Analysis of genome integrity in primary murine B-cells reveals how depleting 26S proteasome activity enhanced cell survival following treatment with topoisomerase poisons.

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.

Ribosome assembly is monitored to promote proteostatis through a system whereby unassembled ribosomal proteins lead to activation of heat shock factor 1 and inactivation of the RP gene activator Ifh1.

CryoEM structures of open gyrase A dimers and DNA in two states representing steps either prior to or after passage through the DNA-gate, show where a putative T-segment is found.

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.

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.