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.

Establishment of replication-timing involves Fkh1-dependent recruitment and execution of DDK function in G1 phase resulting in dynamic relocalization of origins within the nucleus in anticipation of CDK-dependent origin activation.

Replication origins in yeast are more widespread than previously believed.

Replication origins are fundamental organizers and regulators of gene activity through embryonic development.

The mechanism of Dbf4-dependent kinase (DDK) recruitment to replication origins and its regulation by the checkpoint have been identified.

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.

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.

Mathematical modeling and data analysis show that, over evolutionary times, the yeast temporal program of replication strives to avoid stalling events and minimize interference between neighbor origins.

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.

Mapping DNA replication timing, allied to genetic analysis of a RecQ repair helicase, reveals that antigenic variation in the African trypanosome may be initiated by locus-specific, replication-derived sequence instability.