A widely studied chromatin modification associated with gene promoters is important for proper gene expression across organismal lifetime.

Epigenetic modifications to DNA can regulate E3 ubiquitin ligase activity in human cells.

A yeast genetic model for studying the function of sister histones in chromatin dynamics.

Nucleosome binding by PRC2 threads H3K27 into its active site via an interaction network set in register by unmodified H3K36.

Epigenomic and transcriptomic analysis reveals that paternal obesity influences sperm histone H3 lysine 4 tri-methylation enrichment and placenta gene expression, which in turn negatively impact its development and function in a manner that may contribute to metabolic disease in offspring.

A lysine-to-methionine mutation in histone H3 dominantly blocks histone H3K9 methylation by trapping its methyltransferase.

Biochemical approaches reveal that an epigenetic histone deacetylase complex called CoREST is slow to deacetylate histone H3 lysine-14 in nucleosomes, and this inhibits demethylation of histone H3 lysine-4 by the CoREST complex.

Mutation of Glycine 34 to Arginine within the N-terminal tail of histone H3 alters post-translational modifications on Lysine 36 and is associated with a delay in replication restart, defective homologous recombination and an increase in genomic instability.

Mutations in budding yeast modeled after cancer-associated isocitrate dehydrogenase mutations lead to stabilization of heterochromatin and enhanced gene silencing through inhibition of specific histone demethylases by the oncometabolite D-2-hydroxyglutarate.

Chemically sumoylated histone H4 shows negative biochemical crosstalk with gene-activating histone acetylation and methylation marks, and directly inhibits RNA polymerase II-mediated gene transcription.