The N-terminal domain in histone 2A serves as an evolutionary tool to enable greater chromatin compaction when genome size is disproportionately larger than the nuclear volume across eukaryotes.

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

Condensation and segregation of chromosomes during mitosis is caused by a combination of short-range interactions between nucleosomes and the long-range contraction of chromosome arms mediated by condensin.

Building on previous work (Syrjänen, Pellegrini, & Davies, 2014), it is shown that SYCP3 contributes to the architecture of meiotic chromosomes through local bridging interactions that result in large-scale compaction of the chromosome axis.

Direct recordings from the human hippocampus reveal the neural mechanisms that orchestrate recollection of past experiences.

Linker histone H1.8 shapes mitotic chromosomes by tuning the number and size of condensin-dependent DNA loops and suppressing condensin and DNA topoisomerase II-dependent individualization.

Chromatin gradually rearranges during epidermal stem cell differentiation, while transcription of a differentiation-associated gene is extremely dynamic.

The kinase that controls maternal mRNA translation is regulated by phosphorylation of its activating subunit to restrict kinase activity to the developmental window between meiosis completion and early embryogenesis.

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

Models of chromosome compaction by condensins demonstrate that two-sided loop extrusion and long residence times are required for high compaction, suggesting a tight coupling between these two properties in vivo.