Identification of novel components and regulators of heterochromatin reveals a spatially complex and dynamic organization.

Cooperative association of a histone-binding complex with pairs of appropriately modified nucleosomes, which form fundamental units of binding, mediates selective heterochromatin assembly and spreading.

Redundant pathways prevent heterochromatin spreading and ectopic heterochromatin assembly; and plasticity of heterochromatin assembly allows cells to adapt to heterochromatin stress.

Heterochromatin is established at nucleation sites associated with open chromatin and RNA transcripts and matures into stable domains if they are found near transposable elements targeted by maternally deposited piRNAs.

Epigenetic restriction of herpes simplex virus occurs in a biphasic manner, in which ATRX maintains viral heterochromatin after an initial phase of chromatin deposition.

Large regions of foreign DNA inserted into mammalian chromosomes assemble into H3K9me3-heterochromatin and result in increased condensin loading with organisation into shorter mitotic chromosome loops than endogenous DNA.

Transposon activation during male gametogenesis is caused by interactions between DNA demethylation and linker histone H1, developmental depletion of which promotes pollen fertility.

Set1 has roles in chromatin organization and transcriptome control that are largely independent of histone H3 lysine 4 methylation.

Genetic and biochemical studies show that a conserved ribosome biogenesis complex also localizes to heterochromatin, where it triggers RNA degradation and promotes the spreading and epigenetic inheritance of histone methylation.

The piRNA pathway regulates satellite DNAs in the Drosophila melanogaster germline and affects heterochromatin establishment at pericentromeric satellite DNA in embryos, implying a general role for piRNAs in ensuring genome stability.