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Journal articles on the topic 'DNA replication'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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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 (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 b

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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 (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 b

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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 (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 inco

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4

Liu, Guoqi, Michelle Malott, and Michael Leffak. "Multiple Functional Elements Comprise a Mammalian Chromosomal Replicator." Molecular and Cellular Biology 23, no. 5 (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 contain

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5

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 (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 replicat

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6

Moiseeva, Tatiana N., Yandong Yin, Michael J. Calderon, et al. "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 (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

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7

Takebayashi, Shin-ichiro, Tyrone Ryba, Kelsey Wimbish, et al. "The Temporal Order of DNA Replication Shaped by Mammalian DNA Methyltransferases." Cells 10, no. 2 (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

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8

Thomas, David C., John D. Roberts, Ralph D. Sabatino, et al. "Fidelity of mammalian DNA replication and replicative DNA polymerases." Biochemistry 30, no. 51 (1991): 11751–59. http://dx.doi.org/10.1021/bi00115a003.

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9

Greci, Mark D., and Stephen D. Bell. "Archaeal DNA Replication." Annual Review of Microbiology 74, no. 1 (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

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10

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 (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 relativel

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11

Manuel, S. Valenzuela. "Initiation of DNA Replication and Cancer." Biohelikon 1, no. 1 (2013): 1–4. https://doi.org/10.5281/zenodo.810511.

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DNA replication, the key determinant of cell proliferation, is a highly regulated process whose objective is to ensure that the genetic information encoded in the chromosomes is faithfully transmitted from parental to progeny cells. Failure in this regulation could lead to abnormal proliferation and genomic instability, the hallmarks of cancer cells. The initiation step in DNA replication constitutes the main target in the alteration of cell proliferation. Initiation of DNA replication requires the activation of thousands of origins of DNA replication (ORIs) which fire only once, in a pre-dete

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12

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

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13

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

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14

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

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15

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

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16

Sobeck, Alexandra, Stacie Stone, Vincenzo Costanzo, et al. "Fanconi Anemia Proteins Are Required To Prevent Accumulation of Replication-Associated DNA Double-Strand Breaks." Molecular and Cellular Biology 26, no. 2 (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

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17

Nasheuer, Heinz Peter, and Anna Marie Meaney. "Starting DNA Synthesis: Initiation Processes during the Replication of Chromosomal DNA in Humans." Genes 15, no. 3 (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 a

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18

Stoeber, Kai, Thea D. Tlsty, Lisa Happerfield, et al. "DNA replication licensing and human cell proliferation." Journal of Cell Science 114, no. 11 (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 pre

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19

Weitzman, Matthew D., and Amélie Fradet-Turcotte. "Virus DNA Replication and the Host DNA Damage Response." Annual Review of Virology 5, no. 1 (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,

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20

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 (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 con

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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 (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 con

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22

Danovich, R. M., and N. Frenkel. "Herpes simplex virus induces the replication of foreign DNA." Molecular and Cellular Biology 8, no. 8 (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 invol

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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 (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 invol

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24

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 (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 sh

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25

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

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26

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

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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 (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 e

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28

Wanka, F. "Functional aspects of the nuclear matrix." Acta Biochimica Polonica 42, no. 2 (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 expose

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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 (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 prolifera

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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 (1997): 270–78. http://dx.doi.org/10.1182/blood.v90.1.270.270_270_278.

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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 huma

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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 (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

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Robinson, D. R., and K. Gull. "The configuration of DNA replication sites within the Trypanosoma brucei kinetoplast." Journal of Cell Biology 126, no. 3 (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 techn

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33

Bashir, Tarig, Jean Rommelaere, and Celina Cziepluch. "In Vivo Accumulation of Cyclin A and Cellular Replication Factors in Autonomous Parvovirus Minute Virus of Mice-Associated Replication Bodies." Journal of Virology 75, no. 9 (2001): 4394–98. http://dx.doi.org/10.1128/jvi.75.9.4394-4398.2001.

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ABSTRACT Autonomous parvovirus minute virus of mice (MVM) DNA replication is strictly dependent on cellular factors expressed during the S phase of the cell cycle. Here we report that MVM DNA replication proceeds in specific nuclear structures termed autonomous parvovirus-associated replication bodies, where components of the basic cellular replication machinery accumulate. The presence of DNA polymerases α and δ in these bodies suggests that MVM utilizes partially preformed cellular replication complexes for its replication. The recruitment of cyclin A points to a role for this cell cycle fac

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Sobeck, Alexandra, Stacie Stone, Bendert deGraaf, et al. "Coordinated Chromatin-Association of Fanconi Anemia Network Proteins Requires Replication-Coupled DNA Damage Recognition." Blood 104, no. 11 (2004): 723. http://dx.doi.org/10.1182/blood.v104.11.723.723.

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Abstract Fanconi anemia (FA) is a genetic disorder characterized by hypersensitivity to DNA crosslinking agents and diverse clinical symptoms, including developmental anomalies, progressive bone marrow failure, and predisposition to leukemias and other cancers. FA is genetically heterogeneous, resulting from mutations in any of at least eleven different genes. The FA proteins function together in a pathway composed of a mulitprotein core complex that is required to trigger the DNA-damage dependent activation of the downstream FA protein, FANCD2. This activation is thought to be the key step in

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Yuan, Zuanning, and Huilin Li. "Molecular mechanisms of eukaryotic origin initiation, replication fork progression, and chromatin maintenance." Biochemical Journal 477, no. 18 (2020): 3499–525. http://dx.doi.org/10.1042/bcj20200065.

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Eukaryotic DNA replication is a highly dynamic and tightly regulated process. Replication involves several dozens of replication proteins, including the initiators ORC and Cdc6, replicative CMG helicase, DNA polymerase α-primase, leading-strand DNA polymerase ε, and lagging-strand DNA polymerase δ. These proteins work together in a spatially and temporally controlled manner to synthesize new DNA from the parental DNA templates. During DNA replication, epigenetic information imprinted on DNA and histone proteins is also copied to the daughter DNA to maintain the chromatin status. DNA methyltran

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Müller, Carolin A., and Conrad A. Nieduszynski. "DNA replication timing influences gene expression level." Journal of Cell Biology 216, no. 7 (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 pathw

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Quintini, G., K. Treuner, C. Gruss, and R. Knippers. "Role of amino-terminal histone domains in chromatin replication." Molecular and Cellular Biology 16, no. 6 (1996): 2888–97. http://dx.doi.org/10.1128/mcb.16.6.2888.

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Simian virus 40 minichromosomes were treated with trypsin to specifically remove the amino-terminal histone domains (tails). Trypsin treatment does not affect the spacing and the number of nucleosomes on minichromosomes but indices a more extended conformation, as shown by the reduced sedimentation coefficient of trypsinized minichromosomes compared with the untreated controls. Trypsinized minichromosomes replicate more efficiently than control minichromosomes in in vitro replication assays. The increased template efficiency appears to be due to higher rates of replicative fork movement. In vi

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38

Weerasooriya, Savithri, Katherine A. DiScipio, Anthar S. Darwish, Ping Bai, and Sandra K. Weller. "Herpes simplex virus 1 ICP8 mutant lacking annealing activity is deficient for viral DNA replication." Proceedings of the National Academy of Sciences 116, no. 3 (2018): 1033–42. http://dx.doi.org/10.1073/pnas.1817642116.

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Most DNA viruses that use recombination-dependent mechanisms to replicate their DNA encode a single-strand annealing protein (SSAP). The herpes simplex virus (HSV) single-strand DNA binding protein (SSB), ICP8, is the central player in all stages of DNA replication. ICP8 is a classical replicative SSB and interacts physically and/or functionally with the other viral replication proteins. Additionally, ICP8 can promote efficient annealing of complementary ssDNA and is thus considered to be a member of the SSAP family. The role of annealing during HSV infection has been difficult to assess in pa

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Zhu, Huanbo, Umang Swami, Ranjan Preet, and Jun Zhang. "Harnessing DNA Replication Stress for Novel Cancer Therapy." Genes 11, no. 9 (2020): 990. http://dx.doi.org/10.3390/genes11090990.

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DNA replication is the fundamental process for accurate duplication and transfer of genetic information. Its fidelity is under constant stress from endogenous and exogenous factors which can cause perturbations that lead to DNA damage and defective replication. This can compromise genomic stability and integrity. Genomic instability is considered as one of the hallmarks of cancer. In normal cells, various checkpoints could either activate DNA repair or induce cell death/senescence. Cancer cells on the other hand potentiate DNA replicative stress, due to defective DNA damage repair mechanism an

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40

Hsieh, C. L., R. P. McCloskey, E. Radany, and M. R. Lieber. "V(D)J recombination: evidence that a replicative mechanism is not required." Molecular and Cellular Biology 11, no. 8 (1991): 3972–77. http://dx.doi.org/10.1128/mcb.11.8.3972-3977.1991.

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We examined a series of extrachromosomal DNA substrates for V(D)J recombination under replicating and nonreplicating conditions. Complete and partial replications were examined by monitoring the loss of prokaryote-specific adenine methylation at 14 to 22 MboI-DpnI restriction sites (GATC) on the substrates. Some of these sites are within 2 bases of the signal sequence ends. We found that neither coding joint nor signal joint formation requires substrate replication. After ruling out replication as a substrate requirement, we determined whether replication had any effect on the efficiency of V(

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Hsieh, C. L., R. P. McCloskey, E. Radany, and M. R. Lieber. "V(D)J recombination: evidence that a replicative mechanism is not required." Molecular and Cellular Biology 11, no. 8 (1991): 3972–77. http://dx.doi.org/10.1128/mcb.11.8.3972.

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We examined a series of extrachromosomal DNA substrates for V(D)J recombination under replicating and nonreplicating conditions. Complete and partial replications were examined by monitoring the loss of prokaryote-specific adenine methylation at 14 to 22 MboI-DpnI restriction sites (GATC) on the substrates. Some of these sites are within 2 bases of the signal sequence ends. We found that neither coding joint nor signal joint formation requires substrate replication. After ruling out replication as a substrate requirement, we determined whether replication had any effect on the efficiency of V(

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Shechter, David, Carol Y. Ying, and Jean Gautier. "DNA Unwinding Is an MCM Complex-dependent and ATP Hydrolysis-dependent Process." Journal of Biological Chemistry 279, no. 44 (2004): 45586–93. http://dx.doi.org/10.1074/jbc.m407772200.

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Minichromosome maintenance proteins (Mcm) are essential in all eukaryotes and are absolutely required for initiation of DNA replication. The eukaryotic and archaeal Mcm proteins have conserved helicase motifs and exhibit DNA helicase and ATP hydrolysis activitiesin vitro. Although the Mcm proteins have been proposed to be the replicative helicase, the enzyme that melts the DNA helix at the replication fork, their function during cellular DNA replication elongation is still unclear. Using nucleoplasmic extract (NPE) fromXenopus laeviseggs and six purified polyclonal antibodies generated against

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Nickoloff, Jac A., Aruna S. Jaiswal, Neelam Sharma, et al. "Cellular Responses to Widespread DNA Replication Stress." International Journal of Molecular Sciences 24, no. 23 (2023): 16903. http://dx.doi.org/10.3390/ijms242316903.

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Replicative DNA polymerases are blocked by nearly all types of DNA damage. The resulting DNA replication stress threatens genome stability. DNA replication stress is also caused by depletion of nucleotide pools, DNA polymerase inhibitors, and DNA sequences or structures that are difficult to replicate. Replication stress triggers complex cellular responses that include cell cycle arrest, replication fork collapse to one-ended DNA double-strand breaks, induction of DNA repair, and programmed cell death after excessive damage. Replication stress caused by specific structures (e.g., G-rich sequen

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Ho, Yen-Chih, Chen-Syun Ku, Siang-Sheng Tsai, et al. "PARP1 recruits DNA translocases to restrain DNA replication and facilitate DNA repair." PLOS Genetics 18, no. 12 (2022): e1010545. http://dx.doi.org/10.1371/journal.pgen.1010545.

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Replication fork reversal which restrains DNA replication progression is an important protective mechanism in response to replication stress. PARP1 is recruited to stalled forks to restrain DNA replication. However, PARP1 has no helicase activity, and the mechanism through which PARP1 participates in DNA replication restraint remains unclear. Here, we found novel protein-protein interactions between PARP1 and DNA translocases, including HLTF, SHPRH, ZRANB3, and SMARCAL1, with HLTF showing the strongest interaction among these DNA translocases. Although HLTF and SHPRH share structural and funct

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Keijzers, Guido, Daniela Bakula, Michael Petr, et al. "Human Exonuclease 1 (EXO1) Regulatory Functions in DNA Replication with Putative Roles in Cancer." International Journal of Molecular Sciences 20, no. 1 (2018): 74. http://dx.doi.org/10.3390/ijms20010074.

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Human exonuclease 1 (EXO1), a 5′→3′ exonuclease, contributes to the regulation of the cell cycle checkpoints, replication fork maintenance, and post replicative DNA repair pathways. These processes are required for the resolution of stalled or blocked DNA replication that can lead to replication stress and potential collapse of the replication fork. Failure to restart the DNA replication process can result in double-strand breaks, cell-cycle arrest, cell death, or cellular transformation. In this review, we summarize the involvement of EXO1 in the replication, DNA repair pathways, cell cycle c

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Wang, Lixin, Chii-Mei Lin, Sarah Brooks, Dan Cimbora, Mark Groudine та Mirit I. Aladjem. "The Human β-Globin Replication Initiation Region Consists of Two Modular Independent Replicators". Molecular and Cellular Biology 24, № 8 (2004): 3373–86. http://dx.doi.org/10.1128/mcb.24.8.3373-3386.2004.

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ABSTRACT Previous studies have shown that mammalian cells contain replicator sequences, which can determine where DNA replication initiates. However, the specific sequences that confer replicator activity were not identified. Here we report a detailed analysis of replicator sequences that dictate initiation of DNA replication from the human β-globin locus. This analysis suggests that the β-globin replication initiation region contains two adjacent, redundant replicators. Each replicator was capable of initiating DNA replication independently at ectopic sites. Within each of these two replicato

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Merchant, A. M., Y. Kawasaki, Y. Chen, M. Lei, and B. K. Tye. "A lesion in the DNA replication initiation factor Mcm10 induces pausing of elongation forks through chromosomal replication origins in Saccharomyces cerevisiae." Molecular and Cellular Biology 17, no. 6 (1997): 3261–71. http://dx.doi.org/10.1128/mcb.17.6.3261.

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We describe a new minichromosome maintenance factor, Mcm10, and show that this essential protein is involved in the initiation of DNA replication in Saccharomyces cerevisiae. The mcm10 mutant has an autonomously replicating sequence-specific minichromosome maintenance defect and arrests at the nonpermissive temperature with dumbbell morphology and 2C DNA content. Mcm10 is a nuclear protein that physically interacts with several members of the MCM2-7 family of DNA replication initiation factors. Cloning and sequencing of the MCM10 gene show that it is identical to DNA43, a gene identified indep

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Zhang, Hui. "Regulation of DNA Replication Licensing and Re-Replication by Cdt1." International Journal of Molecular Sciences 22, no. 10 (2021): 5195. http://dx.doi.org/10.3390/ijms22105195.

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In eukaryotic cells, DNA replication licensing is precisely regulated to ensure that the initiation of genomic DNA replication in S phase occurs once and only once for each mitotic cell division. A key regulatory mechanism by which DNA re-replication is suppressed is the S phase-dependent proteolysis of Cdt1, an essential replication protein for licensing DNA replication origins by loading the Mcm2-7 replication helicase for DNA duplication in S phase. Cdt1 degradation is mediated by CRL4Cdt2 ubiquitin E3 ligase, which further requires Cdt1 binding to proliferating cell nuclear antigen (PCNA)

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

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

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