![]() ![]() Excitingly, Dppa2/4 also bind non-ZGA gene promoters, including bivalent promoters ( 6, 9– 11), however the significance of this is unknown. Recently, we and others revealed a role for the small heterodimerising nuclear proteins Developmental Pluripotency Associated 2 (Dppa2) and 4 (Dppa4), in regulating zygotic genome activation (ZGA)-associated transcripts ( 6– 8). Consequently, our understanding of the precise regulation and functional importance of bivalent chromatin is lacking ( 3). Furthermore, it is unknown what effect removal of both H3K4me3 and H3K27me3 at bivalent genes has on development as designing a clean experimental system targeting both without altering the rest of the epigenome is challenging. However, it is largely unclear how these epigenetically primed states are targeted specifically to these promoters ( 3). In pluripotent cells, bivalent chromatin is found at important developmental gene promoters, poising them for future activation or silencing ( 4, 5). This co-occurrence of active associated H3K4me3 and repressive associated H3K27me3 histone modifications is catalysed by Mll2, part of the COMPASS complex ( 1, 2) and Ezh2, part of the Polycomb Repressive 2 (PRC2) complex, respectively (reviewed in ( 3)). Perhaps the best understood example of epigenetic priming is bivalent chromatin. This temporal uncoupling of molecular events is especially fitting in the context of early development where genes that are not yet expressed need to avoid permanent silencing prevalent in the peri-implantation embryo. Epigenetic priming describes the establishment of a competent epigenetic landscape that facilitates efficient transcriptional responses at a future point in time. ![]()
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