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.

Drugs in a curative chemotherapy regimen are independently effective and resisted by different mechanisms, so cancer cells have little chance of surviving all drugs, and this benefit occurs without synergistic interactions.