It is now clear that PcG mediated gene silencing requires H3K27me3; a modification catalyzed by PRC2. H3K27me3 then provides a “docking” site for the CBX components of PRC1 to form a repressive complex 20, 28. In turn, YY1 recruits PRC2 and PRC1 proteins, in addition to H3K27me3, to gene promoters to enhance transcriptional silencing 32. The eviction of EED from the Kiss1 promoter at the onset of the pubertal process would predict a concomitant loss of H3K27me3 at this time. Instead, H3K27me3 content decreased at LP, i.e., by mid-puberty. Contrasting with this protracted pattern of change, the abundance of H3K4me3 and acetylated histone 3 (H3 K9/14ac), two histone marks associated with gene activation 39, 41, increased markedly at LJ, i.e., at the initiation of puberty. Because H3K4me3 is a histone mark that opposes the repressive actions of H3K27me3 43, we examined the association of H3K4me3 to the Kiss1 promoter at mid-puberty, and found it to remain as elevated as in LJ. This developmental profile is consistent with the pattern of bivalent association observed for H3K27me3 and H3K4me3 in the promoter
