Evolutionary adaptation to a constitutive perturbation of DNA replication reveals that adaptive mutations in three conserved pathways interact to restore faithful chromosome replication and segregation.
Duplication of Leishmania chromosomes combines S-phase DNA replication initiated at a single internal region with subtelomeric DNA replication detectable outside S-phase, potentially explaining genome plasticity in this important parasite.
Human cell lines replicate and proliferate without ORC1 or ORC2, two subunits of the replication initiator protein complex ORC, which has till now been considered essential for DNA replication.
The crystal structure of the MCM helicase bound to single-stranded DNA reveals a binding motif that is critical for cell viability, helicase activation and DNA replication.
The universal eukaryotic DNA replication kinetics is the consequence of simple physicochemical rules resulting from the localisation of potential replication origins at discrete sites and the diffusion of limiting origin firing factors in the nuclear space.
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.
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.
Sister chromatid cohesion is established during replication by two independent pathways operating in parallel, one converts chromosomal cohesin into cohesive structures while the other loads cohesin onto nascent DNAs.
Two related DNA replication initiation proteins contribute to the decision of whether to enter a new round of the cell division cycle or enter into a period of proliferative quiescence.
