Replication-transcription conflicts cause pervasive replisome instability.

WRNIP1 has been identified as a pivotal factor in preventing the pathological persistence of R-loop-induced transcription-replication conflicts and the accumulation of DNA damage, thereby ensuring genome integrity.

RNA polymerase recruits the PcrA DNA helicase via a conserved interaction motif in order to remove R-loops and prevent conflicts with replication.

The localization of Rad53 cell cycle checkpoint kinase to many gene promoters and the dynamic changes in response to replication stress suggests that the kinase may coordinate genome stability and gene expression.

Reconstitution of orientation-specific R-loop-replisome collisions with purified proteins reveals the differential impact of R-loop-associated RNA:DNA hybrids and G-quadruplexes on replication fork progression.

The nuclear periphery houses compositionally and functionally distinct domains, one of which provides a 'safe zone' for replication and reassembly of heterochromatic genome regions.

Evolution-guided functional analyses identify an activating adaptor of the dynein intracellular transportation machinery, NINL, as a novel component of the antiviral immune response and reveal a mechanism by which viruses antagonize NINL function in a species-specific manner.

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.

Translesion polymerase kappa promotes replication fork restart to maintain genome stability during conditions of nucleotide deprivation.

During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.