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Journal articles on the topic 'DNA replication'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 October 2024

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1

Avemann, K., R. Knippers, T. Koller, and J. M. Sogo. "Camptothecin, a specific inhibitor of type I DNA topoisomerase, induces DNA breakage at replication forks." Molecular and Cellular Biology 8, no. 8 (August 1988): 3026–34. http://dx.doi.org/10.1128/mcb.8.8.3026-3034.1988.

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The structure of replicating simian virus 40 minichromosomes, extracted from camptothecin-treated infected cells, was investigated by biochemical and electron microscopic methods. We found that camptothecin frequently induced breaks at replication forks close to the replicative growth points. Replication branches were disrupted at about equal frequencies at the leading and the lagging strand sides of the fork. Since camptothecin is known to be a specific inhibitor of type I DNA topoisomerase, we suggest that this enzyme is acting very near the replication forks. This conclusion was supported by experiments with aphidicolin, a drug that blocks replicative fork movement, but did not prevent the camptothecin-induced breakage of replication forks. The drug teniposide, an inhibitor of type II DNA topoisomerase, had only minor effects on the structure of these replicative intermediates.

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2

Avemann, K., R. Knippers, T. Koller, and J. M. Sogo. "Camptothecin, a specific inhibitor of type I DNA topoisomerase, induces DNA breakage at replication forks." Molecular and Cellular Biology 8, no. 8 (August 1988): 3026–34. http://dx.doi.org/10.1128/mcb.8.8.3026.

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The structure of replicating simian virus 40 minichromosomes, extracted from camptothecin-treated infected cells, was investigated by biochemical and electron microscopic methods. We found that camptothecin frequently induced breaks at replication forks close to the replicative growth points. Replication branches were disrupted at about equal frequencies at the leading and the lagging strand sides of the fork. Since camptothecin is known to be a specific inhibitor of type I DNA topoisomerase, we suggest that this enzyme is acting very near the replication forks. This conclusion was supported by experiments with aphidicolin, a drug that blocks replicative fork movement, but did not prevent the camptothecin-induced breakage of replication forks. The drug teniposide, an inhibitor of type II DNA topoisomerase, had only minor effects on the structure of these replicative intermediates.

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3

Swindle, C. Scott, Nianxiang Zou, Brian A. Van Tine, George M. Shaw, Jeffrey A. Engler, and Louise T. Chow. "Human Papillomavirus DNA Replication Compartments in a Transient DNA Replication System." Journal of Virology 73, no. 2 (February 1, 1999): 1001–9. http://dx.doi.org/10.1128/jvi.73.2.1001-1009.1999.

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ABSTRACT Many DNA viruses replicate their genomes at nuclear foci in infected cells. Using indirect immunofluorescence in combination with fluorescence in situ hybridization, we colocalized the human papillomavirus (HPV) replicating proteins E1 and E2 and the replicating origin-containing plasmid to nuclear foci in transiently transfected cells. The host replication protein A (RP-A) was also colocalized to these foci. These nuclear structures were identified as active sites of viral DNA synthesis by bromodeoxyuridine (BrdU) pulse-labeling. Unexpectedly, the great majority of RP-A and BrdU incorporation was found in these HPV replication domains. Furthermore, E1, E2, and RP-A were also colocalized to nuclear foci in the absence of an origin-containing plasmid. These observations suggest a spatial reorganization of the host DNA replication machinery upon HPV DNA replication or E1 and E2 expression. Alternatively, viral DNA replication might be targeted to host nuclear domains that are active during the late S phase, when such domains are limited in number. In a fraction of cells expressing E1 and E2, the promyelocytic leukemia protein, a component of nuclear domain 10 (ND10), was either partially or completely colocalized with E1 and E2. Since ND10 structures were recently hypothesized to be sites of bovine papillomavirus virion assembly, our observation suggests that HPV DNA amplification might be partially coupled to virion assembly.

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Thomas, David C., John D. Roberts, Ralph D. Sabatino, Thomas W. Myers, Cheng Keat Tan, Kathleen M. Downey, Antero G. So, Robert A. Bambara, and Thomas A. Kunkel. "Fidelity of mammalian DNA replication and replicative DNA polymerases." Biochemistry 30, no. 51 (December 1991): 11751–59. http://dx.doi.org/10.1021/bi00115a003.

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5

Takebayashi, Shin-ichiro, Tyrone Ryba, Kelsey Wimbish, Takuya Hayakawa, Morito Sakaue, Kenji Kuriya, Saori Takahashi, et al. "The Temporal Order of DNA Replication Shaped by Mammalian DNA Methyltransferases." Cells 10, no. 2 (January 29, 2021): 266. http://dx.doi.org/10.3390/cells10020266.

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Multiple epigenetic pathways underlie the temporal order of DNA replication (replication timing) in the contexts of development and disease. DNA methylation by DNA methyltransferases (Dnmts) and downstream chromatin reorganization and transcriptional changes are thought to impact DNA replication, yet this remains to be comprehensively tested. Using cell-based and genome-wide approaches to measure replication timing, we identified a number of genomic regions undergoing subtle but reproducible replication timing changes in various Dnmt-mutant mouse embryonic stem (ES) cell lines that included a cell line with a drug-inducible Dnmt3a2 expression system. Replication timing within pericentromeric heterochromatin (PH) was shown to be correlated with redistribution of H3K27me3 induced by DNA hypomethylation: Later replicating PH coincided with H3K27me3-enriched regions. In contrast, this relationship with H3K27me3 was not evident within chromosomal arm regions undergoing either early-to-late (EtoL) or late-to-early (LtoE) switching of replication timing upon loss of the Dnmts. Interestingly, Dnmt-sensitive transcriptional up- and downregulation frequently coincided with earlier and later shifts in replication timing of the chromosomal arm regions, respectively. Our study revealed the previously unrecognized complex and diverse effects of the Dnmts loss on the mammalian DNA replication landscape.

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6

Greci, Mark D., and Stephen D. Bell. "Archaeal DNA Replication." Annual Review of Microbiology 74, no. 1 (September 8, 2020): 65–80. http://dx.doi.org/10.1146/annurev-micro-020518-115443.

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It is now well recognized that the information processing machineries of archaea are far more closely related to those of eukaryotes than to those of their prokaryotic cousins, the bacteria. Extensive studies have been performed on the structure and function of the archaeal DNA replication origins, the proteins that define them, and the macromolecular assemblies that drive DNA unwinding and nascent strand synthesis. The results from various archaeal organisms across the archaeal domain of life show surprising levels of diversity at many levels—ranging from cell cycle organization to chromosome ploidy to replication mode and nature of the replicative polymerases. In the following, we describe recent advances in the field, highlighting conserved features and lineage-specific innovations.

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7

Liu, Guoqi, Michelle Malott, and Michael Leffak. "Multiple Functional Elements Comprise a Mammalian Chromosomal Replicator." Molecular and Cellular Biology 23, no. 5 (March 1, 2003): 1832–42. http://dx.doi.org/10.1128/mcb.23.5.1832-1842.2003.

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ABSTRACT The structure of replication origins in metazoans is only nominally similar to that in model organisms, such as Saccharomyces cerevisiae. By contrast to the compact origins of budding yeast, in metazoans multiple elements act as replication start sites or control replication efficiency. We first reported that replication forks diverge from an origin 5′ to the human c-myc gene and that a 2.4-kb core fragment of the origin displays autonomous replicating sequence activity in plasmids and replicator activity at an ectopic chromosomal site. Here we have used clonal HeLa cell lines containing mutated c-myc origin constructs integrated at the same chromosomal location to identify elements important for DNA replication. Replication activity was measured before or after integration of the wild-type or mutated origins using PCR-based nascent DNA abundance assays. We find that deletions of several segments of the c-myc origin, including the DNA unwinding element and transcription factor binding sites, substantially reduced replicator activity, whereas deletion of the c-myc promoter P1 had only a modest effect. Substitution mutagenesis indicated that the sequence of the DNA unwinding element, rather than the spacing of flanking sequences, is critical. These results identify multiple functional elements essential for c-myc replicator activity.

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8

Kornberg, A. "DNA replication." Journal of Biological Chemistry 263, no. 1 (January 1988): 1–4. http://dx.doi.org/10.1016/s0021-9258(19)57345-8.

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9

van der Vliet, P. C. "DNA replication." Current Opinion in Cell Biology 1, no. 3 (June 1989): 481–87. http://dx.doi.org/10.1016/0955-0674(89)90009-4.

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10

Virshup, D. M. "DNA replication." Current Opinion in Cell Biology 2, no. 3 (June 1990): 453–60. http://dx.doi.org/10.1016/0955-0674(90)90127-z.

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11

Kornberg, Arthur. "DNA replication." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 951, no. 2-3 (December 1988): 235–39. http://dx.doi.org/10.1016/0167-4781(88)90091-7.

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12

Laskey, Ronald. "The Croonian Lecture 2001 Hunting the antisocial cancer cell: MCM proteins and their exploitation." Philosophical Transactions of the Royal Society B: Biological Sciences 360, no. 1458 (June 23, 2005): 1119–32. http://dx.doi.org/10.1098/rstb.2005.1656.

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Replicating large eukaryotic genomes presents the challenge of distinguishing replicated regions of DNA from unreplicated DNA. A heterohexamer of minichromosome maintenance (MCM) proteins is essential for the initiation of DNA replication. MCM proteins are loaded on to unreplicated DNA before replication begins and displaced progressively during replication. Thus, bound MCM proteins license DNA for one, and only one, round of replication and this licence is reissued each time a cell divides. MCM proteins are also the best candidates for the replicative helicases that unwind DNA during replication, but interesting questions arise about how they can perform this role, particularly as they are present on only unreplicated DNA, rather than clustered at replication forks. Although MCM proteins are bound and released cyclically from DNA during the cell cycle, higher eukaryotic cells retain them in the nucleus throughout the cell cycle. In contrast, MCMs are broken down when cells exit the cycle by quiescence or differentiation. We have exploited these observations to develop screening tests for the common carcinomas, starting with an attempt to improve the sensitivity of the smear test for cervical cancer. MCM proteins emerge as exceptionally promising markers for cancer screening and early diagnosis.

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13

Moiseeva, Tatiana N., Yandong Yin, Michael J. Calderon, Chenao Qian, Sandra Schamus-Haynes, Norie Sugitani, Hatice U. Osmanbeyoglu, Eli Rothenberg, Simon C. Watkins, and Christopher J. Bakkenist. "An ATR and CHK1 kinase signaling mechanism that limits origin firing during unperturbed DNA replication." Proceedings of the National Academy of Sciences 116, no. 27 (June 17, 2019): 13374–83. http://dx.doi.org/10.1073/pnas.1903418116.

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DNA damage-induced signaling by ATR and CHK1 inhibits DNA replication, stabilizes stalled and collapsed replication forks, and mediates the repair of multiple classes of DNA lesions. We and others have shown that ATR kinase inhibitors, three of which are currently undergoing clinical trials, induce excessive origin firing during unperturbed DNA replication, indicating that ATR kinase activity limits replication initiation in the absence of damage. However, the origins impacted and the underlying mechanism(s) have not been described. Here, we show that unperturbed DNA replication is associated with a low level of ATR and CHK1 kinase signaling and that inhibition of this signaling induces dormant origin firing at sites of ongoing replication throughout the S phase. We show that ATR and CHK1 kinase inhibitors induce RIF1 Ser2205 phosphorylation in a CDK1-dependent manner, which disrupts an interaction between RIF1 and PP1 phosphatase. Thus, ATR and CHK1 signaling suppresses CDK1 kinase activity throughout the S phase and stabilizes an interaction between RIF1 and PP1 in replicating cells. PP1 dephosphorylates key CDC7 and CDK2 kinase substrates to inhibit the assembly and activation of the replicative helicase. This mechanism limits origin firing during unperturbed DNA replication in human cells.

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14

Nasheuer, Heinz Peter, and Anna Marie Meaney. "Starting DNA Synthesis: Initiation Processes during the Replication of Chromosomal DNA in Humans." Genes 15, no. 3 (March 14, 2024): 360. http://dx.doi.org/10.3390/genes15030360.

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The initiation reactions of DNA synthesis are central processes during human chromosomal DNA replication. They are separated into two main processes: the initiation events at replication origins, the start of the leading strand synthesis for each replicon, and the numerous initiation events taking place during lagging strand DNA synthesis. In addition, a third mechanism is the re-initiation of DNA synthesis after replication fork stalling, which takes place when DNA lesions hinder the progression of DNA synthesis. The initiation of leading strand synthesis at replication origins is regulated at multiple levels, from the origin recognition to the assembly and activation of replicative helicase, the Cdc45–MCM2-7–GINS (CMG) complex. In addition, the multiple interactions of the CMG complex with the eukaryotic replicative DNA polymerases, DNA polymerase α-primase, DNA polymerase δ and ε, at replication forks play pivotal roles in the mechanism of the initiation reactions of leading and lagging strand DNA synthesis. These interactions are also important for the initiation of signalling at unperturbed and stalled replication forks, “replication stress” events, via ATR (ATM–Rad 3-related protein kinase). These processes are essential for the accurate transfer of the cells’ genetic information to their daughters. Thus, failures and dysfunctions in these processes give rise to genome instability causing genetic diseases, including cancer. In their influential review “Hallmarks of Cancer: New Dimensions”, Hanahan and Weinberg (2022) therefore call genome instability a fundamental function in the development process of cancer cells. In recent years, the understanding of the initiation processes and mechanisms of human DNA replication has made substantial progress at all levels, which will be discussed in the review.

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15

Hernández-Tamayo, Rogelio, Luis M. Oviedo-Bocanegra, Georg Fritz, and Peter L. Graumann. "Symmetric activity of DNA polymerases at and recruitment of exonuclease ExoR and of PolA to the Bacillus subtilis replication forks." Nucleic Acids Research 47, no. 16 (June 28, 2019): 8521–36. http://dx.doi.org/10.1093/nar/gkz554.

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AbstractDNA replication forks are intrinsically asymmetric and may arrest during the cell cycle upon encountering modifications in the DNA. We have studied real time dynamics of three DNA polymerases and an exonuclease at a single molecule level in the bacterium Bacillus subtilis. PolC and DnaE work in a symmetric manner and show similar dwell times. After addition of DNA damage, their static fractions and dwell times decreased, in agreement with increased re-establishment of replication forks. Only a minor fraction of replication forks showed a loss of active polymerases, indicating relatively robust activity during DNA repair. Conversely, PolA, homolog of polymerase I and exonuclease ExoR were rarely present at forks during unperturbed replication but were recruited to replications forks after induction of DNA damage. Protein dynamics of PolA or ExoR were altered in the absence of each other during exponential growth and during DNA repair, indicating overlapping functions. Purified ExoR displayed exonuclease activity and preferentially bound to DNA having 5′ overhangs in vitro. Our analyses support the idea that two replicative DNA polymerases work together at the lagging strand whilst only PolC acts at the leading strand, and that PolA and ExoR perform inducible functions at replication forks during DNA repair.

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16

Weitzman, Matthew D., and Amélie Fradet-Turcotte. "Virus DNA Replication and the Host DNA Damage Response." Annual Review of Virology 5, no. 1 (September 29, 2018): 141–64. http://dx.doi.org/10.1146/annurev-virology-092917-043534.

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Viral DNA genomes have limited coding capacity and therefore harness cellular factors to facilitate replication of their genomes and generate progeny virions. Studies of viruses and how they interact with cellular processes have historically provided seminal insights into basic biology and disease mechanisms. The replicative life cycles of many DNA viruses have been shown to engage components of the host DNA damage and repair machinery. Viruses have evolved numerous strategies to navigate the cellular DNA damage response. By hijacking and manipulating cellular replication and repair processes, DNA viruses can selectively harness or abrogate distinct components of the cellular machinery to complete their life cycles. Here, we highlight consequences for viral replication and host genome integrity during the dynamic interactions between virus and host.

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17

Stoeber, Kai, Thea D. Tlsty, Lisa Happerfield, Geraldine A. Thomas, Sergei Romanov, Lynda Bobrow, E. Dillwyn Williams, and Gareth H. Williams. "DNA replication licensing and human cell proliferation." Journal of Cell Science 114, no. 11 (June 1, 2001): 2027–41. http://dx.doi.org/10.1242/jcs.114.11.2027.

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The convergence point of growth regulatory pathways that control cell proliferation is the initiation of genome replication, the core of which is the assembly of pre-replicative complexes resulting in chromatin being ‘licensed’ for DNA replication in the subsequent S phase. We have analysed regulation of the pre-replicative complex proteins ORC, Cdc6, and MCM in cycling and non-proliferating quiescent, differentiated and replicative senescent human cells. Moreover, a human cell-free DNA replication system has been exploited to study the replicative capacity of nuclei and cytosolic extracts prepared from these cells. These studies demonstrate that downregulation of the Cdc6 and MCM constituents of the replication initiation pathway is a common downstream mechanism for loss of proliferative capacity in human cells. Furthermore, analysis of MCM protein expression in self-renewing, stable and permanent human tissues shows that the three classes of tissue have developed very different growth control strategies with respect to replication licensing. Notably, in breast tissue we found striking differences between the proportion of mammary acinar cells that express MCM proteins and those labelled with conventional proliferation markers, raising the intriguing possibility that progenitor cells of some tissues are held in a prolonged G1 phase or ‘in-cycle arrest’. We conclude that biomarkers for replication-licensed cells detect, in addition to actively proliferating cells, cells with growth potential, a concept that has major implications for developmental and cancer biology.

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18

Hills, Stephanie A., and John F. X. Diffley. "DNA Replication and Oncogene-Induced Replicative Stress." Current Biology 24, no. 10 (May 2014): R435—R444. http://dx.doi.org/10.1016/j.cub.2014.04.012.

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19

Hills, Stephanie A., and John F. X. Diffley. "DNA Replication and Oncogene-Induced Replicative Stress." Current Biology 24, no. 13 (July 2014): 1563. http://dx.doi.org/10.1016/j.cub.2014.06.016.

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20

Sobeck, Alexandra, Stacie Stone, Vincenzo Costanzo, Bendert de Graaf, Tanja Reuter, Johan de Winter, Michael Wallisch, et al. "Fanconi Anemia Proteins Are Required To Prevent Accumulation of Replication-Associated DNA Double-Strand Breaks." Molecular and Cellular Biology 26, no. 2 (January 15, 2006): 425–37. http://dx.doi.org/10.1128/mcb.26.2.425-437.2006.

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ABSTRACT Fanconi anemia (FA) is a multigene cancer susceptibility disorder characterized by cellular hypersensitivity to DNA interstrand cross-linking agents such as mitomycin C (MMC). FA proteins are suspected to function at the interface between cell cycle checkpoints, DNA repair, and DNA replication. Using replicating extracts from Xenopus eggs, we developed cell-free assays for FA proteins (xFA). Recruitment of the xFA core complex and xFANCD2 to chromatin is strictly dependent on replication initiation, even in the presence of MMC indicating specific recruitment to DNA lesions encountered by the replication machinery. The increase in xFA chromatin binding following treatment with MMC is part of a caffeine-sensitive S-phase checkpoint that is controlled by xATR. Recruitment of xFANCD2, but not xFANCA, is dependent on the xATR-xATR-interacting protein (xATRIP) complex. Immunodepletion of either xFANCA or xFANCD2 from egg extracts results in accumulation of chromosomal DNA breaks during replicative synthesis. Our results suggest coordinated chromatin recruitment of xFA proteins in response to replication-associated DNA lesions and indicate that xFA proteins function to prevent the accumulation of DNA breaks that arise during unperturbed replication.

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21

Enver, T., A. C. Brewer, and R. K. Patient. "Role for DNA replication in beta-globin gene activation." Molecular and Cellular Biology 8, no. 3 (March 1988): 1301–8. http://dx.doi.org/10.1128/mcb.8.3.1301-1308.1988.

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Transcriptional activation of the Xenopus laevis beta-globin gene requires the synergistic action of the simian virus 40 enhancer and DNA replication in DEAE-dextran-mediated HeLa cell transfections. Replication does not act through covalent modification of the template, since its requirement was not obviated by the prior replication of the transfected DNA in eucaryotic cells. Transfection of DNA over a 100-fold range demonstrates that replication does not contribute to gene activation simply increasing template copy number. Furthermore, in cotransfections of replicating and nonreplicating constructs, only replicating templates were transcribed. Replication is not simply a requirement of chromatin assembly, since even unreplicated templates generated nucleosomal ladders. Stimulation of beta-globin transcription by DNA replication, though less marked, was also observed in calcium phosphate transfections. We interpret these results as revealing a dynamic role for replication in gene activation.

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Enver, T., A. C. Brewer, and R. K. Patient. "Role for DNA replication in beta-globin gene activation." Molecular and Cellular Biology 8, no. 3 (March 1988): 1301–8. http://dx.doi.org/10.1128/mcb.8.3.1301.

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Transcriptional activation of the Xenopus laevis beta-globin gene requires the synergistic action of the simian virus 40 enhancer and DNA replication in DEAE-dextran-mediated HeLa cell transfections. Replication does not act through covalent modification of the template, since its requirement was not obviated by the prior replication of the transfected DNA in eucaryotic cells. Transfection of DNA over a 100-fold range demonstrates that replication does not contribute to gene activation simply increasing template copy number. Furthermore, in cotransfections of replicating and nonreplicating constructs, only replicating templates were transcribed. Replication is not simply a requirement of chromatin assembly, since even unreplicated templates generated nucleosomal ladders. Stimulation of beta-globin transcription by DNA replication, though less marked, was also observed in calcium phosphate transfections. We interpret these results as revealing a dynamic role for replication in gene activation.

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23

Danovich, R. M., and N. Frenkel. "Herpes simplex virus induces the replication of foreign DNA." Molecular and Cellular Biology 8, no. 8 (August 1988): 3272–81. http://dx.doi.org/10.1128/mcb.8.8.3272-3281.1988.

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Plasmids containing the simian virus 40 (SV40) DNA replication origin and the large T gene are replicated efficiently in Vero monkey cells but not in rabbit skin cells. Efficient replication of the plasmids was observed in rabbit skin cells infected with herpes simplex virus type 1 (HSV-1) and HSV-2. The HSV-induced replication required the large T antigen and the SV40 replication origin. However, it produced concatemeric molecules resembling replicative intermediates of HSV DNA and was sensitive to phosphonoacetate at concentrations known to inhibit the HSV DNA polymerase. Therefore, it involved the HSV DNA polymerase itself or a viral gene product(s) which was expressed following the replication of HSV DNA. Analyses of test plasmids lacking SV40 or HSV DNA sequences showed that, under some conditions, HSV also induced low-level replication of test plasmids containing no known eucaryotic replication origins. Together, these results show that HSV induces a DNA replicative activity which amplifies foreign DNA. The relevance of these findings to the putative transforming potential of HSV is discussed.

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Danovich, R. M., and N. Frenkel. "Herpes simplex virus induces the replication of foreign DNA." Molecular and Cellular Biology 8, no. 8 (August 1988): 3272–81. http://dx.doi.org/10.1128/mcb.8.8.3272.

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Plasmids containing the simian virus 40 (SV40) DNA replication origin and the large T gene are replicated efficiently in Vero monkey cells but not in rabbit skin cells. Efficient replication of the plasmids was observed in rabbit skin cells infected with herpes simplex virus type 1 (HSV-1) and HSV-2. The HSV-induced replication required the large T antigen and the SV40 replication origin. However, it produced concatemeric molecules resembling replicative intermediates of HSV DNA and was sensitive to phosphonoacetate at concentrations known to inhibit the HSV DNA polymerase. Therefore, it involved the HSV DNA polymerase itself or a viral gene product(s) which was expressed following the replication of HSV DNA. Analyses of test plasmids lacking SV40 or HSV DNA sequences showed that, under some conditions, HSV also induced low-level replication of test plasmids containing no known eucaryotic replication origins. Together, these results show that HSV induces a DNA replicative activity which amplifies foreign DNA. The relevance of these findings to the putative transforming potential of HSV is discussed.

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25

Taricani, Lorena, and Teresa S. F. Wang. "Rad4TopBP1, a Scaffold Protein, Plays Separate Roles in DNA Damage and Replication Checkpoints and DNA Replication." Molecular Biology of the Cell 17, no. 8 (August 2006): 3456–68. http://dx.doi.org/10.1091/mbc.e06-01-0056.

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Rad4TopBP1, a BRCT domain protein, is required for both DNA replication and checkpoint responses. Little is known about how the multiple roles of Rad4TopBP1 are coordinated in maintaining genome integrity. We show here that Rad4TopBP1 of fission yeast physically interacts with the checkpoint sensor proteins, the replicative DNA polymerases, and a WD-repeat protein, Crb3. We identified four novel mutants to investigate how Rad4TopBP1 could have multiple roles in maintaining genomic integrity. A novel mutation in the third BRCT domain of rad4+TopBP1 abolishes DNA damage checkpoint response, but not DNA replication, replication checkpoint, and cell cycle progression. This mutant protein is able to associate with all three replicative polymerases and checkpoint proteins Rad3ATR-Rad26ATRIP, Hus1, Rad9, and Rad17 but has a compromised association with Crb3. Furthermore, the damaged-induced Rad9 phosphorylation is significantly reduced in this rad4TopBP1 mutant. Genetic and biochemical analyses suggest that Crb3 has a role in the maintenance of DNA damage checkpoint and influences the Rad4TopBP1 damage checkpoint function. Taken together, our data suggest that Rad4TopBP1 provides a scaffold to a large complex containing checkpoint and replication proteins thereby separately enforcing checkpoint responses to DNA damage and replication perturbations during the cell cycle.

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26

Pierron, Gérard, Dominick Pallotta, and Marianne Bénard. "The One-Kilobase DNA Fragment Upstream of theardC Actin Gene of Physarum polycephalum Is Both a Replicator and a Promoter." Molecular and Cellular Biology 19, no. 5 (May 1, 1999): 3506–14. http://dx.doi.org/10.1128/mcb.19.5.3506.

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ABSTRACT The 1-kb DNA fragment upstream of the ardC actin gene of Physarum polycephalum promotes the transcription of a reporter gene either in a transient-plasmid assay or as an integrated copy in an ectopic position, defining this region as the transcriptional promoter of the ardC gene (PardC). Since we mapped an origin of replication activated at the onset of S phase within this same fragment, we examined the pattern of replication of a cassette containing the PardCpromoter and the hygromycin phosphotransferase gene, hph, integrated into two different chromosomal sites. In both cases, we show by two-dimensional agarose gel electrophoresis that an efficient, early activated origin coincides with the ectopic PardC fragment. One of the integration sites was a normally late-replicating region. The presence of the ectopic origin converted this late-replicating domain into an early-replicating domain in which replication forks propagate with kinetics indistinguishable from those of the nativePardC replicon. This is the first demonstration that initiation sites for DNA replication in Physarum correspond to cis-acting replicator sequences. This work also confirms the close proximity of a replication origin and a promoter, with both functions being located within the 1-kb proximal region of theardC actin gene. A more precise location of the replication origin with respect to the transcriptional promoter must await the development of a functional autonomously replicating sequence assay inPhysarum.

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27

Montecucco, Alessandra, Rossella Rossi, Giovanni Ferrari, A. Ivana Scovassi, Ennio Prosperi, and Giuseppe Biamonti. "Etoposide Induces the Dispersal of DNA Ligase I from Replication Factories." Molecular Biology of the Cell 12, no. 7 (July 2001): 2109–18. http://dx.doi.org/10.1091/mbc.12.7.2109.

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In eukaryotic cells DNA replication occurs in specific nuclear compartments, called replication factories, that undergo complex rearrangements during S-phase. The molecular mechanisms underlying the dynamics of replication factories are still poorly defined. Here we show that etoposide, an anticancer drug that induces double-strand breaks, triggers the redistribution of DNA ligase I and proliferating cell nuclear antigen from replicative patterns and the ensuing dephosphorylation of DNA ligase I. Moreover, etoposide triggers the formation of RPA foci, distinct from replication factories. The effect of etoposide on DNA ligase I localization is prevented by aphidicolin, an inhibitor of DNA replication, and by staurosporine, a protein kinase inhibitor and checkpoints' abrogator. We suggest that dispersal of DNA ligase I is triggered by an intra-S-phase checkpoint activated when replicative forks meet topoisomerase II-DNA–cleavable complexes. However, etoposide treatment of ataxia telangiectasia cells demonstrated that ataxia-telangiectasia-mutated activity is not required for the disassembly of replication factories and the formation of replication protein A foci.

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28

Robinson, D. R., and K. Gull. "The configuration of DNA replication sites within the Trypanosoma brucei kinetoplast." Journal of Cell Biology 126, no. 3 (August 1, 1994): 641–48. http://dx.doi.org/10.1083/jcb.126.3.641.

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The kinetoplast is a concatenated network of circular DNA molecules found in the mitochondrion of many trypanosomes. This mass of DNA is replicated in a discrete "S" phase in the cell cycle. We have tracked the incorporation of the thymidine analogue 5-bromodeoxyuridine into newly replicated DNA by immunofluorescence and novel immunogold labeling procedures. This has allowed the detection of particular sites of replicated DNA in the replicating and segregating kinetoplast. These studies provide a new method for observing kinetoplast DNA (kDNA) replication patterns at high resolution. The techniques reveal that initially the pattern of replicated DNA is antipodal and can be detected both on isolated complexes and in replicating kDNA in vivo. In Trypanosoma brucei the opposing edges of replicating kDNA never extend around the complete circumference of the network, as seen in other kinetoplastids. Furthermore, crescent-shaped labeling patterns are formed which give way to labeling of most of the replicating kDNA except the characteristic midzone. The configuration of these sites of replicated DNA molecules is different to previous studies on organisms such as Crithidia fasciculata, suggesting differences in the timing of replication of mini and maxicircles and/or organization of the replicative apparatus in the kinetoplast of the African trypanosome.

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29

Müller, Carolin A., and Conrad A. Nieduszynski. "DNA replication timing influences gene expression level." Journal of Cell Biology 216, no. 7 (May 24, 2017): 1907–14. http://dx.doi.org/10.1083/jcb.201701061.

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Eukaryotic genomes are replicated in a reproducible temporal order; however, the physiological significance is poorly understood. We compared replication timing in divergent yeast species and identified genomic features with conserved replication times. Histone genes were among the earliest replicating loci in all species. We specifically delayed the replication of HTA1-HTB1 and discovered that this halved the expression of these histone genes. Finally, we showed that histone and cell cycle genes in general are exempt from Rtt109-dependent dosage compensation, suggesting the existence of pathways excluding specific loci from dosage compensation mechanisms. Thus, we have uncovered one of the first physiological requirements for regulated replication time and demonstrated a direct link between replication timing and gene expression.

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30

Iwasaki, Hiromichi, Peng Huang, Michael J. Keating, and William Plunkett. "Differential Incorporation of Ara-C, Gemcitabine, and Fludarabine Into Replicating and Repairing DNA in Proliferating Human Leukemia Cells." Blood 90, no. 1 (July 1, 1997): 270–78. http://dx.doi.org/10.1182/blood.v90.1.270.

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Abstract The major actions of nucleoside analogs such as arabinosylcytosine (ara-C) and fludarabine occurs after their incorporation into DNA, during either replication or repair synthesis. The metabolic salvage and DNA incorporation of the normal nucleoside, deoxycytidine, is functionally compartmentalized toward repair synthesis in a process regulated by ribonucleotide reductase. The aim of this study was to investigate the metabolic pathways by which nucleoside analogs that do (fludarabine, gemcitabine) or do not (ara-C) affect ribonucleotide reductase are incorporated into DNA in proliferating human leukemia cells. Using alkaline density-gradient centrifugation to separate repaired DNA from replicating DNA and unreplicated parental DNA strands, approximately 60% of ara-C nucleotide in DNA was incorporated by repair synthesis in CCRF-CEM cells; the remainder was incorporated by replication. In contrast, fludarabine and gemcitabine, nucleosides that inhibit ribonucleotide reductase and decreased deoxynucleotide pools, were incorporated mainly within replicating DNA. Hydroxyurea also depleted deoxynucleotide pools and increased the incorporation of ara-C into DNA by replicative synthesis. Stimulation of DNA repair activity by UV irradiation selectively enhanced the incorporation of all nucleosides tested through repair synthesis. These findings suggest that the pathways by which therapeutically useful nucleoside analogs are incorporated into DNA are affected by cellular dNTP pools from de novo synthesis and by the relative activities of DNA repair and replication. The antitumor activity of these drugs may be enhanced by combination with either ribonucleotide reductase inhibitors to increase their incorporation into replicating DNA or with agents that induce DNA damage and evoke the DNA repair process.

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31

Iwasaki, Hiromichi, Peng Huang, Michael J. Keating, and William Plunkett. "Differential Incorporation of Ara-C, Gemcitabine, and Fludarabine Into Replicating and Repairing DNA in Proliferating Human Leukemia Cells." Blood 90, no. 1 (July 1, 1997): 270–78. http://dx.doi.org/10.1182/blood.v90.1.270.270_270_278.

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Abstract:

The major actions of nucleoside analogs such as arabinosylcytosine (ara-C) and fludarabine occurs after their incorporation into DNA, during either replication or repair synthesis. The metabolic salvage and DNA incorporation of the normal nucleoside, deoxycytidine, is functionally compartmentalized toward repair synthesis in a process regulated by ribonucleotide reductase. The aim of this study was to investigate the metabolic pathways by which nucleoside analogs that do (fludarabine, gemcitabine) or do not (ara-C) affect ribonucleotide reductase are incorporated into DNA in proliferating human leukemia cells. Using alkaline density-gradient centrifugation to separate repaired DNA from replicating DNA and unreplicated parental DNA strands, approximately 60% of ara-C nucleotide in DNA was incorporated by repair synthesis in CCRF-CEM cells; the remainder was incorporated by replication. In contrast, fludarabine and gemcitabine, nucleosides that inhibit ribonucleotide reductase and decreased deoxynucleotide pools, were incorporated mainly within replicating DNA. Hydroxyurea also depleted deoxynucleotide pools and increased the incorporation of ara-C into DNA by replicative synthesis. Stimulation of DNA repair activity by UV irradiation selectively enhanced the incorporation of all nucleosides tested through repair synthesis. These findings suggest that the pathways by which therapeutically useful nucleoside analogs are incorporated into DNA are affected by cellular dNTP pools from de novo synthesis and by the relative activities of DNA repair and replication. The antitumor activity of these drugs may be enhanced by combination with either ribonucleotide reductase inhibitors to increase their incorporation into replicating DNA or with agents that induce DNA damage and evoke the DNA repair process.

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32

Wanka, F. "Functional aspects of the nuclear matrix." Acta Biochimica Polonica 42, no. 2 (June 30, 1995): 127–31. http://dx.doi.org/10.18388/abp.1995_4599.

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A model is proposed of the way in which the unwinding of the chromosomal DNA loops is controlled during DNA replication. It is based on the observation of a permanent binding of replication origins to the nuclear matrix and of a transient attachment of replicating DNA regions to sites in the immediate neighbourhood. DNA unwinding is controlled while the replicating loops are reeled through the replication binding sites. Also a mechanism is proposed to explain how the once-per-cycle replication of individual replicons can be controlled. DNA synthesis is initiated at single-stranded loops exposed by tandemly repeated DNA sequences at the replication origins. The single-stranded loops turn into fully double-stranded DNA during replication, becoming inaccessible for a second initiation during the same cell cycle. The configuration competent for initiation is restored by specific protein-DNA rearrangements coupled to mitotic condensation of the matrix into chromosomal scaffolds and its reversal.

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33

Bennett, Joan. "Modeling DNA Replication." American Biology Teacher 60, no. 6 (June 1, 1998): 457–60. http://dx.doi.org/10.2307/4450521.

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34

So, Antero G., and Kathleen M. Downey. "Eukaryotic DNA Replication." Critical Reviews in Biochemistry and Molecular Biology 27, no. 1-2 (January 1992): 129–55. http://dx.doi.org/10.3109/10409239209082561.

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35

Nishitani, Nishitani. "DNA replication licensing." Frontiers in Bioscience 9, no. 1-3 (2004): 2115. http://dx.doi.org/10.2741/1315.

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36

Chow, Louise T., and Thomas R. Broker. "Papillomavirus DNA Replication." Intervirology 37, no. 3-4 (1994): 150–58. http://dx.doi.org/10.1159/000150373.

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37

Campbell, J. L. "Eukaryotic DNA Replication." Annual Review of Biochemistry 55, no. 1 (June 1986): 733–71. http://dx.doi.org/10.1146/annurev.bi.55.070186.003505.

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38

Marians, Kenneth J. "Prokaryotic DNA Replication." Annual Review of Biochemistry 61, no. 1 (June 1992): 673–715. http://dx.doi.org/10.1146/annurev.bi.61.070192.003325.

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39

Kunkel, Thomas A., and Katarzyna Bebenek. "DNA Replication Fidelity." Annual Review of Biochemistry 69, no. 1 (June 2000): 497–529. http://dx.doi.org/10.1146/annurev.biochem.69.1.497.

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40

Leonard, A. C., and M. Mechali. "DNA Replication Origins." Cold Spring Harbor Perspectives in Biology 5, no. 10 (July 9, 2013): a010116. http://dx.doi.org/10.1101/cshperspect.a010116.

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41

Rhind, N., and D. M. Gilbert. "DNA Replication Timing." Cold Spring Harbor Perspectives in Biology 5, no. 8 (July 9, 2013): a010132. http://dx.doi.org/10.1101/cshperspect.a010132.

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42

Moss, B. "Poxvirus DNA Replication." Cold Spring Harbor Perspectives in Biology 5, no. 9 (July 9, 2013): a010199. http://dx.doi.org/10.1101/cshperspect.a010199.

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43

Hoeben, R. C., and T. G. Uil. "Adenovirus DNA Replication." Cold Spring Harbor Perspectives in Biology 5, no. 3 (February 6, 2013): a013003. http://dx.doi.org/10.1101/cshperspect.a013003.

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44

Weinreich, Michael. "DNA replication reconstructed." Nature 519, no. 7544 (March 2015): 418–19. http://dx.doi.org/10.1038/519418a.

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45

Halazonetis, Thanos D. "Conservative DNA Replication." Nature Reviews Molecular Cell Biology 15, no. 5 (March 26, 2014): 300. http://dx.doi.org/10.1038/nrm3784.

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46

Lambert, P. F. "Papillomavirus DNA replication." Journal of Virology 65, no. 7 (1991): 3417–20. http://dx.doi.org/10.1128/jvi.65.7.3417-3420.1991.

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47

Campbell, J. L. "Yeast DNA replication." Journal of Biological Chemistry 268, no. 34 (December 1993): 25261–64. http://dx.doi.org/10.1016/s0021-9258(19)74385-3.

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48

Kelly, T. J. "SV40 DNA replication." Journal of Biological Chemistry 263, no. 34 (December 1988): 17889–92. http://dx.doi.org/10.1016/s0021-9258(19)81296-6.

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49

Diffley, John F. X. "Eukaryotic DNA replication." Current Opinion in Cell Biology 6, no. 3 (June 1994): 368–72. http://dx.doi.org/10.1016/0955-0674(94)90028-0.

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50

Wang, Thomas A., and Joachim J. Li. "Eukaryotic DNA replication." Current Opinion in Cell Biology 7, no. 3 (January 1995): 414–20. http://dx.doi.org/10.1016/0955-0674(95)80098-0.

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