Supplementary Figure 6: H3K9me3 and KAP1 occupancy at HSP90-target ERVs and the effect of stress on ERV transcription
From: The evolutionary capacitor HSP90 buffers the regulatory effects of mammalian endogenous retroviruses
(a) ChIP-qPCR for HSP90 in ESCs. Enrichment is shown as the mean (± SEM). (b) ChIP-qPCR for Kap1 and H3K9me3 in control ESCs and ESCs treated with HSP90 inhibitor. Enrichment is shown as the mean of three independent cell-culture replicates (± SEM) relative to control conditions. The red dotted line indicates the signal intensity in cells not treated with HSP90 inhibitor (c,d) Effect of Kap1 knock-out on H3K9me3 modification at and around HSP90-targeted ERVs, namely IAPEz (c) and MERV-L (d). (e) Experimental design to study the effect of HSP90 inhibition on genes with different strain-specific upstream ERV elements. All genes tested have an ERV either in 129S1 or CASTEiJ strain or both, but no ERV in C57BL6. Effect of HSP90 inhibitor on gene expression was analyzed by quantitative reverse transcription-PCR. Fold Change is shown as a mean of three independent cell-culture experiments (± SEM). (f) Different conditions mimicking environmental stresses upregulate IAPEz and MERV-L in ESC as shown by quantitative PCR. Fold change is shown as means of three independent cell-culture experiments (±SEM).
