The TRAIP ubiquitin ligase is required during mitosis to disassemble the replisome at sites of incomplete DNA replication, and activate the mitotic DNA repair pathway, thus preserving genome integrity.

Replication origins are established throughout the genome with the exception of transcribed genes, and the local chromatin composition likely modulates the density of ORC and MCM as well as origin activation.

Heritable mutations tend to occur within different DNA sequence contexts in different human populations, suggesting that DNA replication and repair often change in efficacy over only a few hundred generations of evolution.

53BP1 and BRCA1 antagonistically control a temporal choice of two distinct pathways to restart stalled replication forks in a DNA double stand repair-independent manner.

The ~20,000 origins of replication in human cell lines that are reproducibly identified by multiple techniques in multiple cell lines are distant from known origin recognition complex and MCM2-7-binding sites.

Biochemical analysis in Xenopus egg extracts reveals that the MutSα mismatch sensor retains the DNA-bound replication clamp to maintain a post-replicative temporal window permissive to strand-specific repair of mismatches.

In contrast to other transcription factors, CTCF and Esrrb rapidly regain binding after replication and remain bound to their targets during mitosis, preserving local nucleosome organization throughout the cell cycle.

Live-cell imaging shows that replication-independent specialized polymerase action is a consequence of lesion processing via NER and impacts cellular survival under stress outside replicative phases of the cell cycle.

E3 ubiquitin ligase Bre1-induced H2B monoubiquitination is epigenetically important for recruiting replication factor Mcm10 and cohesion establishment factors Ctf4, Ctf18 and Eco1 to early replication origins to establish sister chromatid cohesion.

In addition to causing DNA damage, R-loops cause genomic instability by interfering with DNA repair.