Journal articles: 'Eukaryotic cell replication'

1

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Zannis-Hadjopoulos, Maria, and Gerald B. Price. "Eukaryotic DNA replication." Journal of Cellular Biochemistry 75, S32 (1999): 1–14. http://dx.doi.org/10.1002/(sici)1097-4644(1999)75:32+<1::aid-jcb2>3.0.co;2-j.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

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

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

5

Kelly, Thomas, and A. John Callegari. "Dynamics of DNA replication in a eukaryotic cell." Proceedings of the National Academy of Sciences 116, no. 11 (February 4, 2019): 4973–82. http://dx.doi.org/10.1073/pnas.1818680116.

Full text

Abstract:

Each genomic locus in a eukaryotic cell has a distinct average time of replication during S phase that depends on the spatial and temporal pattern of replication initiation events. Replication timing can affect genomic integrity because late replication is associated with an increased mutation rate. For most eukaryotes, the features of the genome that specify the location and timing of initiation events are unknown. To investigate these features for the fission yeast, Schizosaccharomyces pombe, we developed an integrative model to analyze large single-molecule and global genomic datasets. The model provides an accurate description of the complex dynamics of S. pombe DNA replication at high resolution. We present evidence that there are many more potential initiation sites in the S. pombe genome than previously identified and that the distribution of these sites is primarily determined by two factors: the sequence preferences of the origin recognition complex (ORC), and the interference of transcription with the assembly or stability of prereplication complexes (pre-RCs). We suggest that in addition to directly interfering with initiation, transcription has driven the evolution of the binding properties of ORC in S. pombe and other eukaryotic species to target pre-RC assembly to regions of the genome that are less likely to be transcribed.

APA, Harvard, Vancouver, ISO, and other styles

6

Bielinsky, A. K., and S. A. Gerbi. "Where it all starts: eukaryotic origins of DNA replication." Journal of Cell Science 114, no. 4 (February 15, 2001): 643–51. http://dx.doi.org/10.1242/jcs.114.4.643.

Full text

Abstract:

Chromosomal origins of DNA replication in eukaryotic cells not only are crucial for understanding the basic process of DNA duplication but also provide a tool to analyze how cell cycle regulators are linked to the replication machinery. During the past decade much progress has been made in identifying replication origins in eukaryotic genomes. More recently, replication initiation point (RIP) mapping has allowed us to detect start sites for DNA synthesis at the nucleotide level and thus to monitor replication initiation events at the origin very precisely. Beyond giving us the precise positions of start sites, the application of RIP mapping in yeast and human cells has revealed a single, defined start point at which replication initiates, a scenario very reminiscent of transcription initiation. More importantly, studies in yeast have shown that the binding site for the initiator, the origin recognition complex (ORC), lies immediately adjacent to the replication start point, which suggests that ORC directs the initiation machinery to a distinct site. Therefore, in our pursuit of identifying ORC-binding sites in higher eukaryotes, RIP mapping may lead the way.

APA, Harvard, Vancouver, ISO, and other styles

7

Walter, Johannes, and John Newport. "Initiation of Eukaryotic DNA Replication." Molecular Cell 5, no. 4 (April 2000): 617–27. http://dx.doi.org/10.1016/s1097-2765(00)80241-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Kearsey, Stephen E., Karim Labib, and Domenico Maiorano. "Cell cycle control of eukaryotic DNA replication." Current Opinion in Genetics & Development 6, no. 2 (April 1996): 208–14. http://dx.doi.org/10.1016/s0959-437x(96)80052-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Blow, J. Julian. "Eukaryotic DNA replication reconstituted outside the cell." BioEssays 8, no. 5 (May 1988): 149–52. http://dx.doi.org/10.1002/bies.950080505.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Hubscher, U., and JM Sogo. "The Eukaryotic DNA Replication Fork." Physiology 12, no. 3 (June 1, 1997): 125–31. http://dx.doi.org/10.1152/physiologyonline.1997.12.3.125.

Full text

Abstract:

Before a cell divides into two identical daughter cells, the entire genome must be replicated faithfully. The mechanistic details of this complex macromolecular process, called DNA replication, have recently been clarified. We focus on the current knowledge at the eukaryotic DNA replication fork at the levels of DNA and chromatin.

APA, Harvard, Vancouver, ISO, and other styles

11

Diffley, John F. X. "Early events in eukaryotic DNA replication." Trends in Cell Biology 2, no. 10 (October 1992): 298–303. http://dx.doi.org/10.1016/0962-8924(92)90119-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

MacNeill, Stuart A. "Structure and function of the GINS complex, a key component of the eukaryotic replisome." Biochemical Journal 425, no. 3 (January 15, 2010): 489–500. http://dx.doi.org/10.1042/bj20091531.

Full text

Abstract:

High-fidelity chromosomal DNA replication is fundamental to all forms of cellular life and requires the complex interplay of a wide variety of essential and non-essential protein factors in a spatially and temporally co-ordinated manner. In eukaryotes, the GINS complex (from the Japanese go-ichi-ni-san meaning 5-1-2-3, after the four related subunits of the complex Sld5, Psf1, Psf2 and Psf3) was recently identified as a novel factor essential for both the initiation and elongation stages of the replication process. Biochemical analysis has placed GINS at the heart of the eukaryotic replication apparatus as a component of the CMG [Cdc45–MCM (minichromosome maintenance) helicase–GINS] complex that most likely serves as the replicative helicase, unwinding duplex DNA ahead of the moving replication fork. GINS homologues are found in the archaea and have been shown to interact directly with the MCM helicase and with primase, suggesting a central role for the complex in archaeal chromosome replication also. The present review summarizes current knowledge of the structure, function and evolution of the GINS complex in eukaryotes and archaea, discusses possible functions of the GINS complex and highlights recent results that point to possible regulation of GINS function in response to DNA damage.

APA, Harvard, Vancouver, ISO, and other styles

13

Moreno, Sara Priego, and Agnieszka Gambus. "Mechanisms of eukaryotic replisome disassembly." Biochemical Society Transactions 48, no. 3 (June 3, 2020): 823–36. http://dx.doi.org/10.1042/bst20190363.

Full text

Abstract:

DNA replication is a complex process that needs to be executed accurately before cell division in order to maintain genome integrity. DNA replication is divided into three main stages: initiation, elongation and termination. One of the key events during initiation is the assembly of the replicative helicase at origins of replication, and this mechanism has been very well described over the last decades. In the last six years however, researchers have also focused on deciphering the molecular mechanisms underlying the disassembly of the replicative helicase during termination. Similar to replisome assembly, the mechanism of replisome disassembly is strictly regulated and well conserved throughout evolution, although its complexity increases in higher eukaryotes. While budding yeast rely on just one pathway for replisome disassembly in S phase, higher eukaryotes evolved an additional mitotic pathway over and above the default S phase specific pathway. Moreover, replisome disassembly has been recently found to be a key event prior to the repair of certain DNA lesions, such as under-replicated DNA in mitosis and inter-strand cross-links (ICLs) in S phase. Although replisome disassembly in human cells has not been characterised yet, they possess all of the factors involved in these pathways in model organisms, and de-regulation of many of them are known to contribute to tumorigenesis and other pathological conditions.

APA, Harvard, Vancouver, ISO, and other styles

14

Mirkin, Ekaterina V., and Sergei M. Mirkin. "Replication Fork Stalling at Natural Impediments." Microbiology and Molecular Biology Reviews 71, no. 1 (March 2007): 13–35. http://dx.doi.org/10.1128/mmbr.00030-06.

Full text

Abstract:

SUMMARY Accurate and complete replication of the genome in every cell division is a prerequisite of genomic stability. Thus, both prokaryotic and eukaryotic replication forks are extremely precise and robust molecular machines that have evolved to be up to the task. However, it has recently become clear that the replication fork is more of a hurdler than a runner: it must overcome various obstacles present on its way. Such obstacles can be called natural impediments to DNA replication, as opposed to external and genetic factors. Natural impediments to DNA replication are particular DNA binding proteins, unusual secondary structures in DNA, and transcription complexes that occasionally (in eukaryotes) or constantly (in prokaryotes) operate on replicating templates. This review describes the mechanisms and consequences of replication stalling at various natural impediments, with an emphasis on the role of replication stalling in genomic instability.

APA, Harvard, Vancouver, ISO, and other styles

15

Saugar, Irene, María Ángeles Ortiz-Bazán, and José Antonio Tercero. "Tolerating DNA damage during eukaryotic chromosome replication." Experimental Cell Research 329, no. 1 (November 2014): 170–77. http://dx.doi.org/10.1016/j.yexcr.2014.07.009.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Leatherwood, Janet. "Emerging mechanisms of eukaryotic DNA replication initiation." Current Opinion in Cell Biology 10, no. 6 (December 1998): 742–48. http://dx.doi.org/10.1016/s0955-0674(98)80117-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Stillman, Bruce. "Initiation of Eukaryotic DNA Replication In Vitro." Annual Review of Cell Biology 5, no. 1 (November 1989): 197–245. http://dx.doi.org/10.1146/annurev.cb.05.110189.001213.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Yuan, Zuanning, and Huilin Li. "Molecular mechanisms of eukaryotic origin initiation, replication fork progression, and chromatin maintenance." Biochemical Journal 477, no. 18 (September 24, 2020): 3499–525. http://dx.doi.org/10.1042/bcj20200065.

Full text

Abstract:

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 methyltransferase 1 is primarily responsible for copying the parental DNA methylation pattern into the nascent DNA. Epigenetic information encoded in histones is transferred via a more complex and less well-understood process termed replication-couple nucleosome assembly. Here, we summarize the most recent structural and biochemical insights into DNA replication initiation, replication fork elongation, chromatin assembly and maintenance, and related regulatory mechanisms.

APA, Harvard, Vancouver, ISO, and other styles

19

Wolffe, A. P. "Implications of DNA replication for eukaryotic gene expression." Journal of Cell Science 99, no. 2 (June 1, 1991): 201–6. http://dx.doi.org/10.1242/jcs.99.2.201.

Full text

Abstract:

DNA replication has a key role in many developmental processes. Recent progress in understanding events at the replication fork suggests mechanisms for both establishing and maintaining programs of eukaryotic gene activity. In this review, I discuss the consequences of replication fork passage for preexisting chromatin structures and describe how the mechanism of nucleosome assembly at the replication fork may facilitate the formation of either transcriptionally active or repressed chromatin.

APA, Harvard, Vancouver, ISO, and other styles

20

Walters, Alison D., and James P. J. Chong. "Methanococcus maripaludis: an archaeon with multiple functional MCM proteins?" Biochemical Society Transactions 37, no. 1 (January 20, 2009): 1–6. http://dx.doi.org/10.1042/bst0370001.

Full text

Abstract:

There are a large number of proteins involved in the control of eukaryotic DNA replication, which act together to ensure DNA is replicated only once every cell cycle. Key proteins involved in the initiation and elongation phases of DNA replication include the MCM (minchromosome maintenance) proteins, MCM2–MCM7, a family of six related proteins believed to act as the replicative helicase. Genome sequencing has revealed that the archaea possess a simplified set of eukaryotic replication homologues. The complexity of the DNA replication machinery in eukaryotes has led to a number of archaeal species being adapted as model organisms for the study of the DNA replication process. Most archaea sequenced to date possess a single MCM homologue that forms a hexameric complex. Recombinant MCMs from several archaea have been used in the biochemical characterization of the protein, revealing that the MCM complex has ATPase, DNA-binding and -unwinding activities. Unusually, the genome of the methanogenic archaeon Methanococcus maripaludis contains four MCM homologues, all of which contain the conserved motifs required for function. The availability of a wide range of genetic tools for the manipulation of M. maripaludis and the relative ease of growth of this organism in the laboratory makes it a good potential model for studying the role of multiple MCMs in DNA replication.

APA, Harvard, Vancouver, ISO, and other styles

21

Novak, B., A. Csikasz-Nagy, B. Gyorffy, K. Nasmyth, and J. J. Tyson. "Model scenarios for evolution of the eukaryotic cell cycle." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 353, no. 1378 (December 29, 1998): 2063–76. http://dx.doi.org/10.1098/rstb.1998.0352.

Full text

Abstract:

Progress through the division cycle of present day eukaryotic cells is controlled by a complex network consisting of (i) cyclin–dependent kinases (CDKs) and their associated cyclins, (ii) kinases and phosphatases that regulate CDK activity, and (iii) stoichiometric inhibitors that sequester cyclin–CDK dimers. Presumably regulation of cell division in the earliest ancestors of eukaryotes was a considerably simpler affair. Nasmyth (1995) recently proposed a mechanism for control of a putative, primordial, eukaryotic cell cycle, based on antagonistic interactions between a cyclin–CDK and the anaphase promoting complex (APC) that labels the cyclin subunit for proteolysis. We recast this idea in mathematical form and show that the model exhibits hysteretic behaviour between alternative steady states: a G1–like state (APC on, CDK activity low, DNA unreplicated and replication complexes assembled) and an S/M–like state (APC off, CDK activity high, DNA replicated and replication complexes disassembled). In our model, the transition from G1 to S/M (‘Start’) is driven by cell growth, and the reverse transition (‘Finish’) is driven by completion of DNA synthesis and proper alignment of chromosomes on the metaphase plate. This simple and effective mechanism for coupling growth and division and for accurately copying and partitioning a genome consisting of numerous chromosomes, each with multiple origins of replication, could represent the core of the eukaryotic cell cycle. Furthermore, we show how other controls could be added to this core and speculate on the reasons why stoichiometric inhibitors and CDK inhibitory phosphorylation might have been appended to the primitive alternation between cyclin accumulation and degradation.

APA, Harvard, Vancouver, ISO, and other styles

22

Dutta, Anindya, and Stephen P. Bell. "INITIATION OF DNA REPLICATION IN EUKARYOTIC CELLS." Annual Review of Cell and Developmental Biology 13, no. 1 (November 1997): 293–332. http://dx.doi.org/10.1146/annurev.cellbio.13.1.293.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Kitamura, Etsushi, J. Julian Blow, and Tomoyuki U. Tanaka. "Live-Cell Imaging Reveals Replication of Individual Replicons in Eukaryotic Replication Factories." Cell 125, no. 7 (June 2006): 1297–308. http://dx.doi.org/10.1016/j.cell.2006.04.041.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Hyrien, Olivier. "How MCM loading and spreading specify eukaryotic DNA replication initiation sites." F1000Research 5 (August 24, 2016): 2063. http://dx.doi.org/10.12688/f1000research.9008.1.

Full text

Abstract:

DNA replication origins strikingly differ between eukaryotic species and cell types. Origins are localized and can be highly efficient in budding yeast, are randomly located in early fly and frog embryos, which do not transcribe their genomes, and are clustered in broad (10-100 kb) non-transcribed zones, frequently abutting transcribed genes, in mammalian cells. Nonetheless, in all cases, origins are established during the G1-phase of the cell cycle by the loading of double hexamers of the Mcm 2-7 proteins (MCM DHs), the core of the replicative helicase. MCM DH activation in S-phase leads to origin unwinding, polymerase recruitment, and initiation of bidirectional DNA synthesis. Although MCM DHs are initially loaded at sites defined by the binding of the origin recognition complex (ORC), they ultimately bind chromatin in much greater numbers than ORC and only a fraction are activated in any one S-phase. Data suggest that the multiplicity and functional redundancy of MCM DHs provide robustness to the replication process and affect replication time and that MCM DHs can slide along the DNA and spread over large distances around the ORC. Recent studies further show that MCM DHs are displaced along the DNA by collision with transcription complexes but remain functional for initiation after displacement. Therefore, eukaryotic DNA replication relies on intrinsically mobile and flexible origins, a strategy fundamentally different from bacteria but conserved from yeast to human. These properties of MCM DHs likely contribute to the establishment of broad, intergenic replication initiation zones in higher eukaryotes.

APA, Harvard, Vancouver, ISO, and other styles

25

Coffman, Frederick D., Mai-Ling Reyes, Monique Brown, W. Clark Lambert, and Stanley Cohen. "Localization of ORC1 During the Cell Cycle in Human Leukemia Cells." Analytical Cellular Pathology 34, no. 6 (2011): 355–61. http://dx.doi.org/10.1155/2011/173174.

Full text

Abstract:

The interaction of the origin recognition complex (ORC) with replication origins is a critical parameter in eukaryotic replication initiation. In mammals the ORC remains bound except during mitosis, thus the localization of ORC complexes allows localization of origins. A monoclonal antibody that recognizes human ORC1 was used to localize ORC complexes in populations of human MOLT-4 cells separated by cell cycle position using centrifugal elutriation. ORC1 staining in cells in early G1 is diffuse and primarily peripheral. As the cells traverse G1, ORC1 accumulates and becomes more localized towards the center of the nucleus, however around the G1/S boundary the staining pattern changes and ORC1 appears peripheral. By mid to late S phase ORC1 immunofluorescence is again concentrated at the nuclear center. During anaphase, ORC1 staining is localized mainly in the pericentriolar regions. These findings suggest that concerted movements of origin DNA sequences in addition to the previously documented assembly and disassembly of protein complexes are an important aspect of replication initiation loci in eukaryotes.

APA, Harvard, Vancouver, ISO, and other styles

26

Kunkel, Thomas A., and Peter M. Burgers. "Dividing the workload at a eukaryotic replication fork." Trends in Cell Biology 18, no. 11 (November 2008): 521–27. http://dx.doi.org/10.1016/j.tcb.2008.08.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

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

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

28

Huberman, Joel A. "Cell cycle control of initiation of eukaryotic DNA replication." Chromosoma 100, no. 7 (August 1991): 419–23. http://dx.doi.org/10.1007/bf00364551.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

DePamphilis, Melvin L. "Initiation of DNA replication in eukaryotic chromosomes." Journal of Cellular Biochemistry 72, S30-31 (1998): 8–17. http://dx.doi.org/10.1002/(sici)1097-4644(1998)72:30/31+<8::aid-jcb3>3.0.co;2-r.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Diffley, John F. X. "Quality control in the initiation of eukaryotic DNA replication." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1584 (December 27, 2011): 3545–53. http://dx.doi.org/10.1098/rstb.2011.0073.

Full text

Abstract:

Origins of DNA replication must be regulated to ensure that the entire genome is replicated precisely once in each cell cycle. In human cells, this requires that tens of thousands of replication origins are activated exactly once per cell cycle. Failure to do so can lead to cell death or genome rearrangements such as those associated with cancer. Systems ensuring efficient initiation of replication, while also providing a robust block to re-initiation, play a crucial role in genome stability. In this review, I will discuss some of the strategies used by cells to ensure once per cell cycle replication and provide a quantitative framework to evaluate the relative importance and efficiency of individual pathways involved in this regulation.

APA, Harvard, Vancouver, ISO, and other styles

31

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 (August 23, 2004): 45586–93. http://dx.doi.org/10.1074/jbc.m407772200.

Full text

Abstract:

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 each of theXenopusMcm proteins, we have demonstrated that Mcm proteins are required during DNA replication and DNA unwinding after initiation of replication. Quantitative depletion of Mcms from the NPE results in normal replication and unwinding, confirming that Mcms are required before pre-replicative complex assembly and dispensable thereafter. Replication and unwinding are inhibited when pooled neutralizing antibodies against the six different Mcm2–7 proteins are added during NPE incubation. Furthermore, replication is blocked by the addition of the Mcm antibodies after an initial period of replication in the NPE, visualized by a pulse of radiolabeled nucleotide at the same time as antibody addition. Addition of the cyclin-dependent kinase 2 inhibitor p21cip1specifically blocks origin firing but does not prevent helicase action. When p21cip1is added, followed by the non-hydrolyzable analog ATPγS to block helicase function, unwinding is inhibited, demonstrating that plasmid unwinding is specifically attributable to an ATP hydrolysis-dependent function. These data support the hypothesis that the Mcm protein complex functions as the replicative helicase.

APA, Harvard, Vancouver, ISO, and other styles

32

Tanny, Robyn E., David M. MacAlpine, Hannah G. Blitzblau, and Stephen P. Bell. "Genome-wide Analysis of Re-replication Reveals Inhibitory Controls That Target Multiple Stages of Replication Initiation." Molecular Biology of the Cell 17, no. 5 (May 2006): 2415–23. http://dx.doi.org/10.1091/mbc.e05-11-1037.

Full text

Abstract:

DNA replication must be tightly controlled during each cell cycle to prevent unscheduled replication and ensure proper genome maintenance. The currently known controls that prevent re-replication act redundantly to inhibit pre-replicative complex (pre-RC) assembly outside of the G1-phase of the cell cycle. The yeast Saccharomyces cerevisiae has been a useful model organism to study how eukaryotic cells prevent replication origins from reinitiating during a single cell cycle. Using a re-replication-sensitive strain and DNA microarrays, we map sites across the S. cerevisiae genome that are re-replicated as well as sites of pre-RC formation during re-replication. Only a fraction of the genome is re-replicated by a subset of origins, some of which are capable of multiple reinitiation events. Translocation experiments demonstrate that origin-proximal sequences are sufficient to predispose an origin to re-replication. Origins that reinitiate are largely limited to those that can recruit Mcm2-7 under re-replicating conditions; however, the formation of a pre-RC is not sufficient for reinitiation. Our findings allow us to categorize origins with respect to their propensity to reinitiate and demonstrate that pre-RC formation is not the only target for the mechanisms that prevent genomic re-replication.

APA, Harvard, Vancouver, ISO, and other styles

33

Krings, Gregor, and Deepak Bastia. "Molecular Architecture of a Eukaryotic DNA Replication Terminus-Terminator ProteinComplex." Molecular and Cellular Biology 26, no. 21 (August 28, 2006): 8061–74. http://dx.doi.org/10.1128/mcb.01102-06.

Full text

Abstract:

ABSTRACT DNA replication forks pause at programmed fork barriers within nontranscribed regions of the ribosomal DNA (rDNA) genes of many eukaryotes to coordinate and regulate replication, transcription, and recombination. The mechanism of eukaryotic fork arrest remains unknown. In Schizosaccharomyces pombe, the promiscuous DNA binding protein Sap1 not only causes polar fork arrest at the rDNA fork barrier Ter1 but also regulates mat1 imprinting at SAS1 without fork pausing. Towards an understanding of eukaryotic fork arrest, we probed the interactions of Sap1 with Ter1 as contrasted with SAS1. The Sap1 dimer bound Ter1 with high affinity at one face of the DNA, contacting successive major grooves. The complex displayed translational symmetry. In contrast, Sap1 subunits approached SAS1 from opposite helical faces, forming a low-affinity complex with mirror image rotational symmetry. The alternate symmetries were reflected in distinct Sap1-induced helical distortions. Importantly, modulating protein-DNA interactions of the fork-proximal Sap1 subunit with the nonnatural binding site DR2 affected blocking efficiency without changes in binding affinity or binding mode but with alterations in Sap1-induced DNA distortion. The results reveal that Sap1-DNA affinity alone is insufficient to account for fork arrest and suggest that Sap1 binding-induced structural changes may result in formation of a competent fork-blocking complex.

APA, Harvard, Vancouver, ISO, and other styles

34

Tarrason Risa, Gabriel, Fredrik Hurtig, Sian Bray, Anne E. Hafner, Lena Harker-Kirschneck, Peter Faull, Colin Davis, et al. "The proteasome controls ESCRT-III–mediated cell division in an archaeon." Science 369, no. 6504 (August 6, 2020): eaaz2532. http://dx.doi.org/10.1126/science.aaz2532.

Full text

Abstract:

Sulfolobus acidocaldarius is the closest experimentally tractable archaeal relative of eukaryotes and, despite lacking obvious cyclin-dependent kinase and cyclin homologs, has an ordered eukaryote-like cell cycle with distinct phases of DNA replication and division. Here, in exploring the mechanism of cell division in S. acidocaldarius, we identify a role for the archaeal proteasome in regulating the transition from the end of one cell cycle to the beginning of the next. Further, we identify the archaeal ESCRT-III homolog, CdvB, as a key target of the proteasome and show that its degradation triggers division by allowing constriction of the CdvB1:CdvB2 ESCRT-III division ring. These findings offer a minimal mechanism for ESCRT-III–mediated membrane remodeling and point to a conserved role for the proteasome in eukaryotic and archaeal cell cycle control.

APA, Harvard, Vancouver, ISO, and other styles

35

Broderick, Ronan, and Heinz-Peter Nasheuer. "Regulation of Cdc45 in the cell cycle and after DNA damage." Biochemical Society Transactions 37, no. 4 (July 22, 2009): 926–30. http://dx.doi.org/10.1042/bst0370926.

Full text

Abstract:

The Cdc (cell division cycle) 45 protein has a central role in the regulation of the initiation and elongation stages of eukaryotic chromosomal DNA replication. In addition, it is the main target for a Chk1 (checkpoint kinase 1)-dependent Cdc25/CDK2 (cyclin-dependent kinase 2)-independent DNA damage checkpoint signal transduction pathway following low doses of BPDE (benzo[a]pyrene dihydrodiol epoxide) treatment, which causes DNA damage similar to UV-induced adducts. Cdc45 interacts physically and functionally with the putative eukaryotic replicative DNA helicase, the MCM (mini-chromosome maintenance) complex, and forms a helicase active ‘supercomplex’, the CMG [Cdc45–MCM2–7–GINS (go-ichi-ni-san)] complex. These known protein–protein interactions, as well as unknown interactions and post-translational modifications, may be important for the regulation of Cdc45 and the initiation of DNA replication following DNA damage. Future studies will help to elucidate the molecular basis of this newly identified S-phase checkpoint pathway which has Cdc45 as a target.

APA, Harvard, Vancouver, ISO, and other styles

36

Pollok, S., J. Stoepel, C. Bauerschmidt, E. Kremmer, and H. P. Nasheuer. "Regulation of eukaryotic DNA replication at the initiation step." Biochemical Society Transactions 31, no. 1 (February 1, 2003): 266–69. http://dx.doi.org/10.1042/bst0310266.

Full text

Abstract:

The studies of cell growth and division have remained at the centre of biomedical research for more than 100 years. The combination of genetic, biochemical, molecular and cell biological techniques recently yielded a burst in what is known of the molecular control of cell growth processes. The initiation of DNA replication is crucial for the stability of the genetic information of a cell. Two factors, Cdc45p (cell division cycle 45p) and DNA polymerase α-primase, are necessary in this process. Depending on growth signals, Cdc45p is expressed as a late protein. New phosphorylation-specific antibodies specifically recognize the phosphorylated subunit, p68, of the four subunit DNA polymerase α-primase and show that the phosphorylated polypeptide is exclusively nuclear.

APA, Harvard, Vancouver, ISO, and other styles

37

Yardimci, Hasan, Anna B. Loveland, Satoshi Habuchi, Antoine M. van Oijen, and Johannes C. Walter. "Uncoupling of Sister Replisomes during Eukaryotic DNA Replication." Molecular Cell 40, no. 5 (December 2010): 834–40. http://dx.doi.org/10.1016/j.molcel.2010.11.027.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

WU, Jia Rui. "Regulation of eukaryotic DNA replication and nuclear structure." Cell Research 9, no. 3 (September 1999): 163–70. http://dx.doi.org/10.1038/sj.cr.7290014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

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

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

40

Depamphilis, Melvin L. "Origins of DNA replication that function in eukaryotic cells." Current Opinion in Cell Biology 5, no. 3 (June 1993): 434–41. http://dx.doi.org/10.1016/0955-0674(93)90008-e.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Cavalier-Smith, Thomas. "Kingdoms Protozoa and Chromista and the eozoan root of the eukaryotic tree." Biology Letters 6, no. 3 (December 23, 2009): 342–45. http://dx.doi.org/10.1098/rsbl.2009.0948.

Full text

Abstract:

I discuss eukaryotic deep phylogeny and reclassify the basal eukaryotic kingdom Protozoa and derived kingdom Chromista in the light of multigene trees. I transfer the formerly protozoan Heliozoa and infrakingdoms Alveolata and Rhizaria into Chromista, which is sister to kingdom Plantae and arguably originated by synergistic double internal enslavement of green algal and red algal cells. I establish new subkingdoms (Harosa; Hacrobia) for the expanded Chromista. The protozoan phylum Euglenozoa differs immensely from other eukaryotes in its nuclear genome organization (trans-spliced multicistronic transcripts), mitochondrial DNA organization, cytochrome c -type biogenesis, cell structure and arguably primitive mitochondrial protein-import and nuclear DNA prereplication machineries. The bacteria-like absence of mitochondrial outer-membrane channel Tom40 and DNA replication origin-recognition complexes from trypanosomatid Euglenozoa roots the eukaryotic tree between Euglenozoa and all other eukaryotes (neokaryotes), or within Euglenozoa. Given their unique properties, I segregate Euglenozoa from infrakingdom Excavata (now comprising only phyla Percolozoa, Loukozoa, Metamonada), grouping infrakingdoms Euglenozoa and Excavata as the ancestral protozoan subkingdom Eozoa. I place phylum Apusozoa within the derived protozoan subkingdom Sarcomastigota. Clarifying early eukaryote evolution requires intensive study of properties distinguishing Euglenozoa from neokaryotes and Eozoa from neozoa (eukaryotes except Eozoa; ancestrally defined by haem lyase).

APA, Harvard, Vancouver, ISO, and other styles

42

Boos, Dominik, and Pedro Ferreira. "Origin Firing Regulations to Control Genome Replication Timing." Genes 10, no. 3 (March 6, 2019): 199. http://dx.doi.org/10.3390/genes10030199.

Full text

Abstract:

Complete genome duplication is essential for genetic homeostasis over successive cell generations. Higher eukaryotes possess a complex genome replication program that involves replicating the genome in units of individual chromatin domains with a reproducible order or timing. Two types of replication origin firing regulations ensure complete and well-timed domain-wise genome replication: (1) the timing of origin firing within a domain must be determined and (2) enough origins must fire with appropriate positioning in a short time window to avoid inter-origin gaps too large to be fully copied. Fundamental principles of eukaryotic origin firing are known. We here discuss advances in understanding the regulation of origin firing to control firing time. Work with yeasts suggests that eukaryotes utilise distinct molecular pathways to determine firing time of distinct sets of origins, depending on the specific requirements of the genomic regions to be replicated. Although the exact nature of the timing control processes varies between eukaryotes, conserved aspects exist: (1) the first step of origin firing, pre-initiation complex (pre-IC formation), is the regulated step, (2) many regulation pathways control the firing kinase Dbf4-dependent kinase, (3) Rif1 is a conserved mediator of late origin firing and (4) competition between origins for limiting firing factors contributes to firing timing. Characterization of the molecular timing control pathways will enable us to manipulate them to address the biological role of replication timing, for example, in cell differentiation and genome instability.

APA, Harvard, Vancouver, ISO, and other styles

43

Bogan, Joseph A., Darren A. Natale, and Melvin L. Depamphilis. "Initiation of eukaryotic DNA replication: conservative or liberal?" Journal of Cellular Physiology 184, no. 2 (2000): 139–50. http://dx.doi.org/10.1002/1097-4652(200008)184:2<139::aid-jcp1>3.0.co;2-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Burgers, Peter M. J. "Polymerase Dynamics at the Eukaryotic DNA Replication Fork." Journal of Biological Chemistry 284, no. 7 (October 3, 2008): 4041–45. http://dx.doi.org/10.1074/jbc.r800062200.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Patel, Prasanta K., Benoit Arcangioli, Stephen P. Baker, Aaron Bensimon, and Nicholas Rhind. "DNA Replication Origins Fire Stochastically in Fission Yeast." Molecular Biology of the Cell 17, no. 1 (January 2006): 308–16. http://dx.doi.org/10.1091/mbc.e05-07-0657.

Full text

Abstract:

DNA replication initiates at discrete origins along eukaryotic chromosomes. However, in most organisms, origin firing is not efficient; a specific origin will fire in some but not all cell cycles. This observation raises the question of how individual origins are selected to fire and whether origin firing is globally coordinated to ensure an even distribution of replication initiation across the genome. We have addressed these questions by determining the location of firing origins on individual fission yeast DNA molecules using DNA combing. We show that the firing of replication origins is stochastic, leading to a random distribution of replication initiation. Furthermore, origin firing is independent between cell cycles; there is no epigenetic mechanism causing an origin that fires in one cell cycle to preferentially fire in the next. Thus, the fission yeast strategy for the initiation of replication is different from models of eukaryotic replication that propose coordinated origin firing.

APA, Harvard, Vancouver, ISO, and other styles

46

Masai, Hisao, Zhiying You, and Ken-ichi Arai. "Control of DNA Replication: Regulation and Activation of Eukaryotic Replicative Helicase, MCM." IUBMB Life (International Union of Biochemistry and Molecular Biology: Life) 57, no. 4-5 (May 1, 2005): 323–35. http://dx.doi.org/10.1080/15216540500092419.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Mass, Gilad, Tamar Nethanel, and Gabriel Kaufmann. "The Middle Subunit of Replication Protein A Contacts Growing RNA-DNA Primers in Replicating Simian Virus 40 Chromosomes." Molecular and Cellular Biology 18, no. 11 (November 1, 1998): 6399–407. http://dx.doi.org/10.1128/mcb.18.11.6399.

Full text

Abstract:

ABSTRACT The eukaryotic single-stranded DNA binding protein replication protein A (RPA) participates in major DNA transactions. RPA also interacts through its middle subunit (Rpa2) with regulators of the cell division cycle and of the response to DNA damage. A specific contact between Rpa2 and nascent simian virus 40 DNA was revealed by in situ UV cross-linking. The dynamic attributes of the cross-linked DNA, namely, its size distribution, RNA primer content, and replication fork polarity, were determined. These data suggest that Rpa2 contacts the early DNA chain intermediates synthesized by DNA polymerase α-primase (RNA-DNA primers) but not more advanced products. Possible signaling functions of Rpa2 are discussed, and current models of eukaryotic lagging-strand DNA synthesis are evaluated in view of our results.

APA, Harvard, Vancouver, ISO, and other styles

48

Reusswig, Karl-Uwe, and Boris Pfander. "Control of Eukaryotic DNA Replication Initiation—Mechanisms to Ensure Smooth Transitions." Genes 10, no. 2 (January 29, 2019): 99. http://dx.doi.org/10.3390/genes10020099.

Full text

Abstract:

DNA replication differs from most other processes in biology in that any error will irreversibly change the nature of the cellular progeny. DNA replication initiation, therefore, is exquisitely controlled. Deregulation of this control can result in over-replication characterized by repeated initiation events at the same replication origin. Over-replication induces DNA damage and causes genomic instability. The principal mechanism counteracting over-replication in eukaryotes is a division of replication initiation into two steps—licensing and firing—which are temporally separated and occur at distinct cell cycle phases. Here, we review this temporal replication control with a specific focus on mechanisms ensuring the faultless transition between licensing and firing phases.

APA, Harvard, Vancouver, ISO, and other styles

49

Yoshimochi, Takehiro, Ryosuke Fujikane, Miyuki Kawanami, Fujihiko Matsunaga, and Yoshizumi Ishino. "The GINS Complex from Pyrococcus furiosus Stimulates the MCM Helicase Activity." Journal of Biological Chemistry 283, no. 3 (November 5, 2007): 1601–9. http://dx.doi.org/10.1074/jbc.m707654200.

Full text

Abstract:

Pyrococcus furiosus, a hyperthermophilic Archaea, has homologs of the eukaryotic MCM (mini-chromosome maintenance) helicase and GINS complex. The MCM and GINS proteins are both essential factors to initiate DNA replication in eukaryotic cells. Many biochemical characterizations of the replication-related proteins have been reported, but it has not been proved that the homologs of each protein are also essential for replication in archaeal cells. Here, we demonstrated that the P. furiosus GINS complex interacts with P. furiosus MCM. A chromatin immunoprecipitation assay revealed that the GINS complex is detected preferentially at the oriC region on Pyrococcus chromosomal DNA during the exponential growth phase but not in the stationary phase. Furthermore, the GINS complex stimulates both the ATPase and DNA helicase activities of MCM in vitro. These results strongly suggest that the archaeal GINS is involved in both the initiation and elongation processes of DNA replication in P. furiosus, as observed in eukaryotic cells.

APA, Harvard, Vancouver, ISO, and other styles

50

Lewis, Jacob S., Lisanne M. Spenkelink, Grant D. Schauer, Olga Yurieva, Stefan H. Mueller, Varsha Natarajan, Gurleen Kaur, et al. "Tunability of DNA Polymerase Stability during Eukaryotic DNA Replication." Molecular Cell 77, no. 1 (January 2020): 17–25. http://dx.doi.org/10.1016/j.molcel.2019.10.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Eukaryotic cell replication'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles