The glucocorticoid receptor (GR) is a hormone-inducible transcription factor involved in metabolic and anti-inflammatory gene expression responses. What determines the specific genes that the GR regulates remains unclear.
To investigate what controls interaction between GR binding sites and their target genes, the Reddy lab, along with Charlie Gersbach and Greg Crawford, used in situ Hi-C to generate high-resolution, genome-wide maps of chromatin interactions before and after glucocorticoid treatment. They found that GR binding to the genome typically does not cause new chromatin interactions to target genes, but instead acts through chromatin interactions that already exist prior to hormone treatment.
Their findings, published online on July 18 in Cell Systems, offer new insights into the mechanisms underlying glucocorticoid-mediated gene activation and repression.