Project description:In this study, we mapped modification of lysine 4 and lysine 27 of histone H3 genome-wide in a series of mouse embryonic stem cells (mESCs) varying in DNA methylation levels based on knock-out and reconstitution of DNA methyltransferases (DNMTs). We extend previous studies showing cross-talk between DNA methylation and histone modifications by examining a breadth of histone modifications, causal relationships, and direct effects. Our data shows a causal regulation of H3K27me3 at gene promoters as well as H3K27ac and H3K27me3 at tissue-specific enhancers. We also identify isoform differences between DNMT family members. This study provides a comprehensive resource for the study of the complex interplay between DNA methylation and histone modification landscape. Histone ChIP-seq of H3K4me3, H3K27me3, H3K4me1, and H3K27ac were performed on wild-type, Dnmt triple knock-out (Dnmt1/3a/3b; TKO), Dnmt double knock-out (Dnmt3a/3b; DKO), and respective reconstitution mouse embryonic stem cell lines
Project description:We characterized the epigenetic landscape of human colorectal cancer (CRC). To this extent, we performed gene expression profiling using high throughput sequencing (RNA-seq) and genome wide binding/occupancy profiling (ChIP-seq) for histone modifications correlated to transcriptional activity, enhancers, elongation and repression (H3K4me3, H3K4me1, H3K27Ac, H3K36me3, H3K27me3) in patient-derived organoids (PDOs), and in normal and tumoral primary colon tissues. We also generated ChIP-seq data for transcription factors YAP/TAZ in human CRC PDOs.
Project description:We characterized the epigenetic landscape of human colorectal cancer (CRC). To this extent, we performed gene expression profiling using high throughput sequencing (RNA-seq) and genome wide binding/occupancy profiling (ChIP-seq) for histone modifications correlated to transcriptional activity, enhancers, elongation and repression (H3K4me3, H3K4me1, H3K27Ac, H3K36me3, H3K27me3) in patient-derived organoids (PDOs), and in normal and tumoral primary colon tissues. We also generated ChIP-seq data for transcription factors YAP/TAZ in human CRC PDOs.
Project description:Regionalized lineage progenitor cells emerged from the onset of gastrulation would facilitate mouse embryonic patterning and build a blueprint for future development. However, the molecular mechanism especially the epigentic mechanism underlying the formation and development of lineage restricted cells has not been fully unveiled. Here,we present a comprehensive landscape of H3K4me3, H3K4me1, H3K9ac, H3K27ac, H3K27me3 and DNA methylation pattern in mouse embryo from pre-streak stage to late-streak stage, and fully analyze the epigenetic mechansim driving the embryonic patterning of mouse gastrula
Project description:To test whether HIF-1a can directly induce Timp1 expression in periosteal cells at the pre-invasive stage of head and neck squamous cell carcinoma (HNSCC), we performed Chromatin immunoprecipitation followed by sequencing (ChIP–seq) on periosteal cells derived from the pre-invasive stage of a mouse HNSCC bone invasion model by using antibodies to acetylated histone H3 Lys27 (H3K27ac), H3K4me3 and HIF-1α.
Project description:we have established TBLC-based differentiation systems to recapitulate the entire pre-implantation development Cleavage under target & tagmentation (CUT&Tag)-sequencing (CUT&Tag) for H3K4me3,H3K27ac,H3K9me3,RNA polymerase II(Pol2) and h3k27me3 in mPSC sand mTBLCs
Project description:Glioblastoma (GBM) is the most aggressive of all primary brain tumours. Here, we perform a multi-omics approach to map the promoter-enhancer interactome and the regulatory landscape of glioblastoma, including RNA-seq, ChIP-seq of histone marks (H3K4me3, H3K27ac, H3K27me3), H3K4me3 HiChIP and ATAC-seq.
Project description:CUT&RUN analysis was performed in Jurkat cells with FKBP knock-in at the MYB locus to analyze DNA bindings of phospho-MYB, H3K27ac, H3K4me3 after dTAG-mediated depletion.
Project description:VHL loss is the most common genetic alteration event in ccRCC, but its effect on epigenetic landscape has not been elucidated previously. By performing histone modifications (H3K27ac, H3K4me1, H3K4me3) from ccRCC cell lines, we describe the genome-wide cis-regulatory landscapes of VHL-deficient ccRCC tumors. We show that ccRCCs exhibit a pervasive gain of enhancers around hypoxic and metabolic transcriptional targets.
Project description:We performed Chromatin Immunoprecipitation followed by deep-sequencing in TPC1 thyroid cancer cell line model, in order to profile the genomic distribution of H3K27ac, H3K4me1 and H3K4me3, epigenetic markers of chromatin functional status. These data were integrated with RUNX2 genomic occupancy to define the nature and the activation status of the RUNX2-associated regions.