Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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

ABSTRACT: 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.

ORGANISM(S): Plasmodium falciparum

SUBMITTER: O Jensen

PROVIDER: E-GEOD-16095 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

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

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Project description:Missense mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines. In contrast to wild-type p53, the mutant p53 (mutp53) protein has lost the transcriptional activity towards pro-apoptotic and growth arrest genes, but retained the property to interact with DNA in a structure-specific fashion. Expression of mutp53 is advantageous for tumor cells, however the molecular mechanism of mutp53 action is still not known. We used the glioblastoma-derived U-251 MG human cell line to analyze DNA binding of mutant p53 (R273H mutation) on a Nimblegen custom 135k tiling array and to correlate mutp53 binding regions with the epigenetic state and occupation by other transcription factors (ETS1 and SP1). We found that mutp53-binding regions are G/C-rich and are located around transcriptional start sites (TSS) of many protein-coding genes, which in most cases are active, but are not always regulated upon transient mutp53 depletion. We propose a model which does not only rely on interactions of mutp53 with diverse transcriptional regulators at active promoters, but primarily is based on a DNA binding activity of mutp53. We designed a Nimblegen custom 135k tiling array that covers a large set of putative and known p53 (wild-type and mutant) target genes in the human genome. For analysis of the epigenetic state of genes covered by the tiling array in control and mutant p53-depleted U251 cells we focused on changes in active histone marks, H3K4me3 and H3K9Ac, and RNA polymerase II recruitment and processivity. H3K4me3 and H3K9Ac marks are enriched in active promoter regions and the phosphorylation of serine 5 (S5-P) and serine 2 (S2-P) in the CTD of RNA polymerase II have been described to define initiated and elongating complexes, respectively. We performed the ChIP-chip experiments for H3K4me3, H3K9Ac, RNA polymerase II (S5-P) and RNA polymerase II (S2-P) from U251 cells transfected with p53-specific siRNA or control siRNA (2 biological replicates each). To analyze binding of mutant p53 to the genes covered by the tiling array we performed mutant p53 ChIP-chip experiments in 4 biological replicates of. In addition, we analyzed the distribution of SP1 and ETS1 binding sites in 3 biological replicates.

Dataset Information

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

Publications

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

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