Methylated DNA Immunoprecipitation (MeDIP) using a custom type 2 diabetes and related phenotypes array
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Gareth Wilson
PROVIDER: E-GEOD-20553 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Custom array designed to tile Linkage Disequilibrium Blocks of T2D GWAS SNPs, monogenic candidates for T2D and Obesity, and all plausible imprinted loci from human and mouse data.
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Project description:This SuperSeries is composed of the following subset Series: GSE27459: Human cerebral cortex DNA methylation by MeDIP-Chip GSE27460: Rhesus macaque cerebral cortex DNA methylation profiling by MeDIP-Chip Refer to individual Series
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Project description:Using meDIP-chip to provide methylation profile in zdp mutant and identify hypermethylated regions comparing to wild type Arabidopsis plants. Examination of zdp mutant's methylome. 4 samples(1 mutant, 1 WT, each has two biological replicates)
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Project description:Malignant melanoma is the most fatal skin cancer with a high degree of genetic and epigenetic aberrations. To investigate the role of DNA methylation on melanoma heterogeneity, we performed methylated DNA immunoprecipitation (MeDIP) microarray analysis of 10 primary melanoma cell cultures. methylated DNA immunoprecipitation (MeDIP) microarray analysis of 10 primary melanoma cell cultures
2014-05-28 | E-GEOD-57971 | biostudies-arrayexpress
Project description:Aberrational epigenetic marks are believed to play a major role in establishing the abnormal features of cancer cells. Rational use and development of drugs aimed at epigenetic processes requires an understanding of the range, extent, and roles of epigenetic reprogramming in cancer cells. Using ChIP-chip and MeDIP-chip approaches, we localized well-established and prevalent epigenetic marks (H3K27me3, H3K4me3, H3K9me3, DNA methylation) on a genome scale in several lines of putative glioma stem cells (brain tumor stem cells, BTSCs) and, for comparison, normal human fetal neural stem cells (fNSCs). We determined a substantial M-bM-^@M-^\coreM-bM-^@M-^] set of promoters possessing each mark in every surveyed BTSC cell type, which largely overlapped the corresponding fNSC sets. However, there was substantial diversity among cell types in mark localization. We observed large differences among cell types in total number of H3K9me3+ positive promoters and peaks and in broad modification areas for H3K27me3 and, to a lesser extent, H3K9me3. We verified that a change in a broad modification (defined as >50 kb peak length) affected gene expression of CACNG7. We detected large numbers of bivalent promoters, but most bivalent promoters did not display direct overlap of contrasting epigenetic marks, but rather occupied nearby regions of the proximal promoter. There were significant differences in the sets of promoters bearing bivalent marks in the different cell types and few consistent differences between fNSCs and BTSCs. Overall, our M-bM-^@M-^\core setM-bM-^@M-^] data establishes sets of potential therapeutic targets, but the diversity in sets of sites and broad modifications among cell types underscores the need to carefully consider BTSC subtype variation in epigenetic therapy. Our results point toward substantial differences among cell types in the activity of the production/maintenance systems for H3K9me3 and for broad regions of modification (H3K27me3 or H3K9me3). Finally, the unexpected diversity in bivalent promoter sets among these multipotent cells indicates that bivalent promoters may play complex roles in the overall biology of these cells. These results provide key information for forming the basis for future rational drug therapy aimed at epigenetic processes in these cells. ChIP-chip and MeDIP-chip localization of histone modifications and DNA methylation in glioma stem cells and fetal neural stem cells comparison of 4 lines of brain tumor stem cells to each other and to normal fetal neural stem cells
2014-08-30 | E-GEOD-60806 | biostudies-arrayexpress
Project description:The analysis of DNA methylation profiles was performed by methylated DNA immunoprecipitation (MeDIP) using anti-5-methylcytidine antibody (Eurogentec, Seraing, Belgium) followed by the Human 244K Agilent CpG island microarray (Agilent, Santa Clara, CA)
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Project description:BackgroundDNA methylation contributes to the regulation of gene expression during development and cellular differentiation. The recently developed Methylated DNA ImmunoPrecipitation (MeDIP) assay allows a comprehensive analysis of this epigenetic mark at the genomic level in normal and disease-derived cells. However, estimating the efficiency of the MeDIP technique is difficult without previous knowledge of the methylation status of a given cell population. Attempts to circumvent this problem have involved the use of in vitro methylated DNA in parallel to the investigated samples. Taking advantage of this stratagem, we sought to improve the sensitivity of the approach and to assess potential biases resulting from DNA amplification and hybridization procedures using MeDIP samples.FindingsWe performed MeDIP assays using in vitro methylated DNA, with or without previous DNA amplification, and hybridization to a human promoter array. We observed that CpG content at gene promoters indeed correlates strongly with the MeDIP signal obtained using in vitro methylated DNA, even when lowering significantly the amount of starting material. In analyzing MeDIP products that were subjected to whole genome amplification (WGA), we also revealed a strong bias against CpG-rich promoters during this amplification procedure, which may potentially affect the significance of the resulting data.ConclusionWe illustrate the use of in vitro methylated DNA to assess the efficiency and accuracy of MeDIP procedures. We report that efficient and reproducible genome-wide data can be obtained via MeDIP experiments using relatively low amount of starting genomic DNA; and emphasize for the precaution that must be taken in data analysis when an additional DNA amplification step is required.
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Project description:Comparing genetic differences between human and nonhuman primates is a fundamental method to dissect the molecular mechanisms underlying the improved human cognitive ability during evolution. Besides DNA sequence divergences, gene regulation differences between human and nonhuman primates have been shown to be more prominent. DNA methylation is an important type of epigenetic modification that plays critical roles in gene regulations. Trans-generational inheritances of DNA methylation in mammals are widely accepted, suggesting the evolutionary role of DNA methylation. To test if DNA methylation has contributed to the evolution of human brain, with the use of MeDIP-Chip and SEQUENOM MassARRAY, we conducted a systematic analysis to identify the differentially methylated DNA regions (DMRs) between human and rhesus macaque in the cerebral cortex. We first identified a total of 150 candidate DMRs by the MeDIP-Chip method, among which 6 DMRs were confirmed by the SEQUENOM MassARRAY method. And 4 of them were further confirmed using independent samples, while the other 2 were failed to test due to technical difficulties. All the 6 DMRs were in CpG islands or close to CpG islands, and a MIR3 repeat element was located in one DMR, but no repeats was found in the other 5 DMRs. For the 6 DMR genes, most have neural related functions, and their proteins tend to be conserved. Additionally, we found the DNA sequence changes at CpG sites contributed to the species-specific DNA methylation. Our study shed light on the researches of trans-generational epigenetic inheritance and the roles of DNA methylation in evolution, especially human evolution. Compare the DNA methylation levels between human and rhesus macaque
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