which prevented the eviction of EED from the Kiss1 promoter at LJ, also prevented the LJ increase in both H3K4me3 and H3K9,14ac abundance (Fig. 5f,g). To determine if the chromatin landscape of the Kiss1 promoter continues to change as the pubertal process unfolds, we measured both H3K27me3 and its opposing counterpart H3K4me3 43 at LP, when the preovulatory surge of gonadotropins take place, and found a significant decrease in H3K27me3 levels, accompanied by persistently elevated levels of H3K4me3 (Supplementary Fig. 6a). Altogether these results are compatible with the notion that a repressive PcG-depending tone on the Kiss1 gene is lifted at the onset of puberty, and the status of the associated chromatin shifts from an inhibitory to an activating configuration, leading to activation of the Kiss1 gene (Supplementary Fig. 6b)
