Histone Modifications in Mammalian Early Embryos

Early mammalian development entails one of the most extensive and physiologically relevant episodes of epigenomic reprogramming. Following fertilization, two highly specialized gametic epigenomes are reset to establish a totipotent zygotic state and are subsequently reorganized to enable lineage specification and pluripotency. A central component of this transition is the dynamic regulation of histone modifications that mark transcriptionally active and inactive chromatin. Studies in mouse embryos have revealed a distinctive sequence of events in which noncanonical, oocyte- and embryo-specific chromatin states are transiently established and then progressively replaced by canonical, somatic-like patterns around zygotic genome activation. However, comparative analyses across mammals demonstrate that several of these features, including broad noncanonical histone domains and Polycomb-mediated imprinting, are not universally conserved and differ substantially in humans and other species. In this chapter, we summarize recent findings on the dynamics of active and inactive histone marks during early embryogenesis, with a focus on principles derived from the mouse model and their limitations. We discuss how histone modifications contribute to transcriptional competence, repression, and lineage priming, how these processes vary across species, and how they together constitute an epigenomic "rebooting" that balances the erasure of parental memory with the preservation of essential regulatory information.