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Mapping of H3, H3K4me3, H3K9me3, and H3K9ac on mixed asexual stages of P. falciparum

ABSTRACT: Epigenome profiling has led to the paradigm that promoters of active genes are decorated with H3K4me3 and H3K9ac marks. Data revealed an extensively euchromatic epigenome with heterochromatin restricted to variant surface antigen gene families (VSA) and a number of genes hitherto unlinked to VSA. The vast majority of the genome shows an unexpected pattern of enrichment of H3K4me3 and H3K9ac at intergenic regions and depletion at genes. Chip-chip (and cDNA) from Plasmodium falciparum strain NF54 asexual blood stages with H3, H3K4me3, H3K9me3 and H3K9ac

ORGANISM(S): Plasmodium falciparum

SUBMITTER: O Jensen

PROVIDER: E-GEOD-15728 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dynamic histone H3 epigenome marking during the intraerythrocytic cycle of Plasmodium falciparum.

Salcedo-Amaya Adriana M AM van Driel Marc A MA Alako Blaise T BT Trelle Morten B MB van den Elzen Antonia M G AM Cohen Adrian M AM Janssen-Megens Eva M EM van de Vegte-Bolmer Marga M Selzer Rebecca R RR Iniguez A Leonardo AL Green Roland D RD Sauerwein Robert W RW Jensen Ole N ON Stunnenberg Hendrik G HG

Proceedings of the National Academy of Sciences of the United States of America 20090602 24

Epigenome profiling has led to the paradigm that promoters of active genes are decorated with H3K4me3 and H3K9ac marks. To explore the epigenome of Plasmodium falciparum asexual stages, we performed MS analysis of histone modifications and found a general preponderance of H3/H4 acetylation and H3K4me3. ChIP-on-chip profiling of H3, H3K4me3, H3K9me3, and H3K9ac from asynchronous parasites revealed an extensively euchromatic epigenome with heterochromatin restricted to variant surface antigen gene ...[more]

PMID: 19497874

Similar Datasets

Dynamic histone H3 epigenome marking during the intraerythrocytic cycle of P. falciparum

Project description:This SuperSeries is composed of the following subset Series: GSE15728: Mapping of H3, H3K4me3, H3K9me3, and H3K9ac on mixed asexual stages of P. falciparum GSE16095: Mapping of H3, H3K4me3 and H3K9ac on Ring and Schizont stages of P. falciparum Refer to individual Series

2010-05-19 | E-GEOD-16096 | biostudies-arrayexpress

Mapping of H3, H3K4me3 and H3K9ac on Ring and Schizont stages of P. falciparum

Project description:Epigenome profiling has led to the paradigm that promoters of active genes are decorated with H3K4me3 and H3K9ac marks. These data on synchronized parasites reveals significant developmental stage specificity of the epigenome. In rings, H3K4me3 and H3K9ac are homogenous across the genes marking active and inactive genes equally, whilst in schizonts they are enriched at the 5âend of active genes. Chip-chip (and cDNA) from Plasmodium falciparum strain NF54 Rings and Schizonts with H3, H3K4me3 and H3K9ac.

2010-05-19 | E-GEOD-16095 | biostudies-arrayexpress

Identification of histone modifications in cardiomyocytes of conditional HDAC4 knockout mice

Project description:Histone Deacetylase 4 (HDAC4) is known to contribute to cardiac remodeling processes. We wanted to identify and compare different genome wide targets of HDAC4 to well described interaction partners and its functional consequences. Therefore, we used a model of adult cardiomyocytes isolated from HDAC4 knockout mice and Wildtyp (WT) controls. We looked for HDAC4s contribution to changes of activating histone modifications (H3K4me3, H3K9ac, H3K27ac) and repressive pendants (H3K9me2 and H3K27me3).

2021-09-15 | E-MTAB-7319 | biostudies-arrayexpress

ChIP-seq data of Epstein-Barr Virus Nuclear Antigen Leader ProteinM-BM- (EBNALP)

Project description:Epstein-Barr-Virus (EBV) Nuclear Antigens EBNALP and EBNA2 are co-expressed in EBV infected B-lymphocytes and are critical for Lymphoblastoid Cell Line (LCL) growth. EBNALP removes NCOR1 and RBPJ repressive complexes from promoter and enhancer sites and EBNA2 mostly activates transcription from distal enhancers. ChIP-seqs found EBNALP at 19,224 LCL sites, which were 33% promoter associated. EBNALP was associated with 10 transcription factor (TF) clusters that included YY1(63%), SP1(62%), PAX5(59%), BATF(50%), IRF4(49%), RBPJ(43%), ETS1(39%), PU.1(37%), RAD21(33%), NF-kB(31%), TBLR1(26%), ZNF143(24%), CTCF(23%), SMC3(21%), and EBF(17%). EBNALP sites had higher H3K4me3, H3K9ac, H3K27ac, H2Az, and RNA Pol II signals than EBNA2 sites and had similar transcription effects. EBNALP co-localized with 29% of 19,845 EBNA2 sites. EBNALP/EBNA2 sites were similar to EBNALP sites in promoter localization, associated cell TFs, Pol II, H3K4me3, H3K9ac, H3K27ac, and H2Az signals. EBNALP and EBNA2 promoter sites were more transcriptionally active than EBNALP or EBNA2 promoter sites. EBNALP was at the enhancer or promoter of myc and MYC affected genes, including cyclin D2, and bcl2. EBNALP at promoters with DNA looping and transcription factors, is positioned to deplete repressors from enhancers and promoters, enable chromatin remodeling, and transcription activation. Two EBNALP ChIP-seq replicates from IB4 LCL are analyzed in this study.

2013-07-31 | E-GEOD-49338 | biostudies-arrayexpress

Effect of Gfi1 36N variant on genome-wide H3K9 Acetylation patterns

Project description:ChIP-Seq Analysis of H3K9Ac in pairs of mouse and human samples carrying either the Gfi136S or the GFi136N variants. The objective of the study was to identify the changes in H3K9 acetylation at gene promoters that occur in samples expressing the 36N variant of the Gfi1 gene. 3 pairs of bone-marrow AML samples were obtained from mice where 1 mouse in each pair was homozygous for Gfi136S and 1 heterozygous for Gfi136N, or homozygous for 36N in one case. 2 pairs of AML samples were obtained from human patients were 1 patient was homozygous for Gfi1 36S and one was heterozygous for Gfi1 36N. H3 and H3K9Ac ChIP-Seq was carried out on each sample.

2016-08-01 | E-GEOD-71254 | biostudies-arrayexpress

Chromatin signature of embryonic pluripotency is established during zygotic genome activation [Danio rerio]

Project description:[PROJECT] After fertilization the embryonic genome is inactive until transcription is initiated during the maternal-zygotic transition (MZT). This universal process coincides with the formation of pluripotent cells, which in mammals can be used to generate embryonic stem (ES) cells. To study the changes in chromatin structure that accompany zygotic genome activation and pluripotency, we mapped the genomic locations of histone H3 modifications before and after MZT in zebrafish embryos. Repressive H3 lysine 27 trimethylation (H3K27me3) and activating H3 lysine 4 trimethylation (H3K4me3) are only detected after MZT. H3K4me3 marks more than 80% of genes, including many developmental regulatory genes that are also occupied by H3K27me3. Sequential chromatin immunoprecipitation demonstrates that both methylation marks occupy the same promoter regions, revealing that the bivalent chromatin domains found in cultured ES cells also exist in embryos. In addition, we find a large group of genes that are monovalently marked by H3K4me3 but not H3K27me3. These H3K4me3 monovalent genes are neither expressed nor stably bound by RNA polymerase II. Closer inspection of in vitro data sets reveals similar monovalent H3K4me3 domains in ES cells. The analysis of an inducible transgene indicates that H3K4me3 domains can form in the absence of sequence-specific transcriptional activators or stable association with RNA pol II. These results suggest that bivalent and monovalent domains might poise embryonic genes for activation and that the chromatin profile associated with pluripotency is established during MZT. [SAMPLES] ChIPchip analysis of histone modifications (H3K4me3, H3K27me3, H3K36me3) and RNA polymerase II in pre MZT (256-cell) and post MZT (4hpf; dome/30% epiboly) wt zebrafish embryos. H3K4me3, H3K27me3, H3K36me3 and PolII ChIP-chip at 256 cell stage (one replicate) and 4hpf (dome/30% epiboly) (two replicates)

2010-01-25 | E-GEOD-20023 | biostudies-arrayexpress

Mapping the Chromatin State Dynamics in Myoblasts

Project description:The chromatin state in developing body parts provides a zip code to cellular populations that direct their cell fates. We used antibodies for H3K4me3, H3K27me3 and Pol2, to identify the chromatin state signature of the Pitx2-null mouse forelimb during mid-gestation, at embryonic day 12. The families of genes marked included those related to transcription, transcriptional regulation, and embryonic organ development. Transcription factors specific for muscle development were characterized by bivalent chromatin, as E12 is a transition time point from embryonic to fetal myogenesis. The identified chromatin state of muscle specific genes was in strong correlation with their observed expression profile. Examination of the histone marks H3K4me3, H3k27me3, and Pol2 in whole E12.5 forelimb tissues from Pitx2 null mice using the Illumina HiSeq 2000

2016-07-17 | E-GEOD-71128 | biostudies-arrayexpress

ChIP-seq mapping of histone modifications in CD14++ CD16- monocytes from septic disease patients

Project description:Chromatin immunoprecipitation with antibodies specific for histone modifications H3K4me3, H3K9ac and H3K27me3 and subsequent high-throughput sequencing were performed on fixed chromatin from two septic disease patients. ChIP-seq

2015-03-01 | E-GEOD-62908 | biostudies-arrayexpress

Nuclear phosphatidylinositol-5-phosphate regulates ING2 stability at discrete chromatin targets in response to DNA damage [ChIP-chip]

Project description:ING2 (inhibitor of growth family member 2) is a component of a chromatin-regulatory complex that represses gene expression and is implicated in cellular processes that promote tumor suppression. However, few direct genomic targets of ING2 have been identified and the mechanism(s) by which ING2 selectively regulates genes remains unknown. Here we provide evidence that direct association of ING2 with the nuclear phosphoinositide phosphatidylinositol-5-phosphate (PtdIns(5)P) regulates a subset of ING2 targets in response to DNA damage. At these target genes, the binding event between ING2 and PtdIns(5)P is required for ING2 promoter occupancy and ING2-associated gene repression. Moreover, depletion of PtdIns(5)P attenuates ING2-mediated regulation of these targets in the presence of DNA damage. Taken together, these findings support a model in which PtdIns(5)P functions as a sub-nuclear trafficking factor that stabilizes ING2 at discrete genomic sites. FLAG-ING2 ChIP-chip of stably-transduced HT1080 cells in the presence of vehicle (DMSO) or etoposide. Each condition is tested in duplicate.

2013-12-31 | E-GEOD-47688 | biostudies-arrayexpress

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