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A complex that includes the protein HP1 binds to specific regulatory DNA sequences to promote local compaction of genomic regions and inhibit associated genes that drive differentiation of specific cell lineages.

Although many species-specific imprinted genes have been identified, how the evolutionary switch from biallelic to imprinted expression occurs is still unknown. Here authors find that lineage-specific ERVs active as oocyte promoters can induce de novo DNA methylation at gDMRs and imprinting.

Standard ChIP-seq protocols require large numbers of cells for high-quality datasets, limiting the application of this technique on rare cell types. Here, Brind’Amour et al. introduce an ultra-low-input ChIP-seq protocol to generate maps of covalent histone marks from as few as 1,000 cells.

The paternal genome in mice undergoes widespread DNA methylation loss post-fertilization. Here, the authors apply allele-specific analysis of WGBS data to show that a number of genomic regions are simultaneously de novo methylated on the paternal genome dependent on maternal DNMT3A activity, which induces transcriptional silencing of this allele in the early embryo.

Maternal SETD2 deficiency leads to loss of H3K36me3, aberrant DNA methylation and ectopic H3K4me3 and H3K27me3 in mouse oocytes. Maternal depletion of SETD2 causes oocyte defects and subsequent zygotic arrest.

Heterochromatin protein 1 (HP1), including HP1 α, β and γ, is a family of non-histone chromatin factors thought to be involved in chromatin organization. Here, the authors show that dimeric HP1β interacts dynamically with H3K9me3, a hallmark of heterochromatin, and bridges condensed chromatin.

Histone acetylation is a ubiquitous hallmark of transcription. Here the authors provide evidence that the majority of histone acetylation is dependent on transcription, specifically due to the requirement of RNAPII for the recruitment and activity of histone acetyltransferases.

Germline genes are repressed by DNA methylation and histone marks. Here, the authors show that specific germline genes hypomethylated pre-implantation are enriched for PRC1.6, H2AK119ub1 and H3K9me3, which coordinately repress their expression.

NSD1, which deposits H3K36me2, is a major regulator of DNA methylation in male but not in female gametogenesis. NSD1 safeguards against H3K27me3-associated transcriptional silencing.

In this Review, Janssen and Lorincz discuss the intricate and multilayered interplay between chromatin marks. Focusing on histone methylation and DNA methylation during mammalian development, they discuss the implications for gene regulation, differentiation and human disease.

De novo DNA methylation during mouse oogenesis occurs within transcribed regions. Here the authors investigate the role of species-specific long terminal repeats (LTRs)-initiated transcription units in regulating the oocyte methylome, identifying syntenic regions in mouse, rat and human with divergent DNA methylation associated with private LITs.

Vitamin C is a direct regulator of Tet enzyme activity and DNA methylation fidelity in mouse ES cells; addition of vitamin C promotes Tet activity, increases 5-hydroxymethlycytosine (5hmC) and DNA demethylation of many gene promoters, upregulates demethylated germline genes, and induces a state that more closely approximates that of the inner cell mass of the blastocyst.

Endogenous retroviruses (ERVs) are widely dispersed in mammalian genomes, and are silenced in somatic cells by DNA methylation. Here, an ERV silencing pathway independent of DNA methylation is shown to operate in embryonic stem cells. The pathway involves the histone H3K9 methyltransferase ESET and might be important for ERV silencing during the stages in embryogenesis when DNA methylation is reprogrammed.

Post-translational histone modifications are important regulators of nuclear reprogramming. A study now reveals that histone lysine demethylase KDM4A-mediated H3K9me3 demethylation in mammalian oocytes is essential for zygotic genome activation and preimplantation development.

A study in this issue demonstrates that epigenome-modifying drugs used in cancer chemotherapy induce transcription from thousands of previously unannotated transcription start sites, most of which are derived from ancient endogenous retroviruses (ERVs). This work, coupled with previous related findings, suggests that induction of ERVs, rather than direct effects on specific genes, may have a central role in the cellular responses to such agents and, in turn, their therapeutic efficacy.

An extensive analysis of HERVH (a primate-specific endogenous retrovirus) expression in human pluripotent stem cells is presented, identifying a sub-population of cells within cultured human embryonic stem cells and induced pluripotent stem cells that has characteristics of naive-state cells — the study provides evidence for a new primate-specific transcriptional circuitry regulating pluripotency.