Genome duplication necessarily involves the replication of imperfect DNA templates and, if
left to their own devices, replication complexes regularly run into problems. The details of …

The progress of replication forks is often threatened in vivo, both by DNA damage and by
proteins bound to the template. Blocked forks must somehow be restarted, and the original …

There is mounting evidence that there are frequent conflicts between complexes that
replicate DNA and those that transcribe the same template, and that these conflicts lead to …

If replication forks are perturbed, a multifaceted response including several DNA repair and
cell cycle checkpoint pathways is activated to ensure faithful DNA replication. Here, we show …

Nucleoprotein complexes present challenges to genome stability by acting as potent blocks
to replication. One attractive model of how such conflicts are resolved is direct targeting of …

We have discovered a correlation between the ability of Escherichia coli cells to survive
damage to DNA and their ability to modulate RNA polymerase via the stringent response …

PriA helicase is the major DNA replication restart initiator in Escherichia coli and acts to reload
the replicative helicase DnaB back onto the chromosome at repaired replication forks and …

Modification of damaged replication forks is emerging as a crucial factor for efficient chromosomal
duplication and the avoidance of genetic instability. The RecG helicase of Escherichia …

The PriA protein of Escherichia coli provides a vital link between recombination and DNA
replication. To establish the molecular basis for this link, we investigated the ability of PriA to …

… More recent genetic and biochemical data from McGlynn and Lloyd (14) argues that it is …
polymerase modulator (p)ppGpp] or rpo* [mutations in rpoB that mimic the effect of (p)ppGpp …