Epigenetic factors tightly regulate gene expression and thereby could contribute to the subregionally specific deficit in Crem observed in SHRs. To explore this hypothesis, we studied histone post-translational modifications which play well-documented roles in transcriptional regulation. Chromatin from the AcbC and AcbSh were immunoprecipitated with antibodies specific for pan-acetylated histone H3 (H3Ac) and trimethylated histone 3 lysine 4 (H3K4me3), both typically markers of transcriptional activation, and dimethylated histone 3 lysine 9 (H3K9me2), a repressive marker. The profile of H3Ac revealed lower enrichment of this mark close to the transcriptional start site (TSS) in the AcbC of SHRs (t13=3.05, p=0.009, Fig. 2g and Supplementary Fig. 5a), but not the AcbSh (t14=0.72, p>0.05, Supplementary Fig. 5d). Similarly, lower H3K4me3 enrichment was observed in the AcbC of SHRs around the TSS (−0.05 kb relative TSS, t13=2.98, p=0.01) and in a downstream region (+0.17 kb relative TSS, t13=2.49, p=0.02, Fig. 2h and Supplementary Fig. 5b,e). Enrichment of H3K9me2 showed no difference between the rat strains at any examined loci except +0.17 kb downstream the TSS in the AcbSh (t14=3.31, p=0.005, Supplementary Fig. 5c,f). These
