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Global examination of H3K9me3 levels and PEG3 binding sites between WT and KO

ABSTRACT: Global examination of H3K9me3 levels and PEG3 binding sites between WT and KO

PROVIDER: PRJNA750512 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15291788.fastq.gz	Fastqsanger.gz
	SRR15291789.fastq.gz	Fastqsanger.gz
	SRR15291790.fastq.gz	Fastqsanger.gz
	SRR15291791.fastq.gz	Fastqsanger.gz
	SRR15291792.fastq.gz	Fastqsanger.gz

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Global examination of H3K9me3 levels and PEG3 binding sites between WT and KO

Project description:PEG3 (Paternally Expressed Gene 3) is an imprinted gene encoding a DNA-binding protein. In this study, we used MEF cells (Mouse Embryonic Fibroblast). We performed genome-wide ChIP-seq experiments profiling H3K9me3 levels as well as examine the set of genomic targets and also redefines the DNA-binding motif for the imprinted transcription factor, PEG3 in the WT and KO of Peg3. The results suggested high levels of H3K9 levels in Peg3-KO MEFs than in Peg3-WT MEFs, whereas several different genes involved several biochemical pathways seems to be have potential binding site for PEG3 protein, which tend to have a distinct profile of binding motif to its binding region. This further suggests that mammalian Peg3 may control its downstream genes in regulating several biological functions and regulate the H3K9 methylation levels.

2021-07-31 | GSE181069 | GEO

Analysis of genome wide H3K9me3 levels in control and ORCA knockdown cells

Project description:Origin Recognition Complex Associated (ORCA) associates with repressive chromatin environments. We carried out H3K9me3 ChIP-seq to determine the affect of ORCA's loss on this repressive mark. Towards this end, we cultured U2OS osteosarcoma cells, performed control and ORCA knockdowns using siRNAs and then carried out H3K9me3 ChIP-seq to determine the regions in the genome which get affected upon ORCA knockdown. Examination of the levels of H3K9me3 in control and ORCA knockdown cells

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Genome-wide maps of H3K9me3 in control ESCs and Rif1 knockdown ESC.

Project description:We found that Rif1 depletion leads to reduced H3K9me3 levels at 1/3 of the H3K9me3-enriched genomic regions (H3K9me3 peaks), and that reduced H3K9me3 de-represses Zscan4 and other genes that are specific to the 2-Cell stage embryo. Examination of H3K9me3 histone modifications in 2 cell types.

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Global examination of LncMyoD binding sites using ChIRP-seq

Project description:Global examination of LncMyoD binding sites using ChIRP-seq

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Profiling of H3K9me3 levels predicts Transcription Factor Activity and Survival in Acute Myeloid Leukemia

Project description:Acute Myeloid Leukemia (AML) is commonly associated with alterations in transcription factors due to altered expression or gene mutations. These changes might induce leukemia specific patterns of histone modifications. We used ChIP-Chip to analyze histone H3 Lysine 9 trimethylation (H3K9me3) patterns in primary AML (n=108), ALL (n=28), CD34+ cells (n=21) and white blood cells (n=15) specimens. Hundreds of promoter regions in AML showed significant alterations in H3K9me3 levels. H3K9me3 deregulation in AML occurred preferentially as a decrease in H3K9me3 levels at core promoter regions. The altered genomic regions showed an overrepresentation of cis-binding sites for ets and c-AMP response elements (CREs) for transcription factors of the CREB/CREM/ATF1 family. The decrease in H3K9me3 levels at CREs was associated with increased CRE-driven promoter activity in AML blasts in vivo. AML specific H3K9me3 patterns were not associated with known cytogenetic abnormalities. But a signature derived from H3K9me3 patterns predicted event free survival in AML patients. Combination of the H3K9me3 signature with established clinical prognostic markers outperformed prognosis prediction based on clinical parameters alone. These findings demonstrate widespread changes of H3K9me3 levels at gene promoters in AML. Signatures of histone modification patterns are associated with patient prognosis in AML.

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Examination of growth mode dependent replication dynamics and expression levels for Vibrio parahaemolyticus RIMD2210633.

Project description:Examination of growth mode dependent replication dynamics and expression levels for Vibrio parahaemolyticus RIMD2210633.

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Project description:We report the placement of the H3K9me3 heterochromatin mark from the filamentous fungus Neurospora crassa in wild type and dim-3 strains. The dim-3 strain has a global reduction in H3K9me3, which results from a causative mutation in importin alpha (NUP-6), a component of the nuclear transport machinery. NUP-6(dim-3) compromises the heterochromatic localization of several components of the DCDC, a histone H3K9 methyltransferase complex, from their sub-nuclear chromatin targets despite appropriate nuclear transport. To determine whether the reduced level of global H3K9me3 observed from isolated histones localizes to A:T rich DNA (genomic DNA destined to become heterochromatin), we performed H3K9me3 ChIP-seq on a dim-3 strain and compared that to a wild type strain.

2015-03-22 | GSE61173 | GEO

Setdb1 is required for persistence of H3K9me3 and repression of endogenous retroviruses in mouse primordial germ cells

Project description:Transcription of endogenous retroviruses (ERVs) is inhibited by de novo DNA methylation during gametogenesis, a process initiated after birth in oocytes and at ~E15.5 in prospermatogonia. Earlier in germline development however, the genome, including most retrotransposons, is progressively demethylated, with young ERVK and ERV1 elements retaining intermediate methylation levels. As DNA methylation reaches a low point in E13.5 primordial germ cells (PGCs) of both sexes, we determined whether retrotransposons are marked by H3K9me3 and H3K27me3 using a recently developed low input ChIP-seq method. Although these repressive histone modifications are predominantly found on distinct genomic regions in E13.5 PGCs, they concurrently mark partially methylated LTRs and LINE1 elements. Germline-specific conditional knock-out (KO) of the H3K9 methyltransferase SETDB1 yields a decrease of both histone marks and DNA methylation at H3K9me3 enriched retrotransposon families. Strikingly, Setdb1-KO E13.5 PGCs show concomitant de-repression of many marked ERVs, including IAP, ETn and ERVK10C elements and ERV-proximal genes, a subset in a sex-dependent manner. Furthermore, Setdb1 deficiency is associated with a reduced number of male PGCs and postnatal hypogonadism in both sexes. Taken together, these observations reveal that SETDB1 is an essential guardian against proviral expression prior to the onset of de novo DNA methylation in the germline. H3K9me3, H3K27me3 and expression profiles in Setdb1 WT, Het and KO male and female E13.5 PGCs.

2014-09-01 | E-GEOD-60377 | biostudies-arrayexpress

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