Environmental stress and transposon transcription in the mammalian brain

Abstract

We recently reported that acute stress causes a substantial upregulation of the epigenetic mark, Histone H3 Lysine 9 Trimethyl (H3K9me3) in the rat hippocampus within an hour of acute stress exposure. To determine the function of this change we used ChIP-sequencing to determine where this silencing mark was being localized. We found that it showed a strong bias toward localization at more active classes of retrotransposable elements and away from genes. Further, we showed that the change was functional in that it reduced transcription of some of these elements (notably the endogenous retrovirus IAP and the B2 SINE). In this commentary we examine these results, which appear to describe a selective genomic stress response and relate it to human health and disease, particularly stress related maladies such as Post-traumatic Stress Disorder, which have recently been shown to have both epigenetic elements in their causation as well as differences in epigenetic marking of retrotransposons in human patients.

Keywords: chromatin; corticosteroid; epigenetic; heterochromatin; hippocampus; post-traumatic stress disorder.

Figure 1. Phylogenetic breakdown of numbers of 5 kb mobile or repetitive element genomic islands showing increased H3Kme3 levels (Stress Up) vs. reduced levels (Stress Down). Adapted from reference .

Figure 2. Levels of the H3K9 specific methyltransferases Suv39h2 mRNA in rat hippocampus under basal conditions and 1 h after acute stress. Adapted from reference .