Project description:This dataset contains ChIP-seq data profiling genomic binding of H3K27ac and H3K4me3 in single cell-derived control, as well as CRISPR/Cas9 induced tRNA gene deletion clones and intergenic region deletion clones in human cancer cell lines HAP1. In this study, we found a large genomic deletion of 10q23 in Cas9 modified clones and further investigate the effect of H3K27ac binding.
Project description:rs2431697 is a SLE risk SNP, genetic and epigenomic analysis indicate that rs2431697-containing region is an enhancer region. To test the function and regulated genes of rs2431697-containing genes, we deleted rs2431697-containing region in U-937 cells, and performed the RNA-seq to detect the gene expression profiles.
Project description:rs2280381 is an autoimmune disease susceptible loci, which have be reported to be associated with SLE, RA and SSc.Genetic and epigenomic analysis indicate that rs2280381-containing region is an enhancer region in monocyte. To test the function and regulated genes of rs228381-containing region, we deleted rs2280381 ~120bp sequence in U-937 cells, and performed the RNA-seq to detect the gene expression profiles.
Project description:rs2280381 is an autoimmune disease susceptible variant, which has been reported to be associated with SLE, RA and SSc. Genetic and epigenomic analysis indicate that the rs2280381-containing region is an enhancer region in monocyte. To test the function and regulated genes of the rs228381-containing region, we deleted the rs2280381 ~120bp sequence in U-937 cells, and performed the RNA-seq to detect the gene expression profiles.
Project description:Genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) associated with increased risk for colorectal cancer (CRC). A molecular understanding of the functional consequences of this genetic variation is complicated because most GWAS SNPs are located in non-coding regions. After identifying H3K27Ac peaks in HCT116 colon cancer cells that harbor SNPs associated with an increased risk for CRC, we used CRISPR/Cas9 nuclease to delete 2 CRC risk-associated H3K27Ac peaks (E7 and E24), a peak that is not associated with CRC risk (18qE) and a region that doesn?t have H3K27Ac peak (18qNE) from HCT116 cells and analyzed effects on the transcriptome and epigenome. We also deleted E7 region from HEK 293 cells and analyzed effects on the transcriptome of HEK 293. We also confirmed the physical interaction between enhancers of our interest and their putative target genes. Analysis of RNA-seq data and ChIP-seq between control clones and enhancer deleted clones in HCT116 cell. For Control, gRNA empty vectorplasmid was transfected with Cas9-GFP. For Deletion, gRNAs that have enhancer target sequences were transfected along with Cas9-GFP. Cells with high GFP expression were identified using fluorescence-activated cell sorting. Sorted cells were plated into individual wells of a 24 well plate and then re-plated as single cells in 10cm dishes and subsequently expanded for further analyses. Samples used in this study were clonal populations. Interaction profiling of enhancers of interest with putative target genes using 4C-seq
Project description:To test the genomic region containing rs2431697 whether forms a cognate enhancer-promoter loop with the miR-146a promoter and modulates the expression of miR-146a, we perfomed 4C-seq in U-937 cell line based on the rs2431697 view point and miR-146a promoter view point.
Project description:This dataset contains Xdrop followed by oxford nanopore long read sequencing performed in target tRNA gene deletion (t8) and intergenic region deletion (i50) clones in HepG2 . By applying de novo assembly based approach to Xdrop-LRS data, we identified Cas9-induced on-target genomic alteration.
Project description:We performed RNA-Seq analysis of wildtype and three EPAS1-/- 786-O single cell clones generated by CRISPR/Cas9 to identify the HIF-2a-responsive genes in this cell line. Samples from wildtype 786-O cells treated with DMSO or HIF-2a antagonist compound C2 were also included in this analysis.
Project description:Mus musculus macrophages were derived from bone marrow, and treated with the supernatant of of DYRK1B-deletion (multiple clones) or Wildtype mKpc4 cells.
