Project description:Genome-wide maps of cytosine methylation, cytosine hydroxylmethylation and small non coding RNAs in mouse ES cells and upon guided differentiation to mesoendoderm cells. Mouse embryonic stem cells (E14) were guided differentiated into mesoendoderm lineages by activin-A induction. cells in three time points (day0, day4 and day6) were collected. The genome-wide studies on three cell types were summerized as following: cytosine methylation data were generated using methylated DNA immunoprecipitation followed by sequencing (MeDIP-seq) and DNA digestion by methyl-sensitive restriction enzymes followed by sequencing (MRE-seq); DNA product for 5-hmC_ChIP-seq is generated by a selctive chemical labeling method (Nat. Biotechnol. 2011, 29, 68-72). E14 Day0 data for MRE-seq and MeDIP-seq are released first in previous publication and included in prior series GSE36114 ChIP-seq, 5-hmC-seq, MeDIP-Seq, MRE-Seq, ncRNA-Seq, and RNA-seq on activin-induced differentiating ES cells at 3 time points.
Project description:We generated two types 5-methylcytosine (5-mC) data in E14 mouse embryonic stem cells, using methylated DNA immunoprecipitation followed by sequencing (MeDIP-seq) and DNA digestion by methyl-sensitive restriction enzymes followed by sequencing (MRE-seq). Examination of 2 histone modifications and methylation in mouse embryonic stem cells
Project description:Genome-wide maps of cytosine methylation, cytosine hydroxylmethylation and small non coding RNAs in mouse ES cells and upon guided differentiation to mesoendoderm cells. Mouse embryonic stem cells (E14) were guided differentiated into mesoendoderm lineages by activin-A induction. cells in three time points (day0, day4 and day6) were collected. The genome-wide studies on three cell types were summerized as following: cytosine methylation data were generated using methylated DNA immunoprecipitation followed by sequencing (MeDIP-seq) and DNA digestion by methyl-sensitive restriction enzymes followed by sequencing (MRE-seq); DNA product for 5-hmC_ChIP-seq is generated by a selctive chemical labeling method (Nat. Biotechnol. 2011, 29, 68-72). E14 Day0 data for MRE-seq and MeDIP-seq are released first in previous publication and included in prior series GSE36114
Project description:Classically, there are two types of endometrial cancer, endometrioid adenocarcinoma (EAC), or Type I; and uterine papillary serous carcinoma (UPSC), or Type II. These two types of cancers exhibit distinct DNA methylation levels in promoters of many genes. In EAC, many tumor suppressor genes were silenced due to DNA hypermethylation at their promoter region. However, promoters of many of these genes remained unmethylated in UPSC. Here, we described complete DNA methylome maps of endometrioid adenocarcinoma, uterine papillary serous carcinoma, and normal endometrium, by applying a combined strategy of methylated DNA immunoprecipitation sequencing (MeDIP-seq) and methylation-sensitive restriction enzyme sequencing (MRE-seq). We took a complementary and orthogonal approach to identify DNA methylation changes unique to the two endometrial cancer subtypes in an unbiased fashion. We generated complete DNA methylome maps for endometrioid adenocarcinoma (EAC, three samples), uterine papillary serous carcinomas (UPSC, three samples), and normal endometrium (pooled samples) by integrating data from methylated DNA immunoprecipitation sequencing (MeDIP-seq) and methylation-sensitive restriction enzyme sequencing (MRE-seq).
Project description:We generated two types 5-methylcytosine (5-mC) data in E14 mouse embryonic stem cells, using methylated DNA immunoprecipitation followed by sequencing (MeDIP-seq) and DNA digestion by methyl-sensitive restriction enzymes followed by sequencing (MRE-seq).
Project description:Understanding the impact of DNA methylation within different disease contexts often requires accurate assessment of these modifications in a genome-wide fashion. Frequently, patient-derived tissue stored in long-term hospital tissue banks have been preserved using formalin-fixation paraffin-embedding (FFPE). While these samples can comprise valuable resources for studying disease, the fixation process ultimately compromises the DNA’s integrity and leads to degradation. Degraded DNA can complicate CpG methylome profiling using traditional techniques, particularly when performing methylation sensitive restriction enzyme sequencing (MRE-seq), yielding high backgrounds and resulting in lowered library complexity. Here, we provide results using our new MRE-seq protocol (Capture MRE-seq), tailored to preserving unmethylated CpG information when using samples with highly degraded DNA. The results using Capture MRE-seq correlate well (0.92) with traditional MRE-seq calls when profiling non-degraded samples, and can recover unmethylated regions in highly degraded samples when traditional MRE-seq fails, which we validate using bisulfite sequencing-based data (WGBS) as well as methylated DNA immunoprecipitation followed by sequencing (MeDIP-seq).
Project description:Genome-wide analysis of histone modification (H2AZ, H3K27ac, H3K27me3, H3K36me3, H3K4me1, H3K4me2, H3K4me3 and H3K9me3), protein-DNA binding (TAF1, P300, Pou5f1 and Nanog), cytosine methylation and transcriptome data in mouse and human ES cells and pig iPS cells We generated histone modification data (H2AZ, H3K27ac, H3K27me3, H3K36me3, H3K4me1, H3K4me2, H3K4me3 and H3K9me3) and protein-DNA binding data (TAF1, P300, Pou5f1 and Nanog) using Chromatin Immunoprecipitation followed by short sequencing (ChIP-seq), cytosine methylation data using methylated DNA immunoprecipitation followed by sequencing (MeDIP-seq) and DNA digestion by methyl-sensitive restriction enzymes followed by sequencing (MRE-seq), transcriptome data with RNA short sequencing (RNA-seq) in human embryonic stem cells, mouse embryonic stem cells, pig induced pluripotent stem cells and mouse embryonic stem cells under activin-A-induced-differentiation. Examination of 8 histone modifications, 4 protein-DNA binding, cytosine methylation and transcriptome in human embryonic stem cells, mouse embryonic stem cells, pig induced pluripotent stem cells and mouse embryonic stem cells under activin-A-induced-differentiation.
