BACH1 recruits STAT3 to enhance leukemia inhibitory factor receptor activity and augments the self-renewal capacity of mouse embryonic stem cells [ChIP-seq]

The relationship between enhancer region chromatin accessibility of the Leukemia Inhibitory Factor Receptor (Lifr) gene and the regulation of self-renewal in mouse embryonic stem cells (mESCs)remains poorly understood. In this study, we elucidate the BACH1 enhances the activity of Lifr enhancer by recruiting STAT3 and activates the LIFR-STAT3 signaling pathway by promoting the LIFR expression, thereby maintaining the self-renewal of mESCs. Our results complement a novel insight into the regulatory role of BACH1 in maintaining the self-renewal capacity of mESCs. Overall design: ChIP-seq of the BTB domain and CNC homolog 1 (BACH1) in mouse embryonic stem cells. ChIP-seq of BACH1 in BACH1-KO mouse embryonic stem cells . Bach1-KO mESCs were generated by using CRISPR/Cas9 genome editing technology. ChIP-seq of the histone modification H3K27ac in mouse embryonic stem cells.