The engagement of DNA crossings is shown to license ATP hydrolysis and DNA cleavage by topoisomerase VI, a finding with mechanistic ramifications for related GHKL ATPases and meiotic recombination machineries.

Condensin I maintains chromosome organization throughout metaphase by preventing erroneous topoisomerase II-dependent sister chromatid re-entanglements.

The first genetic compelling evidence for post-meiotic DNA double-strand breaks and its relation to chromatin remodeling in haploid pronuclei is shown.

SPRTN is a protease essential for the repair of cytotoxic DNA-protein cross links and this function is defective in patients afflicted with Ruijs-Aalfs syndrome -a segmental progeroid syndrome.

The scaffolding that holds chromosome pairs together plays a key role in limiting the levels of double-strand breaks.

Autosomal dominant IRF4 deficiency is the first genetic etiology of Whipple's disease, a very rare chronic condition following a rather common infection by Tropheryma whipplei.

Certain types of 3D chromatin loops are easy to predict from existing or easily obtainable 2D information, which benefits gene expression studies in tissues/cells/organisms without extensive pre-existing 3D information.

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.

PLK-1/2-mediated SYP-4 phosphorylation is dependent on crossover precursor formation, triggering a switch in the dynamic state of the synaptonemal complex that reduces the formation of further double-strand breaks at late meiotic prophase.