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Mus musculus

ABSTRACT: UHRF2 regulates local 5-methylcytosine and suppresses spontaneous seizures [MeDIP-Seq, hMeDIP-Seq]

PROVIDER: PRJNA384816 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5487032.fastq.gz	Fastqsanger.gz
	SRR5487033.fastq.gz	Fastqsanger.gz
	SRR5487034.fastq.gz	Fastqsanger.gz
	SRR5487035.fastq.gz	Fastqsanger.gz
	SRR5487036.fastq.gz	Fastqsanger.gz

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UHRF2 regulates local 5-methylcytosine and suppresses spontaneous seizures

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UHRF2 regulates local 5-methylcytosine and suppresses spontaneous seizures [MeDIP-Seq, hMeDIP-Seq]

Project description:5-methylcytosine (5mC) regulates multiple cellular processes and is faithfully maintained following DNA replication. Ubiquitin-like PHD and ring finger domain-containing protein 1 (UHRF1) plays an important role in the maintenance of 5mC levels. Interestingly, UHRF1 has a paralog UHRF2 that has similar sequence and domain architecture, but the biological function of UHRF2 is not clear. Here, we have generated Uhrf2 knockout mice and characterized the role of UHRF2 in vivo. Uhrf2 knockout mice are viable, but the adult mice develop frequent spontaneous seizures and display abnormal electrical activities in brain. To explore possible mechanism beyond these phenomenon, we utilized high-throughput sequencing to identify global expression changes in Uhrf2 knockout mice brains. In addition, we explored genome-wide 5mc profiles in these samples to examine if UHRF2 regulates 5mc levels in specific genome loci.

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UHRF2 regulates local 5-methylcytosine and suppresses spontaneous seizures [RNA-seq]

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TET1 regulates hypoxia-induced epithelial-mesenchymal transition through DNA demethylation (RNA-Seq)

Project description:In order to explore the status of DNA methylation in hypoxia response, we show that TET1, a DNA dioxygenase converting 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC), regulates hypoxia-responsive gene expression. Hypoxia/HIF-2Î± regulates the expression of TET1. Knockdown of TET1 mitigated hypoxia-induced EMT. RNA sequencing and 5hmC sequencing identified the set of TET1-regulated genes. Four samples (Four samples, Hypoxia (scrambled control), Hypoxia (TET1-si), Normoxia (scrambled control) and Normoxia (TET1-si), are performed by RNA-Seq and hMeDIP-Seq RNA-Seq and hMeDIP-Seq

2014-08-01 | E-GEOD-59987 | biostudies-arrayexpress

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Iron-dependent epigenetic modulation promotes pathogenic T cell differentiation in lupus

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Mouse liver MeDIP, hMeDIP and H3K27ac ChIP-seq data sets

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Hydroxylation of 5-methylcytosine by TET2 maintains the active state of the mammalian HOXA cluster (MeDIP-Seq)

Project description:Differentiation is accompanied by extensive epigenomic reprogramming, leading to the repression of stemness factors and the transcriptional maintenance of activated lineage-specific genes. Here we used the mammalian Hoxa cluster of developmental genes as a model system to follow changes in DNA modification patterns during retinoic acid induced differentiation. We found the inactive cluster to be marked by defined patterns of 5-methylcytosine (5mC). Upon the induction of differentiation, the active anterior part of the cluster became increasingly enriched in 5-hydroxymethylcytosine (5hmC), following closely the colinear activation pattern of the gene array, which was paralleled by the reduction of 5mC. Depletion of the 5hmC generating dioxygenase Tet2 impaired the maintenance of Hoxa activity and partially restored 5mC levels. Our results indicate that gene specific 5mC-5hmC conversion by Tet2 is crucial for the maintenance of active chromatin states at lineage-specific loci. Examination of 5-methylcytosine (MeDIP-seq) and 5-hydroxymethylcytosine (hMeDIP-seq) at the HOXA cluster in 2 different developmental stages of a pluripotent cancer cell line.

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Genome-wide distribution of UHRF2 and ZNF618 in 293T cells.

Project description:We have identified ZNF618 as a novel binding partner of UHRF2. We have found that UHRF2 and ZNF618 co-localize at many genomic loci. Examination of genome-wide distribution of SFB-tagged UHRF2 and ZNF618 in 293T cells using ChIP-seq.

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