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Готові списки джерел за темами / Lagging-strand DNA synthesis / Статті в журналах

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Статті в журналах з теми "Lagging-strand DNA synthesis"

Автор: Grafiati

Опубліковано: 4 березня 2024

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1

Giannattasio, Michele, and Dana Branzei. "DNA Replication Through Strand Displacement During Lagging Strand DNA Synthesis in Saccharomyces cerevisiae." Genes 10, no. 2 (2019): 167. http://dx.doi.org/10.3390/genes10020167.

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This review discusses a set of experimental results that support the existence of extended strand displacement events during budding yeast lagging strand DNA synthesis. Starting from introducing the mechanisms and factors involved in leading and lagging strand DNA synthesis and some aspects of the architecture of the eukaryotic replisome, we discuss studies on bacterial, bacteriophage and viral DNA polymerases with potent strand displacement activities. We describe proposed pathways of Okazaki fragment processing via short and long flaps, with a focus on experimental results obtained in Saccha

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2

Hernandez, Alfredo J., Seung-Joo Lee, and Charles C. Richardson. "Primer release is the rate-limiting event in lagging-strand synthesis mediated by the T7 replisome." Proceedings of the National Academy of Sciences 113, no. 21 (2016): 5916–21. http://dx.doi.org/10.1073/pnas.1604894113.

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DNA replication occurs semidiscontinuously due to the antiparallel DNA strands and polarity of enzymatic DNA synthesis. Although the leading strand is synthesized continuously, the lagging strand is synthesized in small segments designated Okazaki fragments. Lagging-strand synthesis is a complex event requiring repeated cycles of RNA primer synthesis, transfer to the lagging-strand polymerase, and extension effected by cooperation between DNA primase and the lagging-strand polymerase. We examined events controlling Okazaki fragment initiation using the bacteriophage T7 replication system. Prim

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3

Koussa, Natasha C., and Duncan J. Smith. "Limiting DNA polymerase delta alters replication dynamics and leads to a dependence on checkpoint activation and recombination-mediated DNA repair." PLOS Genetics 17, no. 1 (2021): e1009322. http://dx.doi.org/10.1371/journal.pgen.1009322.

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DNA polymerase delta (Pol δ) plays several essential roles in eukaryotic DNA replication and repair. At the replication fork, Pol δ is responsible for the synthesis and processing of the lagging-strand. At replication origins, Pol δ has been proposed to initiate leading-strand synthesis by extending the first Okazaki fragment. Destabilizing mutations in human Pol δ subunits cause replication stress and syndromic immunodeficiency. Analogously, reduced levels of Pol δ in Saccharomyces cerevisiae lead to pervasive genome instability. Here, we analyze how the depletion of Pol δ impacts replication

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4

Lukac, David, Zuzana Machacova, and Pavel Moudry. "Emetine blocks DNA replication via proteosynthesis inhibition not by targeting Okazaki fragments." Life Science Alliance 5, no. 12 (2022): e202201560. http://dx.doi.org/10.26508/lsa.202201560.

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DNA synthesis of the leading and lagging strands works independently and cells tolerate single-stranded DNA generated during strand uncoupling if it is protected by RPA molecules. Natural alkaloid emetine is used as a specific inhibitor of lagging strand synthesis, uncoupling leading and lagging strand replication. Here, by analysis of lagging strand synthesis inhibitors, we show that despite emetine completely inhibiting DNA replication: it does not induce the generation of single-stranded DNA and chromatin-bound RPA32 (CB-RPA32). In line with this, emetine does not activate the replication c

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5

Kramer, M. Gabriela, Saleem A. Khan, and Manuel Espinosa. "Lagging-Strand Replication from the ssoA Origin of Plasmid pMV158 in Streptococcus pneumoniae: In Vivo and In Vitro Influences of Mutations in Two ConservedssoA Regions." Journal of Bacteriology 180, no. 1 (1998): 83–89. http://dx.doi.org/10.1128/jb.180.1.83-89.1998.

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ABSTRACT The streptococcal plasmid pMV158 replicates by the rolling-circle mechanism. One feature of this replication mechanism is the generation of single-stranded DNA intermediates which are converted to double-stranded molecules. Lagging-strand synthesis initiates from the plasmid single-stranded origin, sso. We have used the pMV158-derivative plasmid pLS1 (containing the ssoA type of lagging-strand origin) and a set of pLS1 derivatives with mutations in two conserved regions of the ssoA (the recombination site B [RSB] and a conserved 6-nucleotide sequence [CS-6]) to identify sequences impo

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6

Spiering, Michelle M., Philip Hanoian, Swathi Gannavaram, and Stephen J. Benkovic. "RNA primer–primase complexes serve as the signal for polymerase recycling and Okazaki fragment initiation in T4 phage DNA replication." Proceedings of the National Academy of Sciences 114, no. 22 (2017): 5635–40. http://dx.doi.org/10.1073/pnas.1620459114.

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The opposite strand polarity of duplex DNA necessitates that the leading strand is replicated continuously whereas the lagging strand is replicated in discrete segments known as Okazaki fragments. The lagging-strand polymerase sometimes recycles to begin the synthesis of a new Okazaki fragment before finishing the previous fragment, creating a gap between the Okazaki fragments. The mechanism and signal that initiate this behavior—that is, the signaling mechanism—have not been definitively identified. We examined the role of RNA primer–primase complexes left on the lagging ssDNA from primer syn

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7

Parenteau, Julie, and Raymund J. Wellinger. "Accumulation of Single-Stranded DNA and Destabilization of Telomeric Repeats in Yeast Mutant Strains Carrying a Deletion of RAD27." Molecular and Cellular Biology 19, no. 6 (1999): 4143–52. http://dx.doi.org/10.1128/mcb.19.6.4143.

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ABSTRACT The Saccharomyces cerevisiae RAD27 gene encodes the yeast homologue of the mammalian FEN-1 nuclease, a protein that is thought to be involved in the processing of Okazaki fragments during DNA lagging-strand synthesis. One of the predicted DNA lesions occurring in rad27 strains is the presence of single-stranded DNA of the template strand for lagging-strand synthesis. We examined this prediction by analyzing the terminal DNA structures generated during telomere replication in rad27strains. The lengths of the telomeric repeat tracts were found to be destabilized in rad27 strains, indica

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8

Serra-Cardona, Albert, Chuanhe Yu, Xinmin Zhang, et al. "A mechanism for Rad53 to couple leading- and lagging-strand DNA synthesis under replication stress in budding yeast." Proceedings of the National Academy of Sciences 118, no. 38 (2021): e2109334118. http://dx.doi.org/10.1073/pnas.2109334118.

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In response to DNA replication stress, DNA replication checkpoint kinase Mec1 phosphorylates Mrc1, which in turn activates Rad53 to prevent the generation of deleterious single-stranded DNA, a process that remains poorly understood. We previously reported that lagging-strand DNA synthesis proceeds farther than leading strand in rad53-1 mutant cells defective in replication checkpoint under replication stress, resulting in the exposure of long stretches of the leading-strand templates. Here, we show that asymmetric DNA synthesis is also observed in mec1-100 and mrc1-AQ cells defective in replic

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9

Sparks, Melanie A., Peter M. Burgers та Roberto Galletto. "Pif1, RPA, and FEN1 modulate the ability of DNA polymerase δ to overcome protein barriers during DNA synthesis". Journal of Biological Chemistry 295, № 47 (2020): 15883–91. http://dx.doi.org/10.1074/jbc.ra120.015699.

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Successful DNA replication requires carefully regulated mechanisms to overcome numerous obstacles that naturally occur throughout chromosomal DNA. Scattered across the genome are tightly bound proteins, such as transcription factors and nucleosomes, that are necessary for cell function, but that also have the potential to impede timely DNA replication. Using biochemically reconstituted systems, we show that two transcription factors, yeast Reb1 and Tbf1, and a tightly positioned nucleosome, are strong blocks to the strand displacement DNA synthesis activity of DNA polymerase δ. Although the bl

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10

Nasheuer, Heinz Peter, and Nichodemus O. Onwubiko. "Lagging Strand Initiation Processes in DNA Replication of Eukaryotes—Strings of Highly Coordinated Reactions Governed by Multiprotein Complexes." Genes 14, no. 5 (2023): 1012. http://dx.doi.org/10.3390/genes14051012.

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In their influential reviews, Hanahan and Weinberg coined the term ‘Hallmarks of Cancer’ and described genome instability as a property of cells enabling cancer development. Accurate DNA replication of genomes is central to diminishing genome instability. Here, the understanding of the initiation of DNA synthesis in origins of DNA replication to start leading strand synthesis and the initiation of Okazaki fragment on the lagging strand are crucial to control genome instability. Recent findings have provided new insights into the mechanism of the remodelling of the prime initiation enzyme, DNA

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11

Liu, Guoqi, Xiaomi Chen, and Michael Leffak. "Oligodeoxynucleotide Binding to (CTG) · (CAG) Microsatellite Repeats Inhibits Replication Fork Stalling, Hairpin Formation, and Genome Instability." Molecular and Cellular Biology 33, no. 3 (2012): 571–81. http://dx.doi.org/10.1128/mcb.01265-12.

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ABSTRACT(CTG)n· (CAG)ntrinucleotide repeat (TNR) expansion in the 3′ untranslated region of the dystrophia myotonica protein kinase (DMPK) gene causes myotonic dystrophy type 1. However, a direct link between TNR instability, the formation of noncanonical (CTG)n· (CAG)nstructures, and replication stress has not been demonstrated. In a human cell model, we found that (CTG)45· (CAG)45causes local replication fork stalling, DNA hairpin formation, and TNR instability. Oligodeoxynucleotides (ODNs) complementary to the (CTG)45· (CAG)45lagging-strand template eliminated DNA hairpin formation on leadi

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12

Kulczyk, Arkadiusz W., Arne Moeller, Peter Meyer, Piotr Sliz, and Charles C. Richardson. "Cryo-EM structure of the replisome reveals multiple interactions coordinating DNA synthesis." Proceedings of the National Academy of Sciences 114, no. 10 (2017): E1848—E1856. http://dx.doi.org/10.1073/pnas.1701252114.

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We present a structure of the ∼650-kDa functional replisome of bacteriophage T7 assembled on DNA resembling a replication fork. A structure of the complex consisting of six domains of DNA helicase, five domains of RNA primase, two DNA polymerases, and two thioredoxin (processivity factor) molecules was determined by single-particle cryo-electron microscopy. The two molecules of DNA polymerase adopt a different spatial arrangement at the replication fork, reflecting their roles in leading- and lagging-strand synthesis. The structure, in combination with biochemical data, reveals molecular mecha

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13

Gao, Yang, Yanxiang Cui, Tara Fox, et al. "Structures and operating principles of the replisome." Science 363, no. 6429 (2019): eaav7003. http://dx.doi.org/10.1126/science.aav7003.

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Анотація:

Visualization in atomic detail of the replisome that performs concerted leading– and lagging–DNA strand synthesis at a replication fork has not been reported. Using bacteriophage T7 as a model system, we determined cryo–electron microscopy structures up to 3.2-angstroms resolution of helicase translocating along DNA and of helicase-polymerase-primase complexes engaging in synthesis of both DNA strands. Each domain of the spiral-shaped hexameric helicase translocates sequentially hand-over-hand along a single-stranded DNA coil, akin to the way AAA+ ATPases (adenosine triphosphatases) unfold pep

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14

Hiasa, H., and K. J. Marians. "Primase couples leading- and lagging-strand DNA synthesis from oriC." Journal of Biological Chemistry 269, no. 8 (1994): 6058–63. http://dx.doi.org/10.1016/s0021-9258(17)37569-5.

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15

Holt, Ian J., Heather E. Lorimer, and Howard T. Jacobs. "Coupled Leading- and Lagging-Strand Synthesis of Mammalian Mitochondrial DNA." Cell 100, no. 5 (2000): 515–24. http://dx.doi.org/10.1016/s0092-8674(00)80688-1.

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16

Kreisel, Katrin, Martin K. M. Engqvist, Josephine Kalm та ін. "DNA polymerase η contributes to genome-wide lagging strand synthesis". Nucleic Acids Research 47, № 5 (2018): 2425–35. http://dx.doi.org/10.1093/nar/gky1291.

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17

Spiering, Michelle M., Scott W. Nelson, and Stephen J. Benkovic. "Repetitive lagging strand DNA synthesis by the bacteriophage T4 replisome." Molecular BioSystems 4, no. 11 (2008): 1070. http://dx.doi.org/10.1039/b812163j.

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18

Onwubiko, Nichodemus O., Angela Borst, Suraya A. Diaz, et al. "SV40 T antigen interactions with ssDNA and replication protein A: a regulatory role of T antigen monomers in lagging strand DNA replication." Nucleic Acids Research 48, no. 7 (2020): 3657–77. http://dx.doi.org/10.1093/nar/gkaa138.

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Abstract DNA replication is a central process in all living organisms. Polyomavirus DNA replication serves as a model system for eukaryotic DNA replication and has considerably contributed to our understanding of basic replication mechanisms. However, the details of the involved processes are still unclear, in particular regarding lagging strand synthesis. To delineate the complex mechanism of coordination of various cellular proteins binding simultaneously or consecutively to DNA to initiate replication, we investigated single-stranded DNA (ssDNA) interactions by the SV40 large T antigen (Tag

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19

Lee, Joonsoo, Paul D. Chastain, Jack D. Griffith, and Charles C. Richardson. "Lagging strand synthesis in coordinated DNA synthesis by bacteriophage T7 replication proteins." Journal of Molecular Biology 316, no. 1 (2002): 19–34. http://dx.doi.org/10.1006/jmbi.2001.5325.

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20

Yeeles, Joseph T. P. "Discontinuous leading-strand synthesis: a stop–start story." Biochemical Society Transactions 42, no. 1 (2014): 25–34. http://dx.doi.org/10.1042/bst20130262.

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Reconstitution experiments using replication proteins from a number of different model organisms have firmly established that, in vitro, DNA replication is semi-discontinuous: continuous on the leading strand and discontinuous on the lagging strand. The mechanism by which DNA is replicated in vivo is less clear. In fact, there have been many observations of discontinuous replication in the absence of exogenous DNA-damaging agents. It has also been proposed that replication is discontinuous on the leading strand at least in part because of DNA lesion bypass. Several recent studies have revealed

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21

Ohki, Rieko, Toshiki Tsurimoto, and Fuyuki Ishikawa. "In Vitro Reconstitution of the End Replication Problem." Molecular and Cellular Biology 21, no. 17 (2001): 5753–66. http://dx.doi.org/10.1128/mcb.21.17.5753-5766.2001.

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ABSTRACT The end replication problem hypothesis proposes that the ends of linear DNA cannot be replicated completely during lagging strand DNA synthesis. Although the idea has been widely accepted for explaining telomere attrition during cell proliferation, it has never been directly demonstrated. In order to take a biochemical approach to understand how linear DNA ends are replicated, we have established a novel in vitro linear simian virus 40 DNA replication system. In this system, terminally biotin-labeled linear DNAs are conjugated to avidin-coated beads and subjected to replication reacti

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22

Wanrooij, S., J. M. Fuste, G. Farge, Y. Shi, C. M. Gustafsson, and M. Falkenberg. "Human mitochondrial RNA polymerase primes lagging-strand DNA synthesis in vitro." Proceedings of the National Academy of Sciences 105, no. 32 (2008): 11122–27. http://dx.doi.org/10.1073/pnas.0805399105.

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23

Lee, Joonsoo, Paul D. Chastain, Takahiro Kusakabe, Jack D. Griffith, and Charles C. Richardson. "Coordinated Leading and Lagging Strand DNA Synthesis on a Minicircular Template." Molecular Cell 1, no. 7 (1998): 1001–10. http://dx.doi.org/10.1016/s1097-2765(00)80100-8.

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24

Delagoutte, Emmanuelle, and Giuseppe Baldacci. "5′CAG and 5′CTG Repeats Create Differential Impediment to the Progression of a Minimal Reconstituted T4 Replisome Depending on the Concentration of dNTPs." Molecular Biology International 2011 (August 10, 2011): 1–14. http://dx.doi.org/10.4061/2011/213824.

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Instability of repetitive sequences originates from strand misalignment during repair or replicative DNA synthesis. To investigate the activity of reconstituted T4 replisomes across trinucleotide repeats (TNRs) during leading strand DNA synthesis, we developed a method to build replication miniforks containing a TNR unit of defined sequence and length. Each minifork consists of three strands, primer, leading strand template, and lagging strand template with a 5′ single-stranded (ss) tail. Each strand is prepared independently, and the minifork is assembled by hybridization of the three strands

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25

Kadyrov, Farid A., and John W. Drake. "Conditional Coupling of Leading-strand and Lagging-strand DNA Synthesis at Bacteriophage T4 Replication Forks." Journal of Biological Chemistry 276, no. 31 (2001): 29559–66. http://dx.doi.org/10.1074/jbc.m101310200.

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26

Weston-Hafer, K., and D. E. Berg. "Deletions in plasmid pBR322: replication slippage involving leading and lagging strands." Genetics 127, no. 4 (1991): 649–55. http://dx.doi.org/10.1093/genetics/127.4.649.

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Abstract We test here whether a class of deletions likely to result from errors during DNA replication arise preferentially during synthesis of either the leading or the lagging DNA strand. Deletions were obtained by reversion of particular insertion mutant alleles of the pBR322 amp gene. The alleles contain insertions of palindromic DNAs bracketed by 9-bp direct repeats of amp sequence; in addition, bp 2 to 5 in one arm of the palindrome form a direct repeat with 4 bp of adjoining amp sequence. Prior work had shown that reversion to Ampr results from deletions with endpoints in the 8- or 4-bp

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27

Khristich, Alexandra N., Jillian F. Armenia, Robert M. Matera, Anna A. Kolchinski, and Sergei M. Mirkin. "Large-scale contractions of Friedreich’s ataxia GAA repeats in yeast occur during DNA replication due to their triplex-forming ability." Proceedings of the National Academy of Sciences 117, no. 3 (2020): 1628–37. http://dx.doi.org/10.1073/pnas.1913416117.

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Friedreich’s ataxia (FRDA) is a human hereditary disease caused by the presence of expanded (GAA)n repeats in the first intron of the FXN gene [V. Campuzano et al., Science 271, 1423–1427 (1996)]. In somatic tissues of FRDA patients, (GAA)n repeat tracts are highly unstable, with contractions more common than expansions [R. Sharma et al., Hum. Mol. Genet. 11, 2175–2187 (2002)]. Here we describe an experimental system to characterize GAA repeat contractions in yeast and to conduct a genetic analysis of this process. We found that large-scale contraction is a one-step process, resulting in a med

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28

Hamdan, Samir M., Joseph J. Loparo, Masateru Takahashi, Charles C. Richardson, and Antoine M. van Oijen. "Dynamics of DNA replication loops reveal temporal control of lagging-strand synthesis." Nature 457, no. 7227 (2008): 336–39. http://dx.doi.org/10.1038/nature07512.

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29

Hamdan, Samir M., Joseph J. Loparo, Masateru Takahashi, Charles C. Richardson, and Antoine M. Vanoijen. "Dynamics Of DNA Replication Loops Reveal Temporal Control Of Lagging-strand Synthesis." Biophysical Journal 96, no. 3 (2009): 568a. http://dx.doi.org/10.1016/j.bpj.2008.12.3720.

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30

Cerron, Fernando, Grzegorz L. Ciesielski, Laurie S. Kaguni, Francisco J. Cao, and Borja Ibarra. "Mechanism of SSB Displacement by Replicative DNA Polymerases During Lagging Strand Synthesis." Biophysical Journal 116, no. 3 (2019): 74a. http://dx.doi.org/10.1016/j.bpj.2018.11.443.

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31

Hedglin, Mark, Binod Pandey та Stephen J. Benkovic. "Stability of the human polymerase δ holoenzyme and its implications in lagging strand DNA synthesis". Proceedings of the National Academy of Sciences 113, № 13 (2016): E1777—E1786. http://dx.doi.org/10.1073/pnas.1523653113.

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In eukaryotes, DNA polymerase δ (pol δ) is responsible for replicating the lagging strand template and anchors to the proliferating cell nuclear antigen (PCNA) sliding clamp to form a holoenzyme. The stability of this complex is integral to every aspect of lagging strand replication. Most of our understanding comes fromSaccharomyces cerevisaewhere the extreme stability of the pol δ holoenzyme ensures that every nucleobase within an Okazaki fragment is faithfully duplicated before dissociation but also necessitates an active displacement mechanism for polymerase recycling and exchange. However,

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32

Yonesaki, T. "Involvement of a replicative DNA helicase of bacteriophage T4 in DNA recombination." Genetics 138, no. 2 (1994): 247–52. http://dx.doi.org/10.1093/genetics/138.2.247.

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Abstract Bacteriophage T4 gene 41 encodes a replicative DNA helicase that is a subunit of the primosome which is essential for lagging-strand DNA synthesis. A mutation, rrh, was generated and selected in the helicase gene on the basis of limited DNA replication that ceases early. The survival of ultraviolet-irradiated phage and the frequency of genetic recombination are reduced by rrh. In addition, rrh diminishes the production of concatemeric DNA. These results strongly suggest that the gene 41 replicative helicase participates in DNA recombination.

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33

Nakamura, Mirai, Akira Nabetani, Takeshi Mizuno, Fumio Hanaoka та Fuyuki Ishikawa. "Alterations of DNA and Chromatin Structures at Telomeres and Genetic Instability in Mouse Cells Defective in DNA Polymerase α". Molecular and Cellular Biology 25, № 24 (2005): 11073–88. http://dx.doi.org/10.1128/mcb.25.24.11073-11088.2005.

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ABSTRACT Telomere length is controlled by a homeostatic mechanism that involves telomerase, telomere-associated proteins, and conventional replication machinery. Specifically, the coordinated actions of the lagging strand synthesis and telomerase have been argued. Although DNA polymerase α, an enzyme important for the lagging strand synthesis, has been indicated to function in telomere metabolism in yeasts and ciliates, it has not been characterized in higher eukaryotes. Here, we investigated the impact of compromised polymerase α activity on telomeres, using tsFT20 mouse mutant cells harborin

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34

Bullock, P. A., S. Tevosian, C. Jones, and D. Denis. "Mapping initiation sites for simian virus 40 DNA synthesis events in vitro." Molecular and Cellular Biology 14, no. 8 (1994): 5043–55. http://dx.doi.org/10.1128/mcb.14.8.5043-5055.1994.

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Primer RNA-DNA, a small (approximately 30-nucleotide) RNA-DNA hybrid molecule, was identified in recent studies of simian virus 40 DNA synthesis in vitro. The available evidence indicates that primer RNA-DNA is the product of the polymerase alpha-primase complex. Primer RNA-DNA is formed exclusively on lagging-strand DNA templates; it is synthesized initially in the vicinity of the simian virus 40 origin and at later times at sites progressively distal to the origin. To further characterize initiation events, template sequences encoding the 5' ends of both primer RNA and primer DNA, formed dur

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35

Bullock, P. A., S. Tevosian, C. Jones, and D. Denis. "Mapping initiation sites for simian virus 40 DNA synthesis events in vitro." Molecular and Cellular Biology 14, no. 8 (1994): 5043–55. http://dx.doi.org/10.1128/mcb.14.8.5043.

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Анотація:

Primer RNA-DNA, a small (approximately 30-nucleotide) RNA-DNA hybrid molecule, was identified in recent studies of simian virus 40 DNA synthesis in vitro. The available evidence indicates that primer RNA-DNA is the product of the polymerase alpha-primase complex. Primer RNA-DNA is formed exclusively on lagging-strand DNA templates; it is synthesized initially in the vicinity of the simian virus 40 origin and at later times at sites progressively distal to the origin. To further characterize initiation events, template sequences encoding the 5' ends of both primer RNA and primer DNA, formed dur

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36

Gawel, Damian, Magdalena Maliszewska-Tkaczyk, Piotr Jonczyk, Roel M. Schaaper, and Iwona J. Fijalkowska. "Lack of Strand Bias in UV-Induced Mutagenesis in Escherichia coli." Journal of Bacteriology 184, no. 16 (2002): 4449–54. http://dx.doi.org/10.1128/jb.184.16.4449-4454.2002.

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ABSTRACT We have investigated whether UV-induced mutations are created with equal efficiency on the leading and lagging strands of DNA replication. We employed an assay system that permits measurement of mutagenesis in the lacZ gene in pairs of near-identical strains. Within each pair, the strains differ only in the orientation of the lacZ gene with respect to the origin of DNA replication. Depending on this orientation, any lacZ target sequence will be replicated in one orientation as a leading strand and as a lagging strand in the other orientation. In contrast to previous results obtained f

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37

Zhu, Yali, Zetang Wu, M. Cristina Cardoso, and Deborah S. Parris. "Processing of Lagging-Strand Intermediates In Vitro by Herpes Simplex Virus Type 1 DNA Polymerase." Journal of Virology 84, no. 15 (2010): 7459–72. http://dx.doi.org/10.1128/jvi.01875-09.

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ABSTRACT The processing of lagging-strand intermediates has not been demonstrated in vitro for herpes simplex virus type 1 (HSV-1). Human flap endonuclease-1 (Fen-1) was examined for its ability to produce ligatable products with model lagging-strand intermediates in the presence of the wild-type or exonuclease-deficient (exo−) HSV-1 DNA polymerase (pol). Primer/templates were composed of a minicircle single-stranded DNA template annealed to primers that contained 5′ DNA flaps or 5′ annealed DNA or RNA sequences. Gapped DNA primer/templates were extended but not significantly strand displaced

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38

Khan, S. A. "Rolling-circle replication of bacterial plasmids." Microbiology and Molecular Biology Reviews 61, no. 4 (1997): 442–55. http://dx.doi.org/10.1128/mmbr.61.4.442-455.1997.

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Many bacterial plasmids replicate by a rolling-circle (RC) mechanism. Their replication properties have many similarities to as well as significant differences from those of single-stranded DNA (ssDNA) coliphages, which also replicate by an RC mechanism. Studies on a large number of RC plasmids have revealed that they fall into several families based on homology in their initiator proteins and leading-strand origins. The leading-strand origins contain distinct sequences that are required for binding and nicking by the Rep proteins. Leading-strand origins also contain domains that are required

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39

Kuban, Wojciech, Magdalena Banach-Orlowska, Malgorzata Bialoskorska, et al. "Mutator Phenotype Resulting from DNA Polymerase IV Overproduction in Escherichia coli: Preferential Mutagenesis on the Lagging Strand." Journal of Bacteriology 187, no. 19 (2005): 6862–66. http://dx.doi.org/10.1128/jb.187.19.6862-6866.2005.

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ABSTRACT We investigated the mutator effect resulting from overproduction of Escherichia coli DNA polymerase IV. Using lac mutational targets in the two possible orientations on the chromosome, we observed preferential mutagenesis during lagging strand synthesis. The mutator activity likely results from extension of mismatches produced by polymerase III holoenzyme.

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40

Gan, Haiyun, Chuanhe Yu, Sujan Devbhandari, et al. "Checkpoint Kinase Rad53 Couples Leading- and Lagging-Strand DNA Synthesis under Replication Stress." Molecular Cell 68, no. 2 (2017): 446–55. http://dx.doi.org/10.1016/j.molcel.2017.09.018.

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41

Kurat, Christoph F., Joseph T. P. Yeeles, Harshil Patel, Anne Early, and John F. X. Diffley. "Chromatin Controls DNA Replication Origin Selection, Lagging-Strand Synthesis, and Replication Fork Rates." Molecular Cell 65, no. 1 (2017): 117–30. http://dx.doi.org/10.1016/j.molcel.2016.11.016.

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42

Kresge, Nicole, Robert D. Simoni, and Robert L. Hill. "DNA Polymerase and Leading and Lagging Strand Synthesis: the Work of Bruce Alberts." Journal of Biological Chemistry 282, no. 4 (2007): e3-e5. http://dx.doi.org/10.1016/s0021-9258(20)72146-0.

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43

Cerrón, Fernando, Sara de Lorenzo, Kateryna M. Lemishko, et al. "Replicative DNA polymerases promote active displacement of SSB proteins during lagging strand synthesis." Nucleic Acids Research 47, no. 11 (2019): 5723–34. http://dx.doi.org/10.1093/nar/gkz249.

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44

Barry, Jack, Mei Lie Wong,, and Bruce Alberts. "In vitro reconstitution of DNA replication initiated by genetic recombination: a T4 bacteriophage model for a type of DNA synthesis important for all cells." Molecular Biology of the Cell 30, no. 1 (2019): 146–59. http://dx.doi.org/10.1091/mbc.e18-06-0386.

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Using a mixture of 10 purified DNA replication and DNA recombination proteins encoded by the bacteriophage T4 genome, plus two homologous DNA molecules, we have reconstituted the genetic recombination–initiated pathway that initiates DNA replication forks at late times of T4 bacteriophage infection. Inside the cell, this recombination-dependent replication (RDR) is needed to produce the long concatemeric T4 DNA molecules that serve as substrates for packaging the shorter, genome-sized viral DNA into phage heads. The five T4 proteins that catalyze DNA synthesis on the leading strand, plus the p

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45

Bainbridge, Lewis J., Rebecca Teague, and Aidan J. Doherty. "Repriming DNA synthesis: an intrinsic restart pathway that maintains efficient genome replication." Nucleic Acids Research 49, no. 9 (2021): 4831–47. http://dx.doi.org/10.1093/nar/gkab176.

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Abstract To bypass a diverse range of fork stalling impediments encountered during genome replication, cells possess a variety of DNA damage tolerance (DDT) mechanisms including translesion synthesis, template switching, and fork reversal. These pathways function to bypass obstacles and allow efficient DNA synthesis to be maintained. In addition, lagging strand obstacles can also be circumvented by downstream priming during Okazaki fragment generation, leaving gaps to be filled post-replication. Whether repriming occurs on the leading strand has been intensely debated over the past half-centur

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46

Martin, Aegina Adams, Isabelle Dionne, Raymund J. Wellinger та Connie Holm. "The Function of DNA Polymerase α at Telomeric G Tails Is Important for Telomere Homeostasis". Molecular and Cellular Biology 20, № 3 (2000): 786–96. http://dx.doi.org/10.1128/mcb.20.3.786-796.2000.

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ABSTRACT Telomere length control is influenced by several factors, including telomerase, the components of telomeric chromatin structure, and the conventional replication machinery. Although known components of the replication machinery can influence telomere length equilibrium, little is known about why mutations in certain replication proteins cause dramatic telomere lengthening. To investigate the cause of telomere elongation in cdc17/pol1 (DNA polymerase α) mutants, we examined telomeric chromatin, as measured by its ability to repress transcription on telomere-proximal genes, and telomeri

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47

Prelich, Gregory, and Bruce Stillman. "Coordinated leading and lagging strand synthesis during SV40 DNA replication in vitro requires PCNA." Cell 53, no. 1 (1988): 117–26. http://dx.doi.org/10.1016/0092-8674(88)90493-x.

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48

Muzi-Falconi, Marco, Michele Giannattasio, Marco Foiani, and Paolo Plevani. "The DNA Polymerase _-Primase Complex: Multiple Functions and Interactions." Scientific World JOURNAL 3 (2003): 21–33. http://dx.doi.org/10.1100/tsw.2003.05.

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DNA polymerase _ (pol _) holds a special position among the growing family of eukaryotic DNA polymerases. In fact, pol _ is associated with DNA primase to form a four subunit complex and, as a consequence, is the only enzyme able to start DNA synthesis de novo. Because of this peculiarity the major role of the DNA polymerase _-primase complex (pol-prim) is in the initiation of DNA replication at chromosomal origins and in the discontinuous synthesis of Okazaki fragments on the lagging strand of the replication fork. However, pol-prim seems to play additional roles in other complex cellular pro

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49

Gangavarapu, Venkateswarlu, Satya Prakash, and Louise Prakash. "Requirement of RAD52 Group Genes for Postreplication Repair of UV-Damaged DNA in Saccharomyces cerevisiae." Molecular and Cellular Biology 27, no. 21 (2007): 7758–64. http://dx.doi.org/10.1128/mcb.01331-07.

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ABSTRACT In Saccharomyces cerevisiae, replication through DNA lesions is promoted by Rad6-Rad18-dependent processes that include translesion synthesis by DNA polymerases η and ζ and a Rad5-Mms2-Ubc13-controlled postreplicational repair (PRR) pathway which repairs the discontinuities in the newly synthesized DNA that form opposite from DNA lesions on the template strand. Here, we examine the contributions of the RAD51, RAD52, and RAD54 genes and of the RAD50 and XRS2 genes to the PRR of UV-damaged DNA. We find that deletions of the RAD51, RAD52, and RAD54 genes impair the efficiency of PRR and

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50

Nethanel, T., and G. Kaufmann. "Two DNA polymerases may be required for synthesis of the lagging DNA strand of simian virus 40." Journal of Virology 64, no. 12 (1990): 5912–18. http://dx.doi.org/10.1128/jvi.64.12.5912-5918.1990.

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