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

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

PROVIDER: PRJNA610801 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11250229_1.fastq.gz	Fastqsanger.gz
	SRR11250229_2.fastq.gz	Fastqsanger.gz
	SRR11250230_1.fastq.gz	Fastqsanger.gz
	SRR11250230_2.fastq.gz	Fastqsanger.gz
	SRR11250231_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 [RNA-Seq]

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

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

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

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Fighting against promoter DNA hyper-methylation: Protective histone modification profiles of stress-resistant intestinal stem cells [RNA-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 | GSE146518 | GEO

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

2020-03-07 | GSE146519 | 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.

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

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H3K4me3 and H3K27me3 modification profiling in early zebrafish embryo

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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.

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BnC03UPL3 promoter

Project description:BnC03UPL3 promoter

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