Filling the gaps in replication restart pathways.
Recent work by clarifies two mechanisms of replication fork assembly in E. coli: in vitro, the presence of a leading nascent strand dictates a PriA/B DnaT-dependent mechanism, whereas a gapped fork specifies PriC-mediated restart.
Lovett
Susan T
ST
Rosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, MA 02454, USA. lovett@brandeis.edu
D000251:Adenosine Triphosphatases / Q000502:physiology*; D004265:DNA Helicases / Q000502:physiology*; D004261:DNA Replication; D004269:DNA, Bacterial / Q000096:biosynthesis*; D004268:DNA-Binding Proteins / Q000502:physiology*; D004926:Escherichia coli / Q000235:genetics*; D029968:Escherichia coli Proteins / Q000502:physiology*
D004269:DNA, Bacterial; D004268:DNA-Binding Proteins; D029968:Escherichia coli Proteins; C086004:PriB protein, E coli; C069995:PriC protein, E coli; D000251:Adenosine Triphosphatases; C506743:priA protein, E coli; D004265:DNA Helicases