GSE131848
Changes in chromatin accessibility in male mouse liver induced by naturally occurring endogenous pulses of plasma growth hormone (GH)-activated STAT5
Sequencing files provided here are mouse liver DNase-seq for male mouse livers collected at either a peak or trough of GH/STAT5 activity. This is part of a larger study that includes DNase-seq in mouse liver from hypophysectomized males, females, and hypox-male mice given a single dose of GH. DNase hypersensitivity site (DHS) analysis of these livers established that the  naturally occurring, endogenous male rhythm of plasma GH pulse-stimulated liver STAT5 activation induces dynamic, repeated cycles of chromatin opening and closing at several thousand liver DHS and comprises a novel mechanism conferring male bias to liver chromatin accessibility. Overall design: DNase-seq of individual male mouse livers obtained from mice euthanized either at a peak or at a trough of STAT5 DNA-binding activity ('STAT5-High' and STAT5-low', respectively), as determined by EMSA analysis. DNase-seq libraries for liver samples G74A_M1 and G74A_M2 differ from all of the other STAT5_High samples, and thus are marked 'outlier', insofar as their STAT5 DNA-binding (EMSA) activity is indicative of a STAT5-high liver, but their DNase-seq profiles were more similar to those of STAT5-low activity livers. In contrast, DNase-seq library for liver sample G92_M5 showed STAT5 DNA-binding (EMSA) activity indicative of a STAT5-low liver, but its DNase-seq profile was more similar to that of STAT5-high activity livers.