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The different polymerases at eukaryotic replication forks achieve their asymmetric placement on the leading and lagging strands through exclusion processes that prevent their function on the 'wrong' strand.

Ubiquitylation of the CMG helicase is inhibited throughout the initiation and elongation phases of chromosome replication by the DNA structure of a replication fork.

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.

Phase separated DNA-free stored forms of RecA dissolve in response to DNA damage to make RecA available for repair and recombination reactions as part of the bacterial (Escherichia coli) SOS response.

Systematic analyses of DNA replication machinery components in human cells reveal a requirement of MCM-dependent de novo loading or mobilization of cohesin at replication forks in establishing sister-chromatid cohesion.

An investigation into 8-oxodeoxguanosine bypass by archaeal DNA polymerases.

A new tumor suppressor function of p21, needed at each undamaged duplication cycle, ensures the adequate execution of the DNA replication program thereby protecting the genome integrity.

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.

Biochemical and biological characterization of insulator complex SUMM4 reveals that, in addition to disrupting enhancer–promoter interactions and establishing chromatin barriers, it functions to delay DNA replication, thus implicating architectural proteins in shaping spatiotemporal patterns of replication.