Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

ChIP-Seq of human normal pancreatic islets with anti-histone antibodies to analyse histone modifications

ABSTRACT: This experiment used ChIP-seq technology to create a genome-wide profile of histone marks in normal human pancreatic islets. In the current work we analyzed two histone marks associated with gene expression (H3K4me3, H3K4me1) and marks associated with gene repression(H3K27me3). Each mark was anayzed using samples obtained from four donors (n=4). Chromatin Immunoprecipitations (ChIPs) for histone marks were performed using specific anti-histone antibodies. Enrichment of each sample was calulated with respect to its individual input using qPCR. Samples were sequenced with Solexa and sequenced DNA from both Input (n=4) and ChIP (n = 4) samples were aligned to the NCBI Genome Build 36.1 Ð Hg18 to determine regions that were enriched for binding by modified histones.

ORGANISM(S): Homo sapiens

SUBMITTER: Reena Bhandare

PROVIDER: E-MTAB-189 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Publications

Genome-wide analysis of histone modifications in human pancreatic islets.

Bhandare Reena R Schug Jonathan J Le Lay John J Fox Alan A Smirnova Olga O Liu Chengyang C Naji Ali A Kaestner Klaus H KH

Genome research 20100224 4

The global diabetes epidemic poses a major challenge. Epigenetic events contribute to the etiology of diabetes; however, the lack of epigenomic analysis has limited the elucidation of the mechanistic basis for this link. To determine the epigenetic architecture of human pancreatic islets we mapped the genome-wide locations of four histone marks: three associated with gene activation-H3K4me1, H3K4me2, and H3K4me3-and one associated with gene repression, H3K27me3. Interestingly, the promoters of t ...[more]

PMID: 20181961

Similar Datasets

Project description:The model describing that aberrant CpG island (CGI) methylation leads to transcription repression of tumor suppressor genes and thereby is implicated in tumor progression has been established in many cancers. However, recent studies indicated aberrantly hypermethylated genes in multiple cancers are already repressed in pre-cancerous tissues despite their promoters are hypomethylated. Here, we hypothesized that the occurrence of CGI promoter hypermethylation in cancers are associated with Polycomb-repressive complex and the associated H3K27me3 mark in pre-cancerous tissues. By using a ChIP-BS-seq technology that examines methylation of the DNA fragments precipitated by the antibodies to histone modifications, we provided direct evidences showing that genes highly enriched with H3K27me3 marks both in cancer and normal cells became aberrantly hypermethylated in CGI promoters in cancer cells in comparison with normal cells. Furthermore, we confirmed that these genes consistently were significantly hypermethylated in TCGA primary cancer in comparison with normal tissues. Thus, we provided direct evidences supporting that the presence of H3K27m3 may serve as a guide to promoter hypermethylation. This will spur future work on epigenetic signature of combined histone and DNA methylation that could define a cancerM-bM-^@M-^Ys epigenetic abnormalities, therefore helping distinguish subtypes of cancers and aiding future diagnosis and therapeutics of cancers. We applied ChIP-BS technology to examine H3K27me3 marks, which are catalyzed by the SET domain histone methyltransferase EZH2 and have a repressive function with 50bp pair-end sequencing. found H3K27me3 marks were enriched preferentially at CpG islands, (+/-500) transcription start sites (TSSs) and exons in two GC cell lines (BGC-823 and AGS). In YH cells, H3K27me3 marks were only preferentially enriched at CpG islands. In contrast, Hela cells presented a reverse pattern with highest H3K27me3 enrichment in intergenic regions. To confirm this result in Hela cells, we performed two independent replicates of ChIP-Seq and ChIP-BS-seq. Cause of useful was relative small. we still sequenced one 100bp pe reads replicate for H3K4me3 and two replicate for H3K27me3 ChIP-BS-seq.

Dataset Information

ChIP-Seq of human normal pancreatic islets with anti-histone antibodies to analyse histone modifications

Publications

Genome-wide analysis of histone modifications in human pancreatic islets.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets