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Influence of histone lysine demethylase JMJD2-specific inhibition on the senescence-associated secretory phenotype developed in human stromal cells upon DNA damage

ABSTRACT: Influence of histone lysine demethylase JMJD2-specific inhibition on the senescence-associated secretory phenotype developed in human stromal cells upon DNA damage

PROVIDER: PRJNA527008 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8728130_1.fastq.gz	Fastqsanger.gz
	SRR8728130_2.fastq.gz	Fastqsanger.gz
	SRR8728140_1.fastq.gz	Fastqsanger.gz
	SRR8728140_2.fastq.gz	Fastqsanger.gz
	SRR8728131_1.fastq.gz	Fastqsanger.gz

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Influence of histone lysine demethylase JMJD2-specific inhibition on the senescence-associated secretory phenotype developed in human stromal cells upon DNA damage

Project description:Recent advances in next generation sequencing (NGS) has revolutionized system-based analysis of genome-wide expression, cellular pathways and responses. We performed this epigenetic study to streamline the transcriptome profiling (RNA-seq) of human stromal cells developing a typical senescence-associated secretory phenotype (SASP) upon stress induced by DNA damage or DNA damage together with pharmacological targeting of JMJD2, a trimethylation-specific demethylase of histone H3K9 and H3K36.

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CpG islands recruit a histone H3 lysine 36 demethylase

Project description:This SuperSeries is composed of the following subset Series: GSE18588: CpG islands recruit a histone H3 lysine 36 demethylase [Illumina sequencing data] GSE21201: CpG islands recruit a histone H3 lysine 36 demethylase [Agilent data] Refer to individual Series

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CpG islands recruit a histone H3 lysine 36 demethylase [Illumina sequencing data]

Project description:Eukaryotic gene expression profiles are largely defined by transcription factors that recognize specific DNA sequences in gene regulatory regions and impact RNA polymerase recruitment and transcription. In addition to specific core promoter regulatory elements, up to 70% of genes in higher eukaryotes are also characterized by an overrepresentation of cytosine/guanine base pairs (CpGs) surrounding promoters and gene regulatory units. These features, called CpG islands, were identified over twenty years ago but there remains little mechanistic evidence to suggest how these enigmatic elements contribute to promoter function, with the exception that they are refractory to epigenetic silencing by DNA methylation. Here we uncover a role for CpG islands in buffering gene regulatory elements from repressive histone H3 lysine 36 methylation by directly recruiting the H3K36 specific lysine demethylase enzyme KDM2A. KDM2A is recruited to CpG islands by a zinc finger CxxC (ZF-CxxC) domain that specifically recognizes CpG DNA and is blocked by DNA methylation. This capacity to sense the epigenetic methylation state of DNA constrains KDM2A to non-methylated CpG islands. Importantly, these observations suggest CpG islands may function to delineate gene regulatory elements from bulk chromatin by recruiting factors that create unique chromatin architecture. This study provides information about binding of lysine demethylase enzyme KDM2A in mouse embryonic stem cells.

2010-04-27 | E-GEOD-18588 | biostudies-arrayexpress

Lysine-specific demethylase 1 metastasis of androgen-independent PCa cells

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Uncoupling Histone Modification Crosstalk by Engineering Lysine Demethylase LSD1

Project description:Biochemical crosstalk between two or more histone modifications is often observed in epigenetic enzyme regulation but its functional significance in cells has been difficult to discern. Prior enzymatic studies have revealed that Lys14 acetylation of histone H3 can inhibit Lys4 demethylation by lysine specific demethylase 1 (LSD1). Here we have engineered a mutant form of LSD1, Y391K, which renders the nucleosome demethylase activity of LSD1 insensitive to Lys14 acetylation. Y391K LSD1 knockin cells show increased repression of a set of genes associated with cellular adhesion. Chromatin profiling revealed that the cis-regulatory regions of these silenced genes display a higher level of H3 Lys14 acetylation than the baseline in unedited, parental cells. Y391K LSD1 knockin cells show diminished H3 mono-methyl Lys4 in the vicinity of these silenced genes, consistent with a role for enhanced LSD1 demethylase activity in these regions. These findings illuminate the functional consequences of disconnecting histone modification crosstalk for a key epigenetic enzyme in gene and chromatin regulation.

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