Project description:Chromatin accessibility was assayed in wildtype or Dppa2 knockout ESC after 26 days of release of the trigger imposed by epigenetic editing. Samples were collected in two clonal knockout and wildtype lines after sorting at FACS of cells which maintained a repressive Esg1-tdTomato (TOMneg) reporter expression after 26 days of DOX washout (release of the trigger).
Project description:Chromatin accessibility was assayed in ESC after epigenetic editing with dCas9::KRAB (or dCas9::GFP as a control) and subsequently in ESC and Endoderm differentiated cells upon release of the trigger. Samples were collected in two biological replicates after 7 days of DOX induction in ESC (epigenetic editing) and after 7 days of DOX washout (release of the trigger) in ESC and Endoderm cells.
Project description:Open chromatin regions were analyzed by ATAC-seq in t(3;8) K562 and wild type K562 to characterize the MYC super-enhancer region. ATAC-seq was performed as described (Buenrostro et al., 2013) with a modification in the lysis buffer to reduce mitochondrial DNA contamination.
Project description:Open chromatin regions were analyzed by ATAC-seq in MUTZ3 and MOLM1 cell lines (both inv(3) AML) to characterize the GATA2 super-enhancer region. ATAC-seq was performed as described (Buenrostro et al., 2013) with a modification in the lysis buffer to reduce mitochondrial DNA contamination.
Project description:The human iPSC line H19101 was differentiated in vitro into cardiomyocytes using a 20-day differentiation protocol (Burridge et al. 2014 PMID 24930130 and Montefiori et al 2018 PMID 29988018 ). 50,000 cardiomyocytes were used in each ATAC-seq experiment. 8 replicates were pooled to obtain the final peak file.
Project description:Transcriptome and epigenome of Treg and effector T cells in various activation states. RNA-seq, ATAC-seq, and histone modification ChIP-seq of sorted cell populations
Project description:Genome Wide Association Studies (GWAS) have been successful in yielding >60 loci for Systemic Lupus Erythematosus (SLE). However, it is known that GWAS just reports genomic signals and not necessarily the precise localization of culprit genes, with eQTL efforts only able to infer causality to a minority of such loci. Thus, we sought to carry out physical and direct ‘variant to gene mapping’ by integrating results from high-throughput chromatin conformation capture and ATAC-seq assays. This experiment refers to the ATAC-seq part of our work. To determine informative proxy SNPs for each of the SLE GWAS sentinel loci, we generated ATAC-seq open chromatin maps for primary human T Follicular Helper (TFH) cells from tonsils of healthy volunteers (3 biological replicates), a model relevant to SLE as TFH operate upstream of the activation of pathogenic autoantibody-producing B cells during the disease. We also generated open chromatin maps for naive CD4-positive helper T cells (3 biological replicates).
Project description:To determine the ability of HNF4A and GATA6 to drive open chromatin formation, either HNF4A or GATA6 were overexpressed in normal oesophageal Het1A cells and ATAC-seq was performed.