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Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells [ChIP-Seq]

ABSTRACT: Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells [ChIP-Seq]

PROVIDER: PRJNA610803 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11250241_1.fastq.gz	Fastqsanger.gz
	SRR11250241_2.fastq.gz	Fastqsanger.gz
	SRR11250242_1.fastq.gz	Fastqsanger.gz
	SRR11250242_2.fastq.gz	Fastqsanger.gz
	SRR11250243_1.fastq.gz	Fastqsanger.gz

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Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells

Project description:Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells

| PRJNA610801 | ENA

Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells [RNA-Seq]

Project description:Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells [RNA-Seq]

| PRJNA610804 | ENA

Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells [ChIP-Seq]

Project description:Aberrant DNA methylation in stem cells is a hallmark of aging and tumor development. Recently, we have suggested that promoter DNA hyper-methylation originates in DNA repair and that even successful DNA repair might confer this kind of epigenetic long-term changes. We here ask for interrelations between promoter DNA methylation and histone modification changes observed in the intestine weeks after irradiation and/or following Msh2 loss. We focus on H3K4me3 recruitment to the promoter of H3K27me3 target genes. By RNA- and histone ChIP- sequencing, we demonstrate that this recruitment occurs without changes of the average gene transcription and does not involve H3K9me3. Applying a mathematical model of epigenetic regulation of transcription, we show that the recruitment can be explained by stronger DNA binding of H3K4me3 and H3K27me3 histone methyl-transferases as a consequence of lower DNA methylation. This scenario implicates stable transcription despite of H3K4me3 recruitment, in agreement with our RNA-seq data. Following several kinds of stress, including moderate irradiation, stress-sensitive intestinal stem cell (ISCs) are known to become replaced by more resistant populations. Our simulation results suggest that the stress-resistant ISCs are largely protected against promoter hyper-methylation of H3K27me3 target genes.

2020-03-07 | GSE146519 | GEO

Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells [RNA-Seq]

2020-03-07 | GSE146518 | GEO

Fighting Against Promoter DNA Hyper-Methylation: Protective Histone Modification Profiles of Stress-Resistant Intestinal Stem Cells.

Project description:Aberrant DNA methylation in stem cells is a hallmark of aging and tumor development. Recently, we have suggested that promoter DNA hyper-methylation originates in DNA repair and that even successful DNA repair might confer this kind of epigenetic long-term change. Here, we ask for interrelations between promoter DNA methylation and histone modification changes observed in the intestine weeks after irradiation and/or following Msh2 loss. We focus on H3K4me3 recruitment to the promoter of H3K27me3 target genes. By RNA- and histone ChIP-sequencing, we demonstrate that this recruitment occurs without changes of the average gene transcription and does not involve H3K9me3. Applying a mathematical model of epigenetic regulation of transcription, we show that the recruitment can be explained by stronger DNA binding of H3K4me3 and H3K27me3 histone methyl-transferases as a consequence of lower DNA methylation. This scenario implicates stable transcription despite of H3K4me3 recruitment, in agreement with our RNA-seq data. Following several kinds of stress, including moderate irradiation, stress-sensitive intestinal stem cell (ISCs) are known to become replaced by more resistant populations. Our simulation results suggest that the stress-resistant ISCs are largely protected against promoter hyper-methylation of H3K27me3 target genes.

| S-EPMC7139626 | biostudies-literature

Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells

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

2020-03-07 | GSE146520 | GEO

H3K4me3 and H3K27me3 modification profiling in early zebrafish embryo

Project description:Multicellular organism requires concise gene regulation during ontogeny and epigenetic modifications, such as DNA methylation and histone modification, facilitate the concise regulation. The conservative reprogramming patterns of DNA methylation in vertebrates have been well described but knowledge of how histone modifications are passed on to zygote from gametes are limited and conservations of histone modifications are not clear.We profiled H3K4me3/H3K27me3 modifications in gametes and early embryos in zebrafish and find out that patterns in gene promoter regions have been largely set to either bivalent or active states in gametes and then passed on to zygote. Bivalent states are partially maintained and active states are restored to match sperm’s pattern. But repressive H3K27me3 modifications as well as stage specific modifications in promoter regions are discarded. Prior to zygotic genome activation, patterns of genes that initialize ZGA have been converted to non-repressive states to coordinate gene expression. Histone modification in hyper methylated promoter peaks are erased independent of DNA methylome reprogramming. Comparative analysis revealed that functions of bivalent and active genes passed on from gametes are conserved in vertebrates and gene age preferences by bivalent and active histone modifications are also confirmed in vertebrates.

2019-04-17 | GSE110663 | GEO

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2010-05-22 | E-GEOD-11956 | biostudies-arrayexpress

HCV Hypo- vs. Hyper-Phosphorylated NS5A Interactome

Project description:Chronic hepatitis C virus (HCV) infection is a leading cause of liver cancer. HCV propagation and oncogenicity depend in part on the phosphorylation states of its non-structural protein 5A (NS5A); however, little is known about how hypo- or hyper-phosphorylated NS5A functions. Here, we segregated hypo- from hyper-phosphorylated NS5A in HCV-infected Huh7.5.1 cells with two custom-made specific antibodies and differentiated their interacting proteins with dimethyl labeling-based quantitative proteomics. Bioinformatics analysis revealed that hyper-phosphorylated NS5A preferentially binds the polymerase II-associated factor 1 complex known to alter host gene expression involved in cancer progression. In contrast, hypo-phosphorylated NS5A binds proteins involved in host antiviral response. Moreover, we found that the hypo-phosphorylated NS5A binds DNA-dependent protein kinase catalytic subunit (DNA-PKcs) predicted to phosphorylate NS5A at serine 232, a key amino acid that governs NS5A transition from hypo- to hyper-phosphorylation state. Inhibition of DNA-PKcs with an inhibitor or via gene-specific knockdown significantly reduced serine 232 phosphorylation and NS5A hyper-phosphorylation. Collectively, we have identified a protein kinase that regulates a delicate balance of NS5A between hypo- and hyper-phosphorylation states respectively involved in host antiviral responses and liver cancer progression.

2019-06-17 | PXD012767 | Pride

BnC03UPL3 promoter

Project description:BnC03UPL3 promoter

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