Project description:To investigate enhancer activity in OE19 cells, we performed ATAC_STARR-seq and CUT&Tag_STARR-seq using antibodies against H3K27ac, BRD4 and MED1 .
Project description:The impact of depleting SAF-A (HNRNPU) on the genome-wide replication timing program in human hTERT-RPE1 cells was assessed by a single-cell replication timing analysis.
Project description:Laser Capture Microdissection (LCM) followed by RNA-seq of apical and basal domains of follicle cells from stage 9-10B Drosophila egg chambers. The experiment is composed of 5 Apical and 5 Basal biological replicates. Each biological replicate consists of a pool of 10 LCM fragments. Each fragment consists of 5-10 adjacent cell domains microdissected from either the apical half or the basal half of the follicular epithelium.
Project description:DNA methylation is essential for silencing transposable elements and some genes in higher eukaryotes, implying that this modification must be tightly controlled. However, accidental changes in DNA methylation can be transmitted through mitosis, as in cancer, or meiosis, leading to epiallelic variation. Here, we demonstrate the existence of an efficient and faithful mechanism that protects against transgenerational loss of DNA methylation in the plant Arabidopsis. This process is specific to the subset of heavily methylated genomic repeats that are targeted by the RNAi machinery, and does not spread into flanking regions. Remethylation is often progressive over two to four sexual generations. This differential and incremental correction of epigenetic defects may preserve genome stability while increasing adaptive opportunities. 2 samples examined: wild type, and ddm1 mutant.
Project description:Ribosome profiling of MDA-MB-231 cells treated with Silvestrol to monitor transcriptome wide, eIF4A-dependent changes in translation efficiency Translation efficiency (TE) of mRNAs dervied from ribosome footprints was monitored in the presence or absence of 25 nM Silvestrol, an inhibitor of eukaryotic translation initiation factor 4A (eIF4A). Transcripts with reduced TE in the presence of Silvestrol were compare to transcripts with reduced TE in the presence of INK128, a catalytic mTOR inhbitor.
Project description:To investigate changes to chromatin accessibility associated with resistance to lapatinib, we performed ATAC-seq on OE19 cells treated with 500 nM lapatinib for 1, 7 and 35 days and vehicle control (DMSO) for 1 day.
Project description:This SuperSeries is composed of the following subset Series: GSE27114: Expression data from REST knock-out versus REST wild type cells during in vitro neurogenesis GSE27148: A comparative epigenomics approach reveals REST as a mediator of Polycomb reprogramming during neuronal differentiation Refer to individual Series
Project description:Transcription factors (TFs) in concert with chromatin pathways stably reset transcriptional programs during differentiation. Yet we know little how local sites of chromatin reprogramming are specified and how the estimated 3000 TF encoded in mammalian genomes contribute to chromatin dynamics. To identify candidate TFs we developed an integrated computational approach (Epi-MARA) that models chromatin dynamics in terms of predicted transcription factor binding sites and show that it correctly predicts key TFs involved in epigenome reorganization. When applied to a time course of genome-wide H3 lysine 27 trimethylation (H3K27me3), a chromatin mark set by the Polycomb system, during neuronal differentiation of murine stem cells Epi-MARA predicted that the repressive transcription factor REST contributes to a gain of H3K27me3 at a subset of promoters during the transition from the stem to the progenitor state. To test this prediction we identified, genome-wide, the actual binding sites of REST and H3K27me3 during the differentiation in cells that are either wildtype or in which REST had been deleted. REST indeed localizes to a subset of sites that gain H3K27me3 in progenitors. Importantly, absence of REST in trans leads to a loss of H3K27me3 predominantly in the neuronal progenitor state and specifically at those regions where REST was bound. This function further requires REST binding sites in cis as their mutation leads to substantial loss of H3K27me3. Taken together we provide a novel approach to identify epigenome and TF crosstalk during cellular reprogramming and prove experimentally the prediction that REST acts as an important recruiter of Polycomb repression during early steps of neurogenesis. Dataset comprises of 15 ChIP-seq samples using chromatin from embryonic stem (ES) and neuronal progentor (NP) of wildtype and RESTko cells, which was immunoprecipitated, using antibodies against REST, H3K27me3, or Suz12