabolic-stress induced mitophagy and autophagy stress responses. Altogether GpC and CpG mitochondrial induce a metabolic challenging environment that is similar to mitochondrial dysfunction in the progression of MASLD.

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Mitochondrial GpC and CpG DNA hypermethylation cause metabolic stress induced mitophagy and cholestophagy [RNA-seq]

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Mitochondrial GpC and CpG DNA Hypermethylation Cause Metabolic Stress-Induced Mitophagy and Cholestophagy.

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by a constant accumulation of lipids in the liver. This hepatic lipotoxicity is associated with a dysregulation of the first step in lipid catabolism, known as beta oxidation, which occurs in the mitochondrial matrix. Eventually, this dysregulation will lead to mitochondrial dysfunction. To evaluate the possible involvement of mitochondrial DNA methylation in this lipid metabolic dysfunction, we investigated the functional metabolic effects of mitochondrial overexpression of CpG (MSssI) and GpC (MCviPI) DNA methyltransferases in relation to gene expression and (mito)epigenetic signatures. Overall, the results show that mitochondrial GpC and, to a lesser extent, CpG methylation increase bile acid metabolic gene expression, inducing the onset of cholestasis through mito-nuclear epigenetic reprogramming. Moreover, both increase the expression of metabolic nuclear receptors and thereby induce basal overactivation of mitochondrial respiration. The latter promotes mitochondrial swelling, favoring lipid accumulation and metabolic-stress-induced mitophagy and autophagy stress responses. In conclusion, both mitochondrial GpC and CpG methylation create a metabolically challenging environment that induces mitochondrial dysfunction, which may contribute to the progression of MASLD.

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DNMT3B PWWP mutations cause hypermethylation of heterochromatin.

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Project description:DNMT3B PWWP mutations cause hypermethylation of heterochromatin (RNA-seq)

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DNMT3B PWWP mutations cause hypermethylation of heterochromatin (ChIP-seq)

Project description:DNMT3B PWWP mutations cause hypermethylation of heterochromatin (ChIP-seq)

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CpG island hypermethylation in human astrocytomas

Project description:Astrocytomas are common and lethal human brain tumors. Here, we have analyzed the methylation status of over 28,000 CpG islands and 18,000 promoters in normal human brain and in astrocytomas of various grades using the methylated-CpG island recovery assay (MIRA). We identified six to seven thousand methylated CpG islands in normal human brain. ~5% of the promoter-associated CpG islands in normal brain are methylated. Promoter CpG island methylation is inversely and intragenic methylation is directly correlated with gene expression levels in brain tissue. In astrocytomas, several hundred CpG islands undergo specific hypermethylation relative to normal brain with 428 methylation peaks common to more than 25% of the tumors. Genes involved in brain development and neuronal differentiation, such as POU4F3, GDNF, OTX2, NEFM, CNTN4, OTP, SIM1, FYN, EN1, CHAT, GSX2, NKX6-1, RAX, PAX6, DLX2, were strongly enriched among genes frequently methylated in tumors. There was an overrepresentation of homeobox genes and 31% of the most commonly methylated genes represent targets of the Polycomb complex. We identified several chromosomal loci in which many (sometimes more than 20) consecutive CpG islands were hypermethylated in tumors. Seven of such loci were near homeobox genes, including the HOXC and HOXD clusters, and the BARHL2, DLX1, and PITX2 genes. Two other clusters of hypermethylated islands were at sequences of recent gene duplication events. Our analysis offers mechanistic insights into brain neoplasia suggesting that methylation of genes involved in neuronal differentiation, perhaps in cooperation with other oncogenic events, may shift the balance from regulated differentiation towards gliomagenesis. Comparison of methylation patterns of 30 astrocytomas and 6 controls

2010-05-16 | E-GEOD-19391 | biostudies-arrayexpress

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