GSE131068
An ER stress inducer decreases the H3k27 trimethylation (H3k27me3) modification of Crytochrome 1 in mouse embryo fibroblasts
The perturbations of ER homeostasis lead to the development of a condition referred to as ER stress. However, the repressive trimethylation on histone H3 lysine 27 (H3k27me3) under ER stress remains largely elusive. Here, we identify a critical role for H3k27me3 to impact the expression of Crytochrome 1 (Cry1). To examine the effect of ER stress on histone modification, MEFs were treated with vehicle 2µg/ml tunicamycin for 6 h. The cell lysate were collected and ChIP-seq assays were performed with the primary H3k27me3 or H3k4me3 antibody. When compared to the Vehicle group, the tunicamycin treatment reduced the 23,008 H3k27me3 peaks. In line with the roles of H3k27me3 in the regulation of gene transcriptions, annotation of the peak in genomic positions to the cloest genes indicated that many peaks were positioned after the transcription start site. Cry1 is one of the most regulated genes. However, the tunicamycin treatment slightly reduced H3k4me3 modification in MEFs. There are only 3109 peaks were decreased by the tunicamycin treatment. These data suggest ER stress selectively regulated H3k27me3 modification in the hisone 3 and reactivate Cry1 gene expression in MEFs. Overall design: Examination of 2 different histone modifications in mouse embryo fibroblasts.