@article {2373,
	title = {Leishmania DNA Replication Timing: A Stochastic Event?},
	journal = {Trends Parasitol},
	volume = {32},
	year = {2016},
	month = {2016 10},
	pages = {755-757},
	abstract = {<p>For eukaryotic genomes, DNA synthesis initiates at multiple discrete regions known as replication origins in a dynamic yet regulated manner to ensure genomic stability. Two recent studies using different approaches reveal few Leishmania origins and that origin firing may proceed in a mainly stochastic manner.</p>
},
	keywords = {Animals, DNA Replication Timing, Drug Delivery Systems, Genomic Instability, Humans, Leishmania, Leishmaniasis, Replication Origin},
	issn = {1471-5007},
	doi = {10.1016/j.pt.2016.05.011},
	author = {Rocha-Granados, Maria C and Klingbeil, Michele M}
}
@article {816,
	title = {A hand-off mechanism for primosome assembly in replication restart.},
	journal = {Mol Cell},
	volume = {26},
	year = {2007},
	month = {2007 Jun 22},
	pages = {781-93},
	abstract = {Collapsed DNA replication forks must be reactivated through origin-independent reloading of the replication machinery (replisome) to ensure complete duplication of cellular genomes. In E. coli, the PriA-dependent pathway is the major replication restart mechanism and requires primosome proteins PriA, PriB, and DnaT for replisome reloading. However, the molecular mechanisms that regulate origin-independent replisome loading are not fully understood. Here, we demonstrate that assembly of primosome protein complexes represents a key regulatory mechanism, as inherently weak PriA-PriB and PriB-DnaT interactions are strongly stimulated by single-stranded DNA. Furthermore, the binding site on PriB for single-stranded DNA partially overlaps the binding sites for PriA and DnaT, suggesting a dynamic primosome assembly process in which single-stranded DNA is handed off from one primosome protein to another as a repaired replication fork is reactivated. This model helps explain how origin-independent initiation of DNA replication is restricted to repaired replication forks, preventing overreplication of the genome.},
	keywords = {Binding Sites, DNA Helicases, DNA Replication, DNA, Bacterial, DNA, Single-Stranded, DNA-Binding Proteins, DNA-Directed DNA Polymerase, Escherichia coli, Escherichia coli Proteins, Genome, Bacterial, Models, Biological, Multienzyme Complexes, Protein Binding, Replication Origin},
	issn = {1097-2765},
	doi = {10.1016/j.molcel.2007.05.012},
	author = {Lopper, Matthew and Boonsombat, Ruethairat and Sandler, Steven J and Keck, James L}
}
@article {828,
	title = {The importance of repairing stalled replication forks.},
	journal = {Nature},
	volume = {404},
	year = {2000},
	month = {2000 Mar 2},
	pages = {37-41},
	abstract = {The bacterial SOS response to unusual levels of DNA damage has been recognized and studied for several decades. Pathways for re-establishing inactivated replication forks under normal growth conditions have received far less attention. In bacteria growing aerobically in the absence of SOS-inducing conditions, many replication forks encounter DNA damage, leading to inactivation. The pathways for fork reactivation involve the homologous recombination systems, are nonmutagenic, and integrate almost every aspect of DNA metabolism. On a frequency-of-use basis, these pathways represent the main function of bacterial DNA recombination systems, as well as the main function of a number of other enzymatic systems that are associated with replication and site-specific recombination.},
	keywords = {Bacteria, Bacterial Proteins, Chromosomes, Bacterial, DNA Replication, DNA, Bacterial, Escherichia coli, Recombination, Genetic, Replication Origin, SOS Response (Genetics)},
	issn = {0028-0836},
	doi = {10.1038/35003501},
	author = {Cox, M M and Goodman, M F and Kreuzer, K N and Sherratt, D J and Sandler, S J and Marians, K J}
}
