Journal articles: 'Asynchronous replication'

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Natanzon, Assaf, and Eitan Bachmat. "Dynamic Synchronous/Asynchronous Replication." ACM Transactions on Storage 9, no. 3 (August 1, 2013): 1–19. http://dx.doi.org/10.1145/2501620.2508011.

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Natanzon, Assaf, and Eitan Bachmat. "Dynamic Synchronous/Asynchronous Replication." ACM Transactions on Storage 9, no. 3 (August 2013): 1–19. http://dx.doi.org/10.1145/2508011.

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Lee, Jia, Susumu Adachi, and Ferdinand Peper. "Reliable Self-Replicating Machines in Asynchronous Cellular Automata." Artificial Life 13, no. 4 (October 2007): 397–413. http://dx.doi.org/10.1162/artl.2007.13.4.397.

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We propose a self-replicating machine that is embedded in a two-dimensional asynchronous cellular automaton with von Neumann neighborhood. The machine dynamically encodes its shape into description signals, and despite the randomness of cell updating, it is able to successfully construct copies of itself according to the description signals. Self-replication on asynchronously updated cellular automata may find application in nanocomputers, where reconfigurability is an essential property, since it allows avoidance of defective parts and simplifies programming of such computers.

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Mikhailova, G. F., V. V. Tsepenko, T. G. Shkavrova, and E. V. Goloub. "Asynchronous replication in oncological patients." Advances in molecular oncology 5, no. 1 (May 14, 2018): 26–34. http://dx.doi.org/10.17650/2313-805x-2018-5-1-26-34.

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Ogura, Yoshitoshi, Naotake Ogasawara, Elizabeth J. Harry, and Shigeki Moriya. "Increasing the Ratio of Soj to Spo0J Promotes Replication Initiation in Bacillus subtilis." Journal of Bacteriology 185, no. 21 (November 1, 2003): 6316–24. http://dx.doi.org/10.1128/jb.185.21.6316-6324.2003.

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ABSTRACT The ParA and ParB protein families are well conserved in bacteria. However, their functions are still unclear. In Bacillus subtilis, Soj and Spo0J are members of these two protein families, respectively. A previous report revealed that replication initiated early and asynchronously in spo0J null mutant cells, as determined by flow cytometry. In this study, we examined the cause of this promotion of replication initiation. Deletion of both the soj and spo0J genes restored the frequency of replication initiation to almost the wild-type level, suggesting that production of Soj in the absence of Spo0J leads to early and asynchronous initiation of replication. Consistent with this suggestion, overproduction of Soj in wild-type cells had the same effect on replication initiation as in the spo0J null mutant, and overproduction of both Soj and Spo0J did not. These results indicate that when the ratio of Soj to Spo0J increases, Soj interferes with tight control of replication initiation and causes early and asynchronous initiation. Whereas replication initiation also occurred significantly earlier in the two spo0J mutants, spo0J14 and spo0J17, it occurred only slightly early in the sojK16Q mutant and was delayed in the sojG12V mutant. Although Soj localized to nucleoids in the spo0J mutants, the two Soj mutant proteins were distributed throughout the cell or localized to cell poles. Thus, interestingly, the promotion of replication initiation seems to correlate with localization of Soj to nucleoids. This may suggest that Soj inhibits transcription of some cell cycle genes and leads to early and asynchronous initiation of replication. In wild-type cells Spo0J counteracts this Soj function.

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Argyriou-Tirita, A., K. Romanakis, P. Kroisel, and O. A. Haas. "Asynchronous Replication Patterns of Imprinted Genes in Triploid Cells." Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (April 1996): 207–12. http://dx.doi.org/10.1017/s0001566000001318.

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Several unique features distinguish imprinted from nonimprinted genes, including the unusual replication behavior the unequal methylation and the differential expression of imprinted alleles [1]. The replication timing in S phase of the two homologous alleles of a normal, nonimprinted gene is highly synchronous [2, 3]. Housekeeping genes replicate early, constitutive heterochromatic regions replicate late and tissue-specific genes replicate earlier when they are expressed than when they are not [2-4]. In contrast, imprinted genes which, by definition, display allele-specific expression replicate asynchronously [2-5].The relative order of replication of homologous alleles as well as that of different loci can be elegantly compared with fluorescence in situ hybridization (FISH) on interphase nuclei [2-5]. Unreplicated DNA segments give singlet hybridization signals in normal diploid cells, while replicated loci are characterized by doublets. The distribution of these two patterns can be used to determine the S phase replication time of any DNA sequence. Moreover, determination of the singlet/doublet ratio allows a good estimation of the degree of replication asynchrony of two homologous alleles [2-5].Using cell lines with deletions, disomies or associated FISH-detectable centromeric satellite polymorphisms, Kitsberg et al. [4] found that the paternal allele was the early replicating one in all the imprinted genes which they had analyzed. Subsequently, however, Knoll et al. [5] detected genes in the imprinted Prader-Willi region on chromosome 15, which also displayed other patterns. Therefore, it seems necessary to specify the relative timing of maternally and paternally derived alleles for each individual asynchronously replicating gene. Unfortunately, this is so far only feasible with a very restricted number of sequences.

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Masika, Hagit, Marganit Farago, Merav Hecht, Reba Condiotti, Kirill Makedonski, Yosef Buganim, Tal Burstyn-Cohen, Yehudit Bergman, and Howard Cedar. "Programming asynchronous replication in stem cells." Nature Structural & Molecular Biology 24, no. 12 (November 13, 2017): 1132–38. http://dx.doi.org/10.1038/nsmb.3503.

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Frolund, S., and R. Guerraoui. "Implementing E-transactions with asynchronous replication." IEEE Transactions on Parallel and Distributed Systems 12, no. 2 (2001): 133–46. http://dx.doi.org/10.1109/71.910869.

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Tsepenko, V. V., G. F. Mikhailova, T. G. Shkavrova, E. V. Goloub, G. O. Rukhadze, and V. Yu Skoropad. "Asynchronous replication of AURKA and TP53 genes in gastric cancer patients and patients with multiple tumors." Advances in molecular oncology 6, no. 2 (July 27, 2019): 42–47. http://dx.doi.org/10.17650/2313-805x-2019-6-2-42-47.

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Background. The correct genome replication is essential for normal cell division to guarantee that genetic information comes changeless through the next cells generations. DNA replication is a strictly regulated and synchronous process and its disturbances could result to mutations appearances. Aberrant time of DNA replication affects on gene expression causes changes of epigenetic modifications and influences on increasing the structural rearrangements leading to enhanced genome disbalance. Replication time failure as asynchronous replication is common for cancerogeneses. The objective of our study was the assessment of asynchronous replication levels in patients with gastric cancer and patients with multiple tumors.Materials and methods. Fluorescence in situ hybridization (FISH) was used for the asynchronous replication of AURKA and TP53 genes analyses. Interphase FISH on lymphocytes of peripheral blood of 37 healthy donors, 19 patients with non-cancer gastrointestinal pathologies, 68 patients with solitary gastric cancer and 39 patients with multiple tumors having gastric cancer and other second synchronous or metachronous tumor was carried out.Results. Values of lymphocytes with asynchronous replication for AURKA were 19.8 ± 0.5 % for control group, 24.7 ± 0.4 % for non-cancer patients, 32.5 ± 0.5 % for gastric cancer patients, 39.5 ± 0.6 % for patients with multiple tumors and 17.3 ± 0.5, 19.5 ± 0.7, 26.1 ± 0.7 and 32.5 ± 0.6 % for TP53 respectively. Differences between cell populations of examined groups had statistical significance with p <0.01 for both studied gene. Also there was statistical difference between gastric cancer patients having distant metastases and gastric cancer patients without metastases for AURKA (34.4 ± 1.0 % vs. 31.7 ± 0.6 %; p = 0.02).Conclusion. High lymphocytes with asynchronous replication level in oncological patients could serve as potential marker of second tumor or possible metastatic process including the earliest stage of it.

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Guikema, Jeroen E. J., Conny de Boer, Jules Gadiot, Ed Schuuring, and Philip M. Kluin. "Altered Replication Timing of IGH Alleles in Burkitt’s Lymphoma Depends on IGH Breakpoint Position." Blood 104, no. 11 (November 16, 2004): 4276. http://dx.doi.org/10.1182/blood.v104.11.4276.4276.

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Abstract Monoallelic expression of immunoglobulin genes is epigenetically regulated and maintained. Asynchronous replication of the IGH alleles has been implicated in allelic exclusion. Usually, the functional IGH allele replicates early in the S-phase of the cell cycle whereas the non-functional allele replicates late. Previously, the intronic enhancer region (Eμ) and the 3′ Cα enhancer region have been designated as putative replication initiation sites. Activity of these replication origins are likely to be involved in regulation of asynchronous replication. By use of interphase and DNA fiber FISH we have performed a detailed analysis of the configuration of the t(8;14) chromosomal translocation in Burkitt’s lymphoma patients and cell lines and showed that the breakpoints in all studied cases were perfectly reciprocal without loss of IGH genomic material. An important implication is that in patients and cell lines harboring a breakpoint in a downstream switch region (Sγ or Sα) the Eμ and the 3′ Cα enhancer region are physically separated from each other, whereas in patients and cell lines with the IGH breakpoint located in the JH-region both enhancer regions remain on the der(14) chromosome. We therefore studied the IGH replication timing in Burkitt’s lymphoma cell lines harboring different IGH breakpoints by use of BrdU-FISH and interphase FISH on sorted cell cycle fractions. In two cell lines with JH-region breakpoints (Jiyoye and DG-75) the t(8;14) was invariably targeted to the late replicating IGH allele. In contrast, in all three cell lines with switch-region breakpoints (CA-46, Namalwa, BL-65) asynchronous replication of the IGH alleles was lost. As the position of the breakpoint in the MYC locus at 8q24 differed substantially between these cell lines (DG-75 and CA-46: intron 1 of the c-myc gene; Jiyoye, Namalwa, and BL-65: 100 kb to >500 kb centromeric from c-myc) it is unlikely that the position of the 8q24 breakpoint is of crucial influence on IGH replication timing. We speculate that the Eμ and the 3′ Cα enhancer region regulate the IGH replication timing in a cis-acting manner as physical separation of both enhancer regions results in loss of asynchronous replication.

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Ruban-Ośmiałowska, Beata, Dagmara Jakimowicz, Aleksandra Smulczyk-Krawczyszyn, Keith F. Chater, and Jolanta Zakrzewska-Czerwińska. "Replisome Localization in Vegetative and Aerial Hyphae of Streptomyces coelicolor." Journal of Bacteriology 188, no. 20 (October 1, 2006): 7311–16. http://dx.doi.org/10.1128/jb.00940-06.

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ABSTRACT Using a functional fusion of DnaN to enhanced green fluorescent protein, we examined the subcellular localization of the replisome machinery in the vegetative mycelium and aerial mycelium of the multinucleoid organism Streptomyces coelicolor. Chromosome replication took place in many compartments of both types of hypha, with the apical compartments of the aerial mycelium exhibiting the highest replication activity. Within a single compartment, the number of “current” ongoing DNA replications was lower than the expected chromosome number, and the appearance of fluorescent foci was often heterogeneous, indicating that this process is asynchronous within compartments and that only selected chromosomes undergo replication.

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Gribnau, Joost, Sandra Luikenhuis, Konrad Hochedlinger, Kim Monkhorst, and Rudolf Jaenisch. "X chromosome choice occurs independently of asynchronous replication timing." Journal of Cell Biology 168, no. 3 (January 24, 2005): 365–73. http://dx.doi.org/10.1083/jcb.200405117.

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In mammals, dosage compensation is achieved by X chromosome inactivation in female cells. Xist is required and sufficient for X inactivation, and Xist gene deletions result in completely skewed X inactivation. In this work, we analyzed skewing of X inactivation in mice with an Xist deletion encompassing sequence 5 KB upstream of the promoter through exon 3. We found that this mutation results in primary nonrandom X inactivation in which the wild-type X chromosome is always chosen for inactivation. To understand the molecular mechanisms that affect choice, we analyzed the role of replication timing in X inactivation choice. We found that the two Xist alleles and all regions tested on the X chromosome replicate asynchronously before the start of X inactivation. However, analysis of replication timing in cell lines with skewed X inactivation showed no preference for one of the two Xist alleles to replicate early in S-phase before the onset of X inactivation, indicating that asynchronous replication timing does not play a role in skewing of X inactivation.

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Benkemoun, Laura, Catherine Descoteaux, Nicolas T. Chartier, Lionel Pintard, and Jean-Claude Labbé. "PAR-4/LKB1 regulates DNA replication during asynchronous division of the early C. elegans embryo." Journal of Cell Biology 205, no. 4 (May 19, 2014): 447–55. http://dx.doi.org/10.1083/jcb.201312029.

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Regulation of cell cycle duration is critical during development, yet the underlying molecular mechanisms are still poorly understood. The two-cell stage Caenorhabditis elegans embryo divides asynchronously and thus provides a powerful context in which to study regulation of cell cycle timing during development. Using genetic analysis and high-resolution imaging, we found that deoxyribonucleic acid (DNA) replication is asymmetrically regulated in the two-cell stage embryo and that the PAR-4 and PAR-1 polarity proteins dampen DNA replication dynamics specifically in the posterior blastomere, independently of regulators previously implicated in the control of cell cycle timing. Our results demonstrate that accurate control of DNA replication is crucial during C. elegans early embryonic development and further provide a novel mechanism by which PAR proteins control cell cycle progression during asynchronous cell division.

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Theophile, D., D. Bérubé, J. Augé, and M. Vekemans. "Absence of Genomic Imprinting at the DiGeorge Locus." Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (April 1996): 277–80. http://dx.doi.org/10.1017/s0001566000001458.

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Fluorescence in situ hybridization (FISH) has been used to visualize specific genomic DNA sequences in interphase nuclei. Timing of replication can be measured by FISH to interphase nuclei: nuclei with a sequence that has not replicated reveal two single signals (G1), whereas those in which the sequence has replicated show two signal doublets (G2). Asynchronous nuclei show a single signal on one allele and a double hybridization dot on the other homologue. In general, most sequences replicate synchronously on the two homologues, with only 10% of nuclei showing an asynchronous hybridization pattern. However, for the sequences known about to be imprinted, approximately 30% of nuclei reveal asynchronous replication. Little is known whether or not the proximal region of chromosome 22, involved in the DiGeorge syndrome [1], is imprinted. We have, therefore, examined the replication timing pattern of the DiGeorge critical region (DGCR).

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Amiel, Aliza, Lydia Avivi, Elena Gaber, and Moshe D. Fejgin. "Asynchronous replication of allelic loci in Down syndrome." European Journal of Human Genetics 6, no. 4 (July 1998): 359–64. http://dx.doi.org/10.1038/sj.ejhg.5200199.

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16

Singh, Nandita, Farah A. W. Ebrahimi, Alexander A. Gimelbrant, Alexander W. Ensminger, Michael R. Tackett, Peimin Qi, Joost Gribnau, and Andrew Chess. "Coordination of the random asynchronous replication of autosomal loci." Nature Genetics 33, no. 3 (February 10, 2003): 339–41. http://dx.doi.org/10.1038/ng1102.

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Mostoslavsky, Raul, Nandita Singh, Toyoaki Tenzen, Maya Goldmit, Chana Gabay, Sharon Elizur, Peimin Qi, et al. "Asynchronous replication and allelic exclusion in the immune system." Nature 414, no. 6860 (November 2001): 221–25. http://dx.doi.org/10.1038/35102606.

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Ding, Zhiming, Xiaofeng Meng, and Shan Wang. "A transactional asynchronous replication scheme for mobile database systems." Journal of Computer Science and Technology 17, no. 4 (July 2002): 389–96. http://dx.doi.org/10.1007/bf02943279.

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Lundgren, M., A. Andersson, L. Chen, P. Nilsson, and R. Bernander. "Three replication origins in Sulfolobus species: Synchronous initiation of chromosome replication and asynchronous termination." Proceedings of the National Academy of Sciences 101, no. 18 (April 23, 2004): 7046–51. http://dx.doi.org/10.1073/pnas.0400656101.

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LaSalle, Janine M., and Marc Lalande. "Domain organization of allele-specific DNA replication within the GABAA receptor gene cluster." Proceedings, annual meeting, Electron Microscopy Society of America 53 (August 13, 1995): 766–67. http://dx.doi.org/10.1017/s0424820100140208.

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Parental imprinting is a gamete-specific modification that distinguishes the paternal and maternal chromosomes in higher eukaryotes, resulting in allele-specific changes in chromatin organization, transcription and replication. One example of parental imprinting in humans is revealed by two distinct genetic diseases, Prader-Willi syndrome (PWS) and Angelman syndrome (AS) which both map to chromosome 15q11-13. PWS is caused by the absence of a paternal contribution to 15q11-13, while AS results from the lack of a maternal copy of the region. Within this chromosomal subregion lies a cluster of GABAA receptor β3 and α5 subunit genes (GABRB3 and GABRA5) which are separated by about 100 kb and arranged in opposite transcritional orientations (Figure 1). Allele-specific asynchronous DNA replication has previously been found to be associated with imprinted chromosomal regions.In order to further study the association between DNA replication and imprinting, allele-specific replication was assayed by fluorescence in situ hybridization (FISH). Biotin-labeled phage probes detected by FITC hybridized to each chromosome as either a singlet (unreplicated state) or a doublet (replicated state). Cells demonstrating asynchronous replication (one singlet and one doublet) for each probe are shown in Figure 2.

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Laish, Ido, Tal Biron-Shental, Hila Katz, Meytal Liberman, Yona Kitay-Cohen, Fred Meir Konikoff, and Aliza Amiel. "Asynchronous Replication in Lymphocytes from Patients with Inflammatory Bowel Disease and Primary Sclerosing Cholangitis." Cytogenetic and Genome Research 145, no. 1 (2015): 35–41. http://dx.doi.org/10.1159/000381406.

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Primary sclerosing cholangitis (PSC) and inflammatory bowel disease (IBD) are associated chronic inflammatory diseases with malignant potential. Loss of replication synchrony during the S-phase of the cell cycle has been shown to be linked to several malignant and premalignant states. This study evaluated temporal differences in replication timing between these diseases. The replication pattern of peripheral blood lymphocytes obtained from patients with PSC and IBD and healthy individuals was analyzed by fluorescence in situ hybridization (FISH) in 2 pairs of alleles, in 15qter and 13qter. Asynchrony was determined by the presence of 1 single and 1 set of double dots in the same cell. Samples from subjects with PSC showed significantly greater temporal differences in replication timing, in contrast to the high level of synchrony observed in samples from healthy individuals (p = 0.045). Samples from IBD patients exhibited a nonsignificant increase in replication asynchrony. We believe that these results reflect impairment in the replication control of structural homologous loci in PSC, and that this phenomenon may be correlated with the inflammation-induced malignant potential of this condition.

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Mah, D. C., P. A. Dijkwel, A. Todd, V. Klein, G. B. Price, and M. Zannis-Hadjopoulos. "ors12, a mammalian autonomously replicating DNA sequence, associates with the nuclear matrix in a cell cycle-dependent manner." Journal of Cell Science 105, no. 3 (July 1, 1993): 807–18. http://dx.doi.org/10.1242/jcs.105.3.807.

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Origin enriched sequence ors8 and ors12, have been isolated previously by extrusion of nascent CV-1 cell DNA from replication bubbles at the onset of S-phase. Both have been shown to direct autonomous DNA replication in vivo and in vitro. Here, we have examined the association of genomic ors8 and ors12 with the nuclear matrix in asynchronous and synchronized CV-1 cells. In asynchronously growing cells, ors8 was found to be randomly distributed, while ors12 was found to be enriched on the nuclear matrix. Using an in vitro binding assay, we determined that ors12 contains two attachment sites, each located in AT-rich domains. Surprisingly, in early and mid-S-phase cells, ors12 homologous sequences were recovered mainly from the DNA loops, while in late-S the majority had shifted to positions on the nuclear matrix. In contrast, the distribution of ors8 over the matrix and loop DNA fractions did not change during the cell cycle. By bromodeoxyuridine substitution of replicating DNA, followed by immunoprecipitation with anti-bromodeoxyuridine antibodies and PCR amplification, we demonstrated that ors12 replicates almost exclusively on the matrix in early and mid-S-phase; replicating ors8 was also found to be enriched on the matrix in early S-phase. Chase experiments showed that the ors12 sequences labelled with bromodeoxyuridine in the first 2 hours of S-phase remain attached to the nuclear matrix, resulting in an accumulation of ors12 on the nuclear matrix at the end of the S period.

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Sullivan, Eric D., Matthew J. Longley, and William C. Copeland. "Polymerase γ efficiently replicates through many natural template barriers but stalls at the HSP1 quadruplex." Journal of Biological Chemistry 295, no. 51 (October 19, 2020): 17802–15. http://dx.doi.org/10.1074/jbc.ra120.015390.

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Faithful replication of the mitochondrial genome is carried out by a set of key nuclear-encoded proteins. DNA polymerase γ is a core component of the mtDNA replisome and the only replicative DNA polymerase localized to mitochondria. The asynchronous mechanism of mtDNA replication predicts that the replication machinery encounters dsDNA and unique physical barriers such as structured genes, G-quadruplexes, and other obstacles. In vitro experiments here provide evidence that the polymerase γ heterotrimer is well-adapted to efficiently synthesize DNA, despite the presence of many naturally occurring roadblocks. However, we identified a specific G-quadruplex–forming sequence at the heavy-strand promoter (HSP1) that has the potential to cause significant stalling of mtDNA replication. Furthermore, this structured region of DNA corresponds to the break site for a large (3,895 bp) deletion observed in mitochondrial disease patients. The presence of this deletion in humans correlates with UV exposure, and we have found that efficiency of polymerase γ DNA synthesis is reduced after this quadruplex is exposed to UV in vitro.

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Bergström, Rosita, Joanne Whitehead, Sreenivasulu Kurukuti, and Rolf Ohlsson. "CTCF Regulates Asynchronous Replication of the Imprinted H19/Igf2 Domain." Cell Cycle 6, no. 4 (February 15, 2007): 450–54. http://dx.doi.org/10.4161/cc.6.4.3854.

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Haikun Liu, Hai Jin, Xiaofei Liao, Chen Yu, and Cheng-Zhong Xu. "Live Virtual Machine Migration via Asynchronous Replication and State Synchronization." IEEE Transactions on Parallel and Distributed Systems 22, no. 12 (December 2011): 1986–99. http://dx.doi.org/10.1109/tpds.2011.86.

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Watanabe, Satoru, Ryudo Ohbayashi, Yuh Shiwa, Aska Noda, Yu Kanesaki, Taku Chibazakura, and Hirofumi Yoshikawa. "Light-dependent and asynchronous replication of cyanobacterial multi-copy chromosomes." Molecular Microbiology 83, no. 4 (January 18, 2012): 856–65. http://dx.doi.org/10.1111/j.1365-2958.2012.07971.x.

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Amiel, Aliza, Avital Korenstein, Elena Gaber, and Lydia Avivi. "Asynchronous replication of alleles in genomes carrying an extra autosome." European Journal of Human Genetics 7, no. 2 (March 1999): 223–30. http://dx.doi.org/10.1038/sj.ejhg.5200267.

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Epner, E., W. C. Forrester, and M. Groudine. "Asynchronous DNA replication within the human beta-globin gene locus." Proceedings of the National Academy of Sciences 85, no. 21 (November 1, 1988): 8081–85. http://dx.doi.org/10.1073/pnas.85.21.8081.

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Adams, Kevin, and Denis Gračanin. "Using adaptive scheduling for increased resiliency in passive asynchronous replication." Innovations in Systems and Software Engineering 3, no. 4 (November 10, 2007): 333–44. http://dx.doi.org/10.1007/s11334-007-0037-9.

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Oldach, Phoebe, and Conrad A. Nieduszynski. "Cohesin-Mediated Genome Architecture Does Not Define DNA Replication Timing Domains." Genes 10, no. 3 (March 4, 2019): 196. http://dx.doi.org/10.3390/genes10030196.

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3D genome organization is strongly predictive of DNA replication timing in mammalian cells. This work tested the extent to which loop-based genome architecture acts as a regulatory unit of replication timing by using an auxin-inducible system for acute cohesin ablation. Cohesin ablation in a population of cells in asynchronous culture was shown not to disrupt patterns of replication timing as assayed by replication sequencing (RepliSeq) or BrdU-focus microscopy. Furthermore, cohesin ablation prior to S phase entry in synchronized cells was similarly shown to not impact replication timing patterns. These results suggest that cohesin-mediated genome architecture is not required for the execution of replication timing patterns in S phase, nor for the establishment of replication timing domains in G1.

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Pantelias, Karachristou, Georgakilas, and Terzoudi. "Interphase Cytogenetic Analysis of Micronucleated and Multinucleated Cells Supports the Premature Chromosome Condensation Hypothesis as the Mechanistic Origin of Chromothripsis." Cancers 11, no. 8 (August 6, 2019): 1123. http://dx.doi.org/10.3390/cancers11081123.

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The discovery of chromothripsis in cancer genomes challenges the long-standing concept of carcinogenesis as the result of progressive genetic events. Despite recent advances in describing chromothripsis, its mechanistic origin remains elusive. The prevailing conception is that it arises from a massive accumulation of fragmented DNA inside micronuclei (MN), whose defective nuclear envelope ruptures or leads to aberrant DNA replication, before main nuclei enter mitosis. An alternative hypothesis is that the premature chromosome condensation (PCC) dynamics in asynchronous micronucleated cells underlie chromosome shattering in a single catastrophic event, a hallmark of chromothripsis. Specifically, when main nuclei enter mitosis, premature chromatin condensation provokes the shattering of chromosomes entrapped inside MN, if they are still undergoing DNA replication. To test this hypothesis, the agent RO-3306, a selective ATP-competitive inhibitor of CDK1 that promotes cell cycle arrest at the G2/M boundary, was used in this study to control the degree of cell cycle asynchrony between main nuclei and MN. By delaying the entrance of main nuclei into mitosis, additional time was allowed for the completion of DNA replication and duplication of chromosomes inside MN. We performed interphase cytogenetic analysis using asynchronous micronucleated cells generated by exposure of human lymphocytes to γ-rays, and heterophasic multinucleated Chinese hamster ovary (CHO) cells generated by cell fusion procedures. Our results demonstrate that the PCC dynamics during asynchronous mitosis in micronucleated or multinucleated cells are an important determinant of chromosome shattering and may underlie the mechanistic origin of chromothripsis.

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O'Keefe, R. T., S. C. Henderson, and D. L. Spector. "Dynamic organization of DNA replication in mammalian cell nuclei: spatially and temporally defined replication of chromosome-specific alpha-satellite DNA sequences." Journal of Cell Biology 116, no. 5 (March 1, 1992): 1095–110. http://dx.doi.org/10.1083/jcb.116.5.1095.

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Five distinct patterns of DNA replication have been identified during S-phase in asynchronous and synchronous cultures of mammalian cells by conventional fluorescence microscopy, confocal laser scanning microscopy, and immunoelectron microscopy. During early S-phase, replicating DNA (as identified by 5-bromodeoxyuridine incorporation) appears to be distributed at sites throughout the nucleoplasm, excluding the nucleolus. In CHO cells, this pattern of replication peaks at 30 min into S-phase and is consistent with the localization of euchromatin. As S-phase continues, replication of euchromatin decreases and the peripheral regions of heterochromatin begin to replicate. This pattern of replication peaks at 2 h into S-phase. At 5 h, perinucleolar chromatin as well as peripheral areas of heterochromatin peak in replication. 7 h into S-phase interconnecting patches of electron-dense chromatin replicate. At the end of S-phase (9 h), replication occurs at a few large regions of electron-dense chromatin. Similar or identical patterns have been identified in a variety of mammalian cell types. The replication of specific chromosomal regions within the context of the BrdU-labeling patterns has been examined on an hourly basis in synchronized HeLa cells. Double labeling of DNA replication sites and chromosome-specific alpha-satellite DNA sequences indicates that the alpha-satellite DNA replicates during mid S-phase (characterized by the third pattern of replication) in a variety of human cell types. Our data demonstrates that specific DNA sequences replicate at spatially and temporally defined points during the cell cycle and supports a spatially dynamic model of DNA replication.

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Leonhardt, Heinrich, Hans-Peter Rahn, Peter Weinzierl, Anje Sporbert, Thomas Cremer, Daniele Zink, and M. Cristina Cardoso. "Dynamics of DNA Replication Factories in Living Cells." Journal of Cell Biology 149, no. 2 (April 17, 2000): 271–80. http://dx.doi.org/10.1083/jcb.149.2.271.

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DNA replication occurs in microscopically visible complexes at discrete sites (replication foci) in the nucleus. These foci consist of DNA associated with replication machineries, i.e., large protein complexes involved in DNA replication. To study the dynamics of these nuclear replication foci in living cells, we fused proliferating cell nuclear antigen (PCNA), a central component of the replication machinery, with the green fluorescent protein (GFP). Imaging of stable cell lines expressing low levels of GFP-PCNA showed that replication foci are heterogeneous in size and lifetime. Time-lapse studies revealed that replication foci clearly differ from nuclear speckles and coiled bodies as they neither show directional movements, nor do they seem to merge or divide. These four dimensional analyses suggested that replication factories are stably anchored in the nucleus and that changes in the pattern occur through gradual, coordinated, but asynchronous, assembly and disassembly throughout S phase.

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Zou, Y., S. M. Gryaznov, J. W. Shay, W. E. Wright, and M. N. Cornforth. "Asynchronous replication timing of telomeres at opposite arms of mammalian chromosomes." Proceedings of the National Academy of Sciences 101, no. 35 (August 20, 2004): 12928–33. http://dx.doi.org/10.1073/pnas.0404106101.

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Bhardwaj, Kshitij, and Steven M. Nowick. "A Continuous-Time Replication Strategy for Efficient Multicast in Asynchronous NoCs." IEEE Transactions on Very Large Scale Integration (VLSI) Systems 27, no. 2 (February 2019): 350–63. http://dx.doi.org/10.1109/tvlsi.2018.2876856.

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Amiel, A., Tali Litmanovich, Elena Gaber, Michael Lishner, Lydia Avivi, and Moshe D. Fejgin. "Asynchronous replication of p53 and 21q22 loci in chronic lymphocytic leukemia." Human Genetics 101, no. 2 (November 17, 1997): 219–22. http://dx.doi.org/10.1007/s004390050619.

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Hanna, Mariam Onsy F., Naglaa A. Zayed, Hatem Darwish, and Samia I. Girgis. "Asynchronous DNA replication and aneuploidy in lymphocytes of hepatocellular carcinoma patients." Cancer Genetics 205, no. 12 (December 2012): 636–43. http://dx.doi.org/10.1016/j.cancergen.2012.10.006.

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Ghosh, Maloy, Michael Kemp, Guoqi Liu, Marion Ritzi, Aloys Schepers, and Michael Leffak. "Differential Binding of Replication Proteins across the Human c-myc Replicator." Molecular and Cellular Biology 26, no. 14 (July 15, 2006): 5270–83. http://dx.doi.org/10.1128/mcb.02137-05.

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ABSTRACT The binding of the prereplication complex proteins Orc1, Orc2, Mcm3, Mcm7, and Cdc6 and the novel DNA unwinding element (DUE) binding protein DUE-B to the endogenous human c-myc replicator was studied by chromatin immunoprecipitation. In G1-arrested HeLa cells, Mcm3, Mcm7, and DUE-B were prominent near the DUE, while Orc1 and Orc2 were least abundant near the DUE and more abundant at flanking sites. Cdc6 binding mirrored that of Orc2 in G1-arrested cells but decreased in asynchronous or M-phase cells. Similarly, the signals from Orc1, Mcm3, and Mcm7 were at background levels in cells arrested in M phase, whereas Orc2 retained the distribution seen in G1-phase cells. Previously shown to cause histone hyperacetylation and delocalization of replication initiation, trichostatin A treatment of cells led to a parallel qualitative change in the distribution of Mcm3, but not Orc2, across the c-myc replicator. Orc2, Mcm3, and DUE-B were also bound at an ectopic c-myc replicator, where deletion of sequences essential for origin activity was associated with the loss of DUE-B binding or the alteration of chromatin structure and loss of Mcm3 binding. These results show that proteins implicated in replication initiation are selectively and differentially bound across the c-myc replicator, dependent on discrete structural elements in DNA or chromatin.

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LI, JIANLI, QINGPING TAN, and LANFANG TAN. "IMPLEMENTING LOW-COST FAULT TOLERANCE VIA HYBRID SYNCHRONOUS/ASYNCHRONOUS CHECKS." Journal of Circuits, Systems and Computers 22, no. 07 (August 2013): 1350058. http://dx.doi.org/10.1142/s0218126613500588.

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As semiconductor technologies scale down to deep sub-micron dimensions, transient faults will soon become a critical reliability concern. Due to their prohibitive costs, traditional high-end solutions are unacceptable for the mainstream commodity market. This paper presents FTPIPE, a hybrid software/hardware solution, which provides sufficient fault coverage with affordable overhead for single-threaded programs running on commodity systems. Leveraging existing exception mechanisms with minor modifications to handle exception-causing faults, FTPIPE focuses on tolerating silent data corruptions by using compile-time analysis and performing selective instruction replication in a modern superscalar pipeline extended with minimal hardware overhead. Unlike existing instruction replication-based solutions, which detect faults by synchronous checks, the FTPIPE platform has exploited a novel hybrid synchronous/asynchronous check method for the replicated instructions. In this manner, better performance can be obtained without degradation of fault coverage. By synchronous checks, the validation of the result of a replicated instruction must be finished before it is committed, whereas such a guarantee is not required by an asynchronous check. Evaluation using a set of nine programs from the Mibench benchmark suite demonstrates that FTPIPE can tolerate 89.8% of transient faults under a modest performance overhead of 20.1%.

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Velichko, Artem K., Nadezhda V. Petrova, Omar L. Kantidze, and Sergey V. Razin. "Dual effect of heat shock on DNA replication and genome integrity." Molecular Biology of the Cell 23, no. 17 (September 2012): 3450–60. http://dx.doi.org/10.1091/mbc.e11-12-1009.

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Heat shock (HS) is one of the better-studied exogenous stress factors. However, little is known about its effects on DNA integrity and the DNA replication process. In this study, we show that in G1 and G2 cells, HS induces a countable number of double-stranded breaks (DSBs) in the DNA that are marked by γH2AX. In contrast, in S-phase cells, HS does not induce DSBs but instead causes an arrest or deceleration of the progression of the replication forks in a temperature-dependent manner. This response also provoked phosphorylation of H2AX, which appeared at the sites of replication. Moreover, the phosphorylation of H2AX at or close to the replication fork rescued the fork from total collapse. Collectively our data suggest that in an asynchronous cell culture, HS might affect DNA integrity both directly and via arrest of replication fork progression and that the phosphorylation of H2AX has a protective effect on the arrested replication forks in addition to its known DNA damage signaling function.

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Dutta, Devkanya, Alexander W. Ensminger, Jacob P. Zucker, and Andrew Chess. "Asynchronous Replication and Autosome-Pair Non-Equivalence in Human Embryonic Stem Cells." PLoS ONE 4, no. 3 (March 27, 2009): e4970. http://dx.doi.org/10.1371/journal.pone.0004970.

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Donley, Nathan, Eric P. Stoffregen, Leslie Smith, Christina Montagna, and Mathew J. Thayer. "Asynchronous Replication, Mono-Allelic Expression, and Long Range Cis-Effects of ASAR6." PLoS Genetics 9, no. 4 (April 4, 2013): e1003423. http://dx.doi.org/10.1371/journal.pgen.1003423.

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Reish, Orit, Ron Gal, Elena Gaber, Carron Sher, Tzvy Bistritzer, and Aliza Amiel. "Asynchronous replication of biallelically expressed loci: A new phenomenon in Turner syndrome." Genetics in Medicine 4, no. 6 (December 2002): 439–43. http://dx.doi.org/10.1097/00125817-200211000-00007.

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Schmidt, M., and B. R. Migeon. "Asynchronous replication of homologous loci on human active and inactive X chromosomes." Proceedings of the National Academy of Sciences 87, no. 10 (May 1, 1990): 3685–89. http://dx.doi.org/10.1073/pnas.87.10.3685.

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Yamauchi, Yasuhiro, Monika A. Ward, and W. Steven Ward. "Asynchronous DNA replication and origin licensing in the mouse one-cell embryo." Journal of Cellular Biochemistry 107, no. 2 (March 19, 2009): 214–23. http://dx.doi.org/10.1002/jcb.22117.

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Moriya, Shigeki, Yoshikazu Kawai, Sakiko Kaji, Adrian Smith, Elizabeth J. Harry, and Jeffery Errington. "Effects of oriC relocation on control of replication initiation in Bacillus subtilis." Microbiology 155, no. 9 (September 1, 2009): 3070–82. http://dx.doi.org/10.1099/mic.0.030080-0.

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In bacteria, DNA replication initiation is tightly regulated in order to coordinate chromosome replication with cell growth. In Escherichia coli, positive factors and negative regulatory mechanisms playing important roles in the strict control of DNA replication initiation have been reported. However, it remains unclear how bacterial cells recognize the right time for replication initiation during the cell cycle. In the Gram-positive bacterium Bacillus subtilis, much less is known about the regulation of replication initiation, specifically, regarding negative control mechanisms which ensure replication initiation only once per cell cycle. Here we report that replication initiation was greatly enhanced in strains that had the origin of replication (oriC) relocated to various loci on the chromosome. When oriC was relocated to new loci further than 250 kb counterclockwise from the native locus, replication initiation became asynchronous and earlier than in the wild-type cells. In two oriC-relocated strains (oriC at argG or pnbA, 25 ° or 30 ° on the 36 ° chromosome map, respectively), DnaA levels were higher than in the wild-type but not enough to cause earlier initiation of replication. Our results suggest that the initiation capacity of replication is accumulated well before the actual time of initiation, and its release may be suppressed by a unique DNA structure formed near the native oriC locus.

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Palanciuc, Dorin, and Florin Pop. "Implementing Replication of Objects in DOORS—The Object-Oriented Runtime System for Edge Computing." Sensors 21, no. 23 (November 26, 2021): 7883. http://dx.doi.org/10.3390/s21237883.

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Aiming for simplicity and efficiency in the domain of edge computing, DOORS is a distributed system expected to scale up to hundreds of nodes, which encapsulates application state and behavior into objects and gives them the ability to exchange asynchronous messages. DOORS offers semi-synchronous replication and the ability to explicitly move objects from one node to another, as methods to achieve scalability and resilience. The present paper gives an outline of the system structure, describes how DOORS implements object replication, and describes a basic set of measurements, yielding an initial set of conclusions for the improvements of the design.

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Saint-Dic, Djenann, Jason Kehrl, Brian Frushour, and Lyn Sue Kahng. "Excess SeqA Leads to Replication Arrest and a Cell Division Defect in Vibrio cholerae." Journal of Bacteriology 190, no. 17 (July 11, 2008): 5870–78. http://dx.doi.org/10.1128/jb.00479-08.

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ABSTRACT Although most bacteria contain a single circular chromosome, some have complex genomes, and all Vibrio species studied so far contain both a large and a small chromosome. In recent years, the divided genome of Vibrio cholerae has proven to be an interesting model system with both parallels to and novel features compared with the genome of Escherichia coli. While factors influencing the replication and segregation of both chromosomes have begun to be elucidated, much remains to be learned about the maintenance of this genome and of complex bacterial genomes generally. An important aspect of replicating any genome is the correct timing of initiation, without which organisms risk aneuploidy. During DNA replication in E. coli, newly replicated origins cannot immediately reinitiate because they undergo sequestration by the SeqA protein, which binds hemimethylated origin DNA. This DNA is already methylated by Dam on the template strand and later becomes fully methylated; aberrant amounts of Dam or the deletion of seqA leads to asynchronous replication. In our study, hemimethylated DNA was detected at both origins of V. cholerae, suggesting that these origins are also subject to sequestration. The overproduction of SeqA led to a loss of viability, the condensation of DNA, and a filamentous morphology. Cells with abnormal DNA content arose in the population, and replication was inhibited as determined by a reduced ratio of origin to terminus DNA in SeqA-overexpressing cells. Thus, excessive SeqA negatively affects replication in V. cholerae and prevents correct progression to downstream cell cycle events such as segregation and cell division.

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Leno, G. H., and R. A. Laskey. "The nuclear membrane determines the timing of DNA replication in Xenopus egg extracts." Journal of Cell Biology 112, no. 4 (February 15, 1991): 557–66. http://dx.doi.org/10.1083/jcb.112.4.557.

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We have exploited a property of chicken erythrocyte nuclei to analyze the regulation of DNA replication in a cell-free system from Xenopus eggs. Many individual demembranated nuclei added to the extract often became enclosed within a common nuclear membrane. Nuclei within such a "multinuclear aggregate" lacked individual membranes but shared the perimeter membrane of the aggregate. Individual nuclei that were excluded from the aggregates initiated DNA synthesis at different times over a 10-12-h period, as judged by incorporation of biotinylated dUTP into discrete replication foci at early times, followed by uniformly intense incorporation at later times. Replication forks were clustered in spots, rings, and horseshoe-shaped structures similar to those described in cultured cells. In contrast to the asynchronous replication seen between individual nuclei, replication within multinuclear aggregates was synchronous. There was a uniform distribution and similar fluorescent intensity of the replication foci throughout all the nuclei enclosed within the same membrane. However, different multinuclear aggregates replicated out of synchrony with each other indicating that each membrane-bound aggregate acts as an individual unit of replication. These data indicate that the nuclear membrane defines the unit of DNA replication and determines the timing of DNA synthesis in egg extract resulting in highly coordinated triggering of DNA replication on the DNA it encloses.

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Pohanka, Tomáš, and Vilém Pechanec. "Evaluation of Replication Mechanisms on Selected Database Systems." ISPRS International Journal of Geo-Information 9, no. 4 (April 17, 2020): 249. http://dx.doi.org/10.3390/ijgi9040249.

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This paper is focused on comparing database replication over spatial data in PostgreSQL and MySQL. Database replication means solving various problems with overloading a single database server with writing and reading queries. There are many replication mechanisms that are able to handle data differently. Criteria for objective comparisons were set for testing and determining the bottleneck of the replication process. The tests were done over the real national vector spatial datasets, namely, ArcCR500, Data200, Natural Earth and Estimated Pedologic-Ecological Unit. HWMonitor Pro was used to monitor the PostgreSQL database, network and system load. Monyog was used to monitor the MySQL activity (data and SQL queries) in real-time. Both database servers were run on computers with the Microsoft Windows operating system. The results from the provided tests of both replication mechanisms led to a better understanding of these mechanisms and allowed informed decisions for future deployment. Graphs and tables include the statistical data and describe the replication mechanisms in specific situations. PostgreSQL with the Slony extension with asynchronous replication synchronized a batch of changes with a high transfer speed and high server load. MySQL with synchronous replication synchronized every change record with low impact on server performance and network bandwidth.

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Journal articles on the topic 'Asynchronous replication'

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