DNA replication sites

Bravo, R., and Macdonald-Bravo, H. 1987. Existence of two populations of cyclin/proliferating cell nuclear antigen during the cell cycle Association with DNA replication sites. J. Cell Biol. 705 1549-1554. 

Results of experiments examining the spatiotemporal dynamics of DNA replication and transcription sites in one-cell embryos were also consistent with the presence of replication-dependent and replication-independent genes (Bouniol-Baly et al., 1997). DNA replication sites were detected by incorporation of digitoxin-modified dUTP (detected with antibodies to digitoxin) and transcription sites were detected by incorporation of BrUTP (detected with anti-BrdU antibodies) following microinjection of both of these nucleotides. While most of the transcription sites did not co-localize with replication sites, there were sites of colocalization. 

Mutations in ribonucleotide reductase that affect either the activity or specificity sites can render the enzyme less susceptible to inhibition by dNTP effectors. Cells carrying these kinds of mutations display both abnormalities in the quantities of dNTPs they contain and so-called mutator phenotypes. That is, cells with mutator phenotypes show increased rates of spontaneous mutation at all genetic loci tested. These findings suggest that when dNTP concentrations are altered at DNA replication sites, the likelihood is increased for replication errors, which lead to mutations. 

Cazzalini O, Perucca P, Riva F et al. P21CDKN1A does not interfere with loading of PCNA at DNA replication sites, but it inibits subsequent binding of DNA polymerase delta at the Gl/S phase transition. Cell Cycle 2003 2 596-603. 

Riva F, Savio M, Cazzalini O et al. Distinct pools of proliferating cell nuclear antigen associated to DNA replication sites Intetact with pl25 subunit of DNA polymerase 5 or DNA ligase 1. Exp Cell Res 2004 293 357-367. 

Mapping of DNA Replication Sites in Situ by Fluorescence Microscopy... 

Dolbeare, F. (1996). Bromodeoxyuridine A diagnostic tool in biology and medicine. 3. Proliferation in normal, injured and diseased tissue, growth factors, differentiation, DNA replication sites and in situ hybridization. Histochem. J. 28, 531 575. 

Fox, M. H., Arndt-Jovin, D. J., Jovin, T. M., Baumann, P. H and Robert-Nicoud, M. (1991). Spatial and temporal distribution of DNA replication sites localized by immunofluorescence andconfocal microscopy in mouse fibroblasts. J. Cell Sci. 99, 247-253. 

Huberman. J. A., Tsai, A., and Deich, R. A. (1973). DNA replication sites within nuclei of mammalian cells. Nature (London) 241, 32-36. 

The multiple sites that serve as origins for DNA replication in eukaryotes are poorly defined except in a few animal viruses and in yeast. However, it is clear that initiation is regulated both spatially and temporaUy, since clusters of adjacent sites initiate rephcation synchronously. There are suggestions that functional domains of chromatin replicate as intact units, implying that the origins of rephcation are specificaUy located with respect to transcription units. 

DNA replication occurs at several sites—called replication bubbles—in each chromosome. The entire process takes about 9 hours in a typical cell. 

In some circumstances, DNA radical lesions can react with an adjacent base or the sugar residues. In these cases, a single radical hit can be transformed into two adjacent damage sites on the DNA. The resulting tandem lesions may present special challenges to DNA replication and repair systems. ... 

In E. coli cells, DNA replication starts at a specific site called oriC. The oriC locus contains only 245 base pairs. Similar sequences are responsible for initiating the synthesis of plasmid and bacteriophage DNA. The oriC nucleotide sequence binds several units of the tetrameric form of the dnaA protein. This protein is named for the gene that encodes it. The dnaB and dnaC proteins then bind to the complex. As a result of binding these proteins, a portion of the helical DNA is unwound. This forces the rest of the DNA into a left-handed double helix that wraps around the proteins to give a structure... 

Induced mutagenesis in Escherichia coli is an active process involving proteins with DNA replication, repair, and recombination functions. The available evidence suggests that mutations are generated at sites where DNA has been damaged and that they arise via an error-prone repair activity. In an attempt to understand what specific contributions to mutagenesis are made by DNA lesions, we have studied the mutational specificity of some carcinogens, such as benzo[a]pyrene and aflatoxin, whose chemical reactions with DNA are... 

Not all mutagenesis in IS. coli is dependent on SOS-processing. Mutations may arise quite simply during DNA replication if a base is substituted by or converted to another, incorrect, base. Consider the consequence of oxidative deamination of the base 5-methylcytosine to thymine. Replication followed by daughter strand segregation will result in a G C base pair having been mutated to an A T base pair. Sites containing 5-methylcytosine are hotspots for G C to A T transitions in 12. coli (24). 

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