Project description:We report the actively transcribed chromatin regions in EndoC-βH1 Cells that are associated with histone H3 lysine 27 acetylation mark.
Project description:EndoC-βH1 is emerging as a critical human β cell model to study the genetic and environmental etiologies of β cell (dys)function and diabetes. Comprehensive knowledge of its molecular landscape is lacking, yet required, for effective use of this model. Here, we report chromosomal (spectral karyotyping), genetic (genotyping), epigenomic (ChIP-seq and ATAC-seq), chromatin interaction (Hi-C and Pol2 ChIA-PET), and transcriptomic (RNA-seq and miRNA-seq) maps of EndoC-βH1. Analyses of these maps define known (e.g., PDX1 and ISL1) and putative (e.g., PCSK1 and mir-375) β cell-specific transcriptional cis-regulatory networks and identify allelic effects on cis-regulatory element use. Importantly, comparison with maps generated in primary human islets and/or β cells indicates preservation of chromatin looping but also highlights chromosomal aberrations and fetal genomic signatures in EndoC-βH1. Together, these maps, and a web application we created for their exploration, provide important tools for the design of experiments to probe and manipulate the genetic programs governing β cell identity and (dys)function in diabetes.
Project description:We generated genome-wide chromatin state and RNA Polymerase II binding maps in mouse erythroid cells by ChIP-Seq. Examination of 4 different histone modifications (H3K4me3, H3K4me1, H3K27me3, H3K27ac) and RNA Polymerase II (RNAP2) binding in mouse erythroid cells (Ter119+).