RNA binding is a key input of an active chromatin complex and maintenance of stem cell fate.

Loop extrusion can robustly compact, segregate and disentangle mammalian chromosomes, suggesting it is a universal mechanism of genome folding during cell division.

Chromatin-binding proteins regulate the effective solvent quality experienced by chromatin and impact global chromatin organization in the nucleus.

Hox genes are activated sequentially and, at the same time, undergo a transition from an inactive to an active chromatin compartment, most likely to prevent posterior genes being activated too early.

The acetylation of histones at specific sites close to DNA can regulate transcription.

Pervasive ‘futile cycling’ by chromatin-modifying factors suggests a mechanism for creating new links in gene regulatory networks.

The lysine acetyltransferases KAT2A and KAT2B regulate the dynamic chromatin association of the tumour suppressor protein PALB2, protecting active genes and promoting DNA damage repair in a context-dependent manner.

Active and repressive chromatin marks, asymmetrically distributed between alleles, distinguish gene bodies subject to epigenetically controlled monoallelic expression on autosomes in human cells.

Silencing of gene regulatory elements by modifications of DNA-bound proteins promotes the progression of early mouse development.

Chromosomal structural ensembles are fluid yet are cell-type-specific, despite apparent disorder, appropriate collective variables uncover evidence of structural transitions associated with gene activity and cell differentiation.