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.

DNA replication fork rate in budding yeast is regulated in response to DNA damage by phosphorylation of two proteins, Mrc1 and Mcm10, by the Rad53 protein kinase.

Although questionable research practices inflate false positive rates, they have little effect on replicability because they also increase power.

Definitions of reproducibility vary considerably across disciplines and overall rates of reproducibility are low irrespective of the definition used.

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.

The speed of replisomes in Escherichia coli depends on temperature and varies along the genome in a wave-like manner, with implications for bacterial physiology.

A detailed model of the T7 replisome with the precise positions of the helicase and polymerase at the replication fork explains how catalysis by the two enzymes is coordinated.

Replication-transcription conflicts cause pervasive replisome instability.

Analysis of experiments on bacteria suggests that the dependence of cell size on growth rate is not an adaptation but a causal consequence of a regulatory mechanism that controls DNA replication.

The unique cell cycle variations of pluripotent stem cells ensures that the first step in DNA replication is particularly fast and this rapid rate, in turn, restrains early differentiation.