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Histone Phosphoacetylation ChIP-seq of Kc167 cells from Drosophila

ABSTRACT: ChIP-seq was performed using Drosophila Kc167 cells using antibodies against H3K4me3 to identify active promoters and H3K4me1 to identify active enhancers. H3K27ac ChIPseq was performed to identify active promoters and enhancers. Once enhancers and promoters were identified, JIL-1 and histone phosphorylation, H3K9acS10ph and H3K27acS28ph, ChIP-seq was performed to look at binding trends. JIL-1 and phosphoacetlation is found at low levels at inactive enhancers and shows increase at active enhancers and promoters.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE36374 | GEO | 2012/03/29

SECONDARY ACCESSION(S): PRJNA153251

REPOSITORIES: GEO

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Histone Phosphoacetylation ChIP-seq of Kc167 cells from Drosophila

Project description:ChIP-seq was performed using Drosophila Kc167 cells using antibodies against H3K4me3 to identify active promoters and H3K4me1 to identify active enhancers. H3K27ac ChIPseq was performed to identify active promoters and enhancers. Once enhancers and promoters were identified, JIL-1 and histone phosphorylation, H3K9acS10ph and H3K27acS28ph, ChIP-seq was performed to look at binding trends. JIL-1 and phosphoacetlation is found at low levels at inactive enhancers and shows increase at active enhancers and promoters. Here we examine histone phosphorylation by JIL-1 and acetylation of H3K27ac by CBP at transcriptionally active vs. inactive promoters and enhancers. ChIP-seq is performed in Kc167 Drosophila cells using antibodies against JIL-1, H3K27acS28ph, H3K9acS10ph, H3K4me3, H3K4me1, and H3K27ac.

2012-03-29 | E-GEOD-36374 | biostudies-arrayexpress

JASPer controls interphase histone H3S10 phosphorylation by chromosomal kinase JIL-1 in Drosophila

Project description:In Drosophila the chromosomal kinase JIL-1 is responsible for most interphase histone H3S10 phosphorylation and has been proposed to protect active chromatin from acquiring heterochromatic marks, like dimethylated histone H3K9 (H3K9me2) and HP1. Here, we show that JIL-1’s targeting to chromatin depends on a PWWP domain-containing protein JASPer (JIL-1 Anchoring and Stabilizing Protein). The JASPer-JIL-1 (JJ)-complex is the major form of the kinase in vivo and is targeted to active genes and telomeric transposons via binding of the PWWP domain of JASPer to H3K36me3 nucleosomes, where the complex modulates the transcriptional output. JIL-1 and JJ-complex depletion in cycling cells lead to small changes in H3K9me2 distribution at active genes and telomeric transposons. Finally, we identify several interactors of the endogenous JJ-complex and propose that JIL-1 not only prevents heterochromatin formation but also coordinates chromatin-based regulation in the transcribed part of the genome.

2019-10-09 | PXD012790 | Pride

Kc167 ORC Localization in hydroxyurea (HU)

Project description:Determination of the genome-wide distribution of ORC by chromatin immunoprecipitation in the Drosophila Kc167 cell line at the beginning of S phase. Kc167 cells were arrested at the G1/S transition with hydroxyurea (HU). Goal was to test whether the ORC binding distribution remained the same between G1 and S.

2014-12-05 | GSE63914 | GEO

Kc167 Mcm2-7 Localization in HU

Project description:Determination of the genome-wide distribution of the Mcm2-7 helicase by chromatin immunoprecipitation in the Drosophila Kc167 cell line at the beginning of S phase. Kc167 cells were arrested at the G1/S transition with hydroxyurea (HU). Goal was to evaluate changes in the genome-wide Mcm2-7 distribution throughout the cell cycle, and how this relates to the excess Mcm2-7 loaded onto chromatin in G1.

2014-11-27 | GSE63680 | GEO

modENCODE RNA-Seq of Drosophila Kc167

Project description:Deep Sequencing of Kc167 mRNA. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

2009-09-10 | GSE18040 | GEO

Kc167 Replication Timing

Project description:modENCODE_submission_668 This submission comes from a modENCODE project of David MacAlpine. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: The relative time of replication for all unique sequences in the Drosophila genome was determined by synchronizing tissue culture cell and differentially labeling early and late replicating intermediates. The differentially labeled replication intermediates were then hybridized to Agilent genomic tiling arrays to identify early and late replicating domains. Keywords: CHIP-chip For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: Kc167; Tissue: embryo-derived cell-line; Genotype: se/e; Sex: Female NUMBER OF REPLICATES: 3; EXPERIMENTAL FACTORS: Cell Line Kc167

2009-07-29 | E-GEOD-17279 | biostudies-arrayexpress

H3K27Ac ChIP-seq profile of human oral epithelial cell line HIOEC

Project description:To identify the active enhancers and promoters in human oral epithelial cell line, we performed H3K27Ac ChIP-seq for HIOEC cell line.

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Kc167 Mcm2-7 Localization in Late S Phase

Project description:Determination of the genome-wide distribution of the Mcm2-7 helicase by chromatin immunoprecipitation in the Drosophila Kc167 cell line at the end of S phase. Kc167 cells were synchronized by first arresting at the G1/S transition with hydroxyurea (HU), and then releasing from the HU arrest point for 6 hours. Goal was to evaluate changes in the genome-wide Mcm2-7 distribution throughout the cell cycle, and how this relates to the excess Mcm2-7 loaded onto chromatin in G1.

2014-12-05 | GSE63913 | GEO

Drosophila melanogaster strain:Kc167

Project description:Drosophila Kc167 and S2 Mcm2-7 ChIP-seq in HU

| PRJNA268524 | ENA

Expression data from Drosophila Kc167 cell line

Project description:The consitutive activation of the JAK/STAT signalling cascade is reponsible for the majority of meyoproliferative disorders in humans, a disease that is also conserved in Drosophila. A gain-of-function mutation in the Drosophila JAK kinase leads to blood cell (haemocyte) overproliferation which eventually is manifested as black melanotic tumors. Haemocyte-like Drosophila Kc167 cells were used to identify downstream target genes of the JAK/STAT pathway which may be responsible for tumour generation and progression.

2009-08-31 | GSE15584 | GEO

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