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Journal articles on the topic 'DNA supercoiling'

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Published: 4 June 2021
Last updated: 25 May 2024

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1

LILLEY, DAVID M. J. "DNA supercoiling." Biochemical Society Transactions 14, no. 2 (1986): 489–93. http://dx.doi.org/10.1042/bst0140489.

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2

Eckdahl, Todd T. "Investigating DNA Supercoiling." American Biology Teacher 61, no. 3 (1999): 214–16. http://dx.doi.org/10.2307/4450653.

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3

King, Graeme A., Federica Burla, Erwin J. G. Peterman, and Gijs J. L. Wuite. "Supercoiling DNA optically." Proceedings of the National Academy of Sciences 116, no. 52 (2019): 26534–39. http://dx.doi.org/10.1073/pnas.1908826116.

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Cellular DNA is regularly subject to torsional stress during genomic processes, such as transcription and replication, resulting in a range of supercoiled DNA structures. For this reason, methods to prepare and study supercoiled DNA at the single-molecule level are widely used, including magnetic, angular-optical, micropipette, and magneto-optical tweezers. However, it is currently challenging to combine DNA supercoiling control with spatial manipulation and fluorescence microscopy. This limits the ability to study complex and dynamic interactions of supercoiled DNA. Here we present a single-molecule assay that can rapidly and controllably generate negatively supercoiled DNA using a standard dual-trap optical tweezers instrument. This method, termed Optical DNA Supercoiling (ODS), uniquely combines the ability to study supercoiled DNA using force spectroscopy, fluorescence imaging of the whole DNA, and rapid buffer exchange. The technique can be used to generate a wide range of supercoiled states, with between <5 and 70% lower helical twist than nonsupercoiled DNA. Highlighting the versatility of ODS, we reveal previously unobserved effects of ionic strength and sequence on the structural state of underwound DNA. Next, we demonstrate that ODS can be used to directly visualize and quantify protein dynamics on supercoiled DNA. We show that the diffusion of the mitochondrial transcription factor TFAM can be significantly hindered by local regions of underwound DNA. This finding suggests a mechanism by which supercoiling could regulate mitochondrial transcription in vivo. Taken together, we propose that ODS represents a powerful method to study both the biophysical properties and biological interactions of negatively supercoiled DNA.
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4

LILLEY, DAVID M. J. "DNA supercoiling and DNA structure." Biochemical Society Transactions 14, no. 2 (1986): 211–13. http://dx.doi.org/10.1042/bst0140211.

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5

Burnier, Y., J. Dorier, and A. Stasiak. "DNA supercoiling inhibits DNA knotting." Nucleic Acids Research 36, no. 15 (2008): 4956–63. http://dx.doi.org/10.1093/nar/gkn467.

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6

Westerhoff, Hans V., Mary H. O’Dea, Anthony Maxwell, and Martin Gellert. "DNA supercoiling by DNA gyrase." Cell Biophysics 12, no. 1 (1988): 157–81. http://dx.doi.org/10.1007/bf02918357.

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7

Witz, Guillaume, Giovanni Dietler, and Andrzej Stasiak. "DNA knots and DNA supercoiling." Cell Cycle 10, no. 9 (2011): 1339–40. http://dx.doi.org/10.4161/cc.10.9.15293.

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8

Hobson, Matthew J., Zev Bryant, and James M. Berger. "Modulated control of DNA supercoiling balance by the DNA-wrapping domain of bacterial gyrase." Nucleic Acids Research 48, no. 4 (2020): 2035–49. http://dx.doi.org/10.1093/nar/gkz1230.

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Abstract Negative supercoiling by DNA gyrase is essential for maintaining chromosomal compaction, transcriptional programming, and genetic integrity in bacteria. Questions remain as to how gyrases from different species have evolved profound differences in their kinetics, efficiency, and extent of negative supercoiling. To explore this issue, we analyzed homology-directed mutations in the C-terminal, DNA-wrapping domain of the GyrA subunit of Escherichia coli gyrase (the ‘CTD’). The addition or removal of select, conserved basic residues markedly impacts both nucleotide-dependent DNA wrapping and supercoiling by the enzyme. Weakening CTD–DNA interactions slows supercoiling, impairs DNA-dependent ATP hydrolysis, and limits the extent of DNA supercoiling, while simultaneously enhancing decatenation and supercoil relaxation. Conversely, strengthening DNA wrapping does not result in a more extensively supercoiled DNA product, but partially uncouples ATP turnover from strand passage, manifesting in futile cycling. Our findings indicate that the catalytic cycle of E. coli gyrase operates at high thermodynamic efficiency, and that the stability of DNA wrapping by the CTD provides one limit to DNA supercoil introduction, beyond which strand passage competes with ATP-dependent supercoil relaxation. These results highlight a means by which gyrase can evolve distinct homeostatic supercoiling setpoints in a species-specific manner.
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9

Schvartzman, Jorge B., Pablo Hernández, Dora B. Krimer, Julien Dorier, and Andrzej Stasiak. "Closing the DNA replication cycle: from simple circular molecules to supercoiled and knotted DNA catenanes." Nucleic Acids Research 47, no. 14 (2019): 7182–98. http://dx.doi.org/10.1093/nar/gkz586.

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AbstractDue to helical structure of DNA, massive amounts of positive supercoils are constantly introduced ahead of each replication fork. Positive supercoiling inhibits progression of replication forks but various mechanisms evolved that permit very efficient relaxation of that positive supercoiling. Some of these mechanisms lead to interesting topological situations where DNA supercoiling, catenation and knotting coexist and influence each other in DNA molecules being replicated. Here, we first review fundamental aspects of DNA supercoiling, catenation and knotting when these qualitatively different topological states do not coexist in the same circular DNA but also when they are present at the same time in replicating DNA molecules. We also review differences between eukaryotic and prokaryotic cellular strategies that permit relaxation of positive supercoiling arising ahead of the replication forks. We end our review by discussing very recent studies giving a long-sought answer to the question of how slow DNA topoisomerases capable of relaxing just a few positive supercoils per second can counteract the introduction of hundreds of positive supercoils per second ahead of advancing replication forks.
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10

Frank-Kamenetskii, Maxim. "Waves of DNA supercoiling." Nature 337, no. 6204 (1989): 206. http://dx.doi.org/10.1038/337206a0.

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11

Pavlicek, Jeffrey W., Elena A. Oussatcheva, Richard R. Sinden, Vladimir N. Potaman, Otto F. Sankey, and Yuri L. Lyubchenko. "Supercoiling-Induced DNA Bending†." Biochemistry 43, no. 33 (2004): 10664–68. http://dx.doi.org/10.1021/bi0362572.

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12

Wang, James C., and A. Simon Lynch. "Transcription and DNA supercoiling." Current Opinion in Genetics & Development 3, no. 5 (1993): 764–68. http://dx.doi.org/10.1016/s0959-437x(05)80096-6.

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13

Giaever, Guri N., Larry Snyder, and James C. Wang. "DNA supercoiling in vivo." Biophysical Chemistry 29, no. 1-2 (1988): 7–15. http://dx.doi.org/10.1016/0301-4622(88)87020-0.

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14

Ma, Jie, and Michelle D. Wang. "DNA supercoiling during transcription." Biophysical Reviews 8, S1 (2016): 75–87. http://dx.doi.org/10.1007/s12551-016-0215-9.

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15

Hsieh, Li-Shan, Richard M. Burger, and Karl Drlica. "Bacterial DNA supercoiling and." Journal of Molecular Biology 219, no. 3 (1991): 443–50. http://dx.doi.org/10.1016/0022-2836(91)90185-9.

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16

Niehus, Eike, Eric Cheng, and Ming Tan. "DNA Supercoiling-Dependent Gene Regulation in Chlamydia." Journal of Bacteriology 190, no. 19 (2008): 6419–27. http://dx.doi.org/10.1128/jb.00431-08.

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ABSTRACT The intracellular pathogen Chlamydia has an unusual developmental cycle marked by temporal expression patterns whose mechanisms of regulation are largely unknown. To examine if DNA topology can regulate chlamydial gene expression, we tested the in vitro activity of five chlamydial promoters at different superhelical densities. We demonstrated for the first time that individual chlamydial promoters show a differential response to changes in DNA supercoiling that correlates with the temporal expression pattern. The promoters for two midcycle genes, ompA and pgk, were responsive to alterations in supercoiling, and promoter activity could be regulated more than eightfold. In contrast, the promoters for three late transcripts, omcAB, hctA, and ltuB, were relatively insensitive to supercoiling, with promoter activity varying by no more than 2.2-fold over a range of superhelicities. To obtain a measure of how DNA supercoiling levels vary during the chlamydial developmental cycle, we recovered the cryptic chlamydial plasmid at different times after infection and assayed its superhelical density. The chlamydial plasmid was most negatively supercoiled at midcycle, with an approximate superhelical density of −0.07. At early and late times, the plasmid was more relaxed, with an approximate superhelicity of −0.03. Thus, we found a correlation between the responsiveness to supercoiling shown by the two midcycle promoters and the increased level of negative supercoiling during mid time points in the developmental cycle. Our results support a model in which the response of individual promoters to alterations in DNA supercoiling can provide a mechanism for global patterns of temporal gene expression in Chlamydia.
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17

Liu, Yan-Jie, Biao Hu, Jia-Bi Zhu, Shan-Jiong Shen, and Guan-Qiao Yu. "nifH Promoter Activity Is Regulated by DNA Supercoiling in Sinorhizobium meliloti." Acta Biochimica et Biophysica Sinica 37, no. 4 (2005): 221–26. http://dx.doi.org/10.1111/j.1745-7270.2005.00037.x.

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AbstractIn prokaryotes, DNA supercoiling regulates the expression of many genes; for example, the expression of Klebsiella pneumoniae nifLA operon depends on DNA negative supercoiling in anaerobically grown cells, which indicates that DNA supercoiling might play a role in gene regulation of the anaerobic response. Since the expression of the nifH promoter in Sinorhizobium meliloti is not repressed by oxygen, it is proposed that the status of DNA supercoiling may not affect the expression of the nifH promoter. We tested this hypothesis by analyzing nifH promoter activity in wild-type and gyr Escherichia coli in the presence and absence of DNA gyrase inhibitors. Our results show that gene expression driven by the S. meliloti nifH promoter requires the presence of active DNA gyrase. Because DNA gyrase increases the number of negative superhelical turns in DNA in the presence of ATP, our data indicate that negative supercoiling is also important for nifH promoter activity. Our study also shows that the DNA supercoiling-dependent S. meliloti nifH promoter activity is related to the trans-acting factors NtrC and NifA that activate it. DNA supercoiling appeared to have a stronger effect on NtrC-activated nifH promoter activity than on NifA-activated promoter activity. Collectively, these results from the S. meliloti nifH promoter model system seem to indicate that, in addition to regulating gene expression during anaerobic signaling, DNA supercoiling may also provide a favorable topology for trans-acting factor binding and promoter activation regardless of oxygen status.
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18

Valdés, Antonio, Lucia Coronel, Belén Martínez-García, et al. "Transcriptional supercoiling boosts topoisomerase II-mediated knotting of intracellular DNA." Nucleic Acids Research 47, no. 13 (2019): 6946–55. http://dx.doi.org/10.1093/nar/gkz491.

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AbstractRecent studies have revealed that the DNA cross-inversion mechanism of topoisomerase II (topo II) not only removes DNA supercoils and DNA replication intertwines, but also produces small amounts of DNA knots within the clusters of nucleosomes that conform to eukaryotic chromatin. Here, we examine how transcriptional supercoiling of intracellular DNA affects the occurrence of these knots. We show that although (−) supercoiling does not change the basal DNA knotting probability, (+) supercoiling of DNA generated in front of the transcribing complexes increases DNA knot formation over 25-fold. The increase of topo II-mediated DNA knotting occurs both upon accumulation of (+) supercoiling in topoisomerase-deficient cells and during normal transcriptional supercoiling of DNA in TOP1 TOP2 cells. We also show that the high knotting probability (Pkn ≥ 0.5) of (+) supercoiled DNA reflects a 5-fold volume compaction of the nucleosomal fibers in vivo. Our findings indicate that topo II-mediated DNA knotting could be inherent to transcriptional supercoiling of DNA and other chromatin condensation processes and establish, therefore, a new crucial role of topoisomerase II in resetting the knotting–unknotting homeostasis of DNA during chromatin dynamics.
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19

El Houdaigui, Bilal, Raphaël Forquet, Thomas Hindré, et al. "Bacterial genome architecture shapes global transcriptional regulation by DNA supercoiling." Nucleic Acids Research 47, no. 11 (2019): 5648–57. http://dx.doi.org/10.1093/nar/gkz300.

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Abstract DNA supercoiling acts as a global transcriptional regulator in bacteria, that plays an important role in adapting their expression programme to environmental changes, but for which no quantitative or even qualitative regulatory model is available. Here, we focus on spatial supercoiling heterogeneities caused by the transcription process itself, which strongly contribute to this regulation mode. We propose a new mechanistic modeling of the transcription-supercoiling dynamical coupling along a genome, which allows simulating and quantitatively reproducing in vitro and in vivo transcription assays, and highlights the role of genes’ local orientation in their supercoiling sensitivity. Consistently with predictions, we show that chromosomal relaxation artificially induced by gyrase inhibitors selectively activates convergent genes in several enterobacteria, while conversely, an increase in DNA supercoiling naturally selected in a long-term evolution experiment with Escherichia coli favours divergent genes. Simulations show that these global expression responses to changes in DNA supercoiling result from fundamental mechanical constraints imposed by transcription, independently from more specific regulation of each promoter. These constraints underpin a significant and predictable contribution to the complex rules by which bacteria use DNA supercoiling as a global but fine-tuned transcriptional regulator.
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20

Jülicher, Frank. "Supercoiling transitions of closed DNA." Physical Review E 49, no. 3 (1994): 2429–35. http://dx.doi.org/10.1103/physreve.49.2429.

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21

Drlica, Karl. "Control of bacterial DNA supercoiling." Molecular Microbiology 6, no. 4 (1992): 425–33. http://dx.doi.org/10.1111/j.1365-2958.1992.tb01486.x.

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22

Marko, J., and E. Siggia. "Fluctuations and supercoiling of DNA." Science 265, no. 5171 (1994): 506–8. http://dx.doi.org/10.1126/science.8036491.

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23

OLSON, WILMA K., and JANET CICARIELLO. "Computer Simulation of DNA Supercoiling." Annals of the New York Academy of Sciences 482, no. 1 Computer Simu (1986): 69–81. http://dx.doi.org/10.1111/j.1749-6632.1986.tb20938.x.

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24

Lazurkin, Yu S. "DNA: supercoiling and alternative structures." Biopolymers and Cell 2, no. 6 (1986): 283–92. http://dx.doi.org/10.7124/bc.0001c5.

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25

Gilbert, Nick, and James Allan. "Supercoiling in DNA and chromatin." Current Opinion in Genetics & Development 25 (April 2014): 15–21. http://dx.doi.org/10.1016/j.gde.2013.10.013.

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26

Klenin, Konstantin V., Alexander V. Vologodskii, Vadim V. Anshelevich, Alexander M. Dykhne, and Maxim D. Frank-Kamenetskii. "Computer simulation of DNA supercoiling." Journal of Molecular Biology 217, no. 3 (1991): 413–19. http://dx.doi.org/10.1016/0022-2836(91)90745-r.

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27

Pruss, Gail J., and Karl Drlica. "DNA supercoiling and prokaryotic transcription." Cell 56, no. 4 (1989): 521–23. http://dx.doi.org/10.1016/0092-8674(89)90574-6.

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28

D’Arrigo, Cristina, Paola Barboro, Michele Mormino, et al. "DNA supercoiling in apoptotic chromatin." Biochemical and Biophysical Research Communications 309, no. 3 (2003): 540–46. http://dx.doi.org/10.1016/j.bbrc.2003.08.036.

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29

Villain, Paul, Violette da Cunha, Etienne Villain, et al. "The hyperthermophilic archaeon Thermococcus kodakarensis is resistant to pervasive negative supercoiling activity of DNA gyrase." Nucleic Acids Research 49, no. 21 (2021): 12332–47. http://dx.doi.org/10.1093/nar/gkab869.

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Abstract In all cells, DNA topoisomerases dynamically regulate DNA supercoiling allowing essential DNA processes such as transcription and replication to occur. How this complex system emerged in the course of evolution is poorly understood. Intriguingly, a single horizontal gene transfer event led to the successful establishment of bacterial gyrase in Archaea, but its emergent function remains a mystery. To better understand the challenges associated with the establishment of pervasive negative supercoiling activity, we expressed the gyrase of the bacterium Thermotoga maritima in a naïve archaeon Thermococcus kodakarensis which naturally has positively supercoiled DNA. We found that the gyrase was catalytically active in T. kodakarensis leading to strong negative supercoiling of plasmid DNA which was stably maintained over at least eighty generations. An increased sensitivity of gyrase-expressing T. kodakarensis to ciprofloxacin suggested that gyrase also modulated chromosomal topology. Accordingly, global transcriptome analyses revealed large scale gene expression deregulation and identified a subset of genes responding to the negative supercoiling activity of gyrase. Surprisingly, the artificially introduced dominant negative supercoiling activity did not have a measurable effect on T. kodakarensis growth rate. Our data suggest that gyrase can become established in Thermococcales archaea without critically interfering with DNA transaction processes.
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30

Dobranowska-Fishell, Alicja, and David E. Pulleyblank. "Yeast plasmids have fewer superhelical turns than predicted by the nucleosome repeat of yeast DNA." Biochemistry and Cell Biology 69, no. 2-3 (1991): 170–77. http://dx.doi.org/10.1139/o91-025.

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The superhelical density of three Saccharomyces cerevisiae plasmids was determined with respect to a defined reference state during vegetative growth and stationary phase. The levels of supercoiling determined were ~20% lower than predicted by comparisons with SV40 DNA and reconstituted minichromosomes using histones from higher eukaryotes. In two different plasmids with the ARS1 origin of replication, the level of supercoiling changed substantially as the host cells entered stationary phase. Supercoiling of the endogenous 2-μm plasmid during vegetative growth was lower than in the ARS1 -containing plasmids but did not change significantly upon entry of the cells into stationary phase.Key words: chromatin structure, nucleosome, yeast, DNA supercoiling.
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31

Valenti, Anna, Giuseppe Perugino, Mosè Rossi, and Maria Ciaramella. "Positive supercoiling in thermophiles and mesophiles: of the good and evil." Biochemical Society Transactions 39, no. 1 (2011): 58–63. http://dx.doi.org/10.1042/bst0390058.

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DNA supercoiling plays essential role in maintaining proper chromosome structure, as well as the equilibrium between genome dynamics and stability under specific physicochemical and physiological conditions. In mesophilic organisms, DNA is negatively supercoiled and, until recently, positive supercoiling was considered a peculiar mark of (hyper)thermophilic archaea needed to survive high temperatures. However, several lines of evidence suggest that negative and positive supercoiling might coexist in both (hyper)thermophilic and mesophilic organisms, raising the possibility that positive supercoiling might serve as a regulator of various cellular events, such as chromosome condensation, gene expression, mitosis, sister chromatid cohesion, centromere identity and telomere homoeostasis.
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32

Maxwell, A. "DNA gyrase and the mechanism of DNA supercoiling." Biochemical Society Transactions 27, no. 3 (1999): A87. http://dx.doi.org/10.1042/bst027a087c.

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33

Geng, Yuncong, Christopher Herrick Bohrer, Nicolás Yehya, et al. "A spatially resolved stochastic model reveals the role of supercoiling in transcription regulation." PLOS Computational Biology 18, no. 9 (2022): e1009788. http://dx.doi.org/10.1371/journal.pcbi.1009788.

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In Escherichia coli, translocation of RNA polymerase (RNAP) during transcription introduces supercoiling to DNA, which influences the initiation and elongation behaviors of RNAP. To quantify the role of supercoiling in transcription regulation, we developed a spatially resolved supercoiling model of transcription. The integrated model describes how RNAP activity feeds back with the local DNA supercoiling and how this mechanochemical feedback controls transcription, subject to topoisomerase activities and stochastic topological domain formation. This model establishes that transcription-induced supercoiling mediates the cooperation of co-transcribing RNAP molecules in highly expressed genes, and this cooperation is achieved under moderate supercoiling diffusion and high topoisomerase unbinding rates. It predicts that a topological domain could serve as a transcription regulator, generating substantial transcriptional noise. It also shows the relative orientation of two closely arranged genes plays an important role in regulating their transcription. The model provides a quantitative platform for investigating how genome organization impacts transcription.
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34

Lilley, David M. J., Dongrong Chen, and Richard P. Bowater. "DNA supercoiling and transcription: topological coupling of promoters." Quarterly Reviews of Biophysics 29, no. 3 (1996): 203–25. http://dx.doi.org/10.1017/s0033583500005825.

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DNA supercoiling is a consequence of the double-stranded nature of DNA. When a linear DNA molecule is ligated into a covalently closed circle, the two strands become intertwined like the links of a chain, and will remain so unless one of the strands is broken. The number of times one strand is linked with the other is described by a fundamental property of DNA supercoiling, the linking number (Lk).
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35

Dorman, Charles J. "Dna Supercoiling and Bacterial Gene Expression." Science Progress 89, no. 3-4 (2006): 151–66. http://dx.doi.org/10.3184/003685006783238317.

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36

FRANCO, ROBERT J., and KARL DRLICA. "Gyrase inhibitors and intracellular DNA supercoiling." Biochemical Society Transactions 14, no. 2 (1986): 499–501. http://dx.doi.org/10.1042/bst0140499.

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37

Corless, Samuel, and Nick Gilbert. "Investigating DNA supercoiling in eukaryotic genomes." Briefings in Functional Genomics 16, no. 6 (2017): 379–89. http://dx.doi.org/10.1093/bfgp/elx007.

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38

Brutzer, Hergen, Nicholas Luzzietti, Daniel Klaue, and Ralf Seidel. "Energetics at the DNA Supercoiling Transition." Biophysical Journal 98, no. 7 (2010): 1267–76. http://dx.doi.org/10.1016/j.bpj.2009.12.4292.

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39

Corless, Samuel, Catherine Naughton, and Nick Gilbert. "Profiling DNA supercoiling domains in vivo." Genomics Data 2 (December 2014): 264–67. http://dx.doi.org/10.1016/j.gdata.2014.07.007.

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40

Guitter, E., and S. Leibler. "On Supercoiling Instability in Closed DNA." Europhysics Letters (EPL) 17, no. 7 (1992): 643–48. http://dx.doi.org/10.1209/0295-5075/17/7/012.

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41

Yang, Yang, Irwin Tobias, and Wilma K. Olson. "Finite element analysis of DNA supercoiling." Journal of Chemical Physics 98, no. 2 (1993): 1673–86. http://dx.doi.org/10.1063/1.464283.

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42

Lim, Wilber, Ferdinando Randisi, Jonathan P. K. Doye, and Ard A. Louis. "The interplay of supercoiling and thymine dimers in DNA." Nucleic Acids Research 50, no. 5 (2022): 2480–92. http://dx.doi.org/10.1093/nar/gkac082.

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Abstract Thymine dimers are a major mutagenic photoproduct induced by UV radiation. While they have been the subject of extensive theoretical and experimental investigations, questions of how DNA supercoiling affects local defect properties, or, conversely, how the presence of such defects changes global supercoiled structure, are largely unexplored. Here, we introduce a model of thymine dimers in the oxDNA forcefield, parametrized by comparison to melting experiments and structural measurements of the thymine dimer induced bend angle. We performed extensive molecular dynamics simulations of double-stranded DNA as a function of external twist and force. Compared to undamaged DNA, the presence of a thymine dimer lowers the supercoiling densities at which plectonemes and bubbles occur. For biologically relevant supercoiling densities and forces, thymine dimers can preferentially segregate to the tips of the plectonemes, where they enhance the probability of a localized tip-bubble. This mechanism increases the probability of highly bent and denatured states at the thymine dimer site, which may facilitate repair enzyme binding. Thymine dimer-induced tip-bubbles also pin plectonemes, which may help repair enzymes to locate damage. We hypothesize that the interplay of supercoiling and local defects plays an important role for a wider set of DNA damage repair systems.
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43

Vayssières, Marlène, Nils Marechal, Long Yun, et al. "Structural basis of DNA crossover capture by Escherichia coli DNA gyrase." Science 384, no. 6692 (2024): 227–32. http://dx.doi.org/10.1126/science.adl5899.

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DNA supercoiling must be precisely regulated by topoisomerases to prevent DNA entanglement. The interaction of type IIA DNA topoisomerases with two DNA molecules, enabling the transport of one duplex through the transient double-stranded break of the other, remains elusive owing to structures derived solely from single linear duplex DNAs lacking topological constraints. Using cryo–electron microscopy, we solved the structure of Escherichia coli DNA gyrase bound to a negatively supercoiled minicircle DNA. We show how DNA gyrase captures a DNA crossover, revealing both conserved molecular grooves that accommodate the DNA helices. Together with molecular tweezer experiments, the structure shows that the DNA crossover is of positive chirality, reconciling the binding step of gyrase-mediated DNA relaxation and supercoiling in a single structure.
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44

Desai, Parth Rakesh, Sumitabha Brahmachari, John F. Marko, Siddhartha Das, and Keir C. Neuman. "Coarse-grained modelling of DNA plectoneme pinning in the presence of base-pair mismatches." Nucleic Acids Research 48, no. 19 (2020): 10713–25. http://dx.doi.org/10.1093/nar/gkaa836.

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Abstract Damaged or mismatched DNA bases result in the formation of physical defects in double-stranded DNA. In vivo, defects in DNA must be rapidly and efficiently repaired to maintain cellular function and integrity. Defects can also alter the mechanical response of DNA to bending and twisting constraints, both of which are important in defining the mechanics of DNA supercoiling. Here, we use coarse-grained molecular dynamics (MD) simulation and supporting statistical-mechanical theory to study the effect of mismatched base pairs on DNA supercoiling. Our simulations show that plectoneme pinning at the mismatch site is deterministic under conditions of relatively high force (>2 pN) and high salt concentration (>0.5 M NaCl). Under physiologically relevant conditions of lower force (0.3 pN) and lower salt concentration (0.2 M NaCl), we find that plectoneme pinning becomes probabilistic and the pinning probability increases with the mismatch size. These findings are in line with experimental observations. The simulation framework, validated with experimental results and supported by the theoretical predictions, provides a way to study the effect of defects on DNA supercoiling and the dynamics of supercoiling in molecular detail.
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45

Shapiro, Adam, Haris Jahic, Swati Prasad, et al. "A Homogeneous, High-Throughput Fluorescence Anisotropy-Based DNA Supercoiling Assay." Journal of Biomolecular Screening 15, no. 9 (2010): 1088–98. http://dx.doi.org/10.1177/1087057110378624.

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The degree of supercoiling of DNA is vital for cellular processes, such as replication and transcription. DNA topology is controlled by the action of DNA topoisomerase enzymes. Topoisomerases, because of their importance in cellular replication, are the targets of several anticancer and antibacterial drugs. In the search for new drugs targeting topoisomerases, a biochemical assay compatible with automated high-throughput screening (HTS) would be valuable. Gel electrophoresis is the standard method for measuring changes in the extent of supercoiling of plasmid DNA when acted upon by topoisomerases, but this is a low-throughput and laborious method. A medium-throughput method was described previously that quantitatively distinguishes relaxed and supercoiled plasmids by the difference in their abilities to form triplex structures with an immobilized oligonucleotide. In this article, the authors describe a homogeneous supercoiling assay based on triplex formation in which the oligonucleotide strand is labeled with a fluorescent dye and the readout is fluorescence anisotropy. The new assay requires no immobilization, filtration, or plate washing steps and is therefore well suited to HTS for inhibitors of topoisomerases. The utility of this assay is demonstrated with relaxation of supercoiled plasmid by Escherichia coli topoisomerase I, supercoiling of relaxed plasmid by E. coli DNA gyrase, and inhibition of gyrase by fluoroquinolones and nalidixic acid.
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46

Ahmed, Syed Moiz, and Peter Dröge. "Chromatin Architectural Factors as Safeguards against Excessive Supercoiling during DNA Replication." International Journal of Molecular Sciences 21, no. 12 (2020): 4504. http://dx.doi.org/10.3390/ijms21124504.

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Key DNA transactions, such as genome replication and transcription, rely on the speedy translocation of specialized protein complexes along a double-stranded, right-handed helical template. Physical tethering of these molecular machines during translocation, in conjunction with their internal architectural features, generates DNA topological strain in the form of template supercoiling. It is known that the build-up of transient excessive supercoiling poses severe threats to genome function and stability and that highly specialized enzymes—the topoisomerases (TOP)—have evolved to mitigate these threats. Furthermore, due to their intracellular abundance and fast supercoil relaxation rates, it is generally assumed that these enzymes are sufficient in coping with genome-wide bursts of excessive supercoiling. However, the recent discoveries of chromatin architectural factors that play important accessory functions have cast reasonable doubts on this concept. Here, we reviewed the background of these new findings and described emerging models of how these accessory factors contribute to supercoil homeostasis. We focused on DNA replication and the generation of positive (+) supercoiling in front of replisomes, where two accessory factors—GapR and HMGA2—from pro- and eukaryotic cells, respectively, appear to play important roles as sinks for excessive (+) supercoiling by employing a combination of supercoil constrainment and activation of topoisomerases. Looking forward, we expect that additional factors will be identified in the future as part of an expanding cellular repertoire to cope with bursts of topological strain. Furthermore, identifying antagonists that target these accessory factors and work synergistically with clinically relevant topoisomerase inhibitors could become an interesting novel strategy, leading to improved treatment outcomes.
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47

Maxwell, A., L. Costenaro, S. Mitelheiser, and A. D. Bates. "Coupling ATP hydrolysis to DNA strand passage in type IIA DNA topoisomerases." Biochemical Society Transactions 33, no. 6 (2005): 1460–64. http://dx.doi.org/10.1042/bst0331460.

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Type IIA topos (topoisomerases) catalyse topological conversions of DNA through the passage of one double strand through a transient break in another. In the case of the archetypal enzyme, DNA gyrase, it has always been apparent that the enzyme couples the free energy of ATP hydrolysis to the introduction of negative supercoiling, and the structural details of this process are now becoming clearer. The homologous type IIA enzymes such as topo IV and eukaryotic topo II also require ATP and it has more recently been shown that the energy of hydrolysis is coupled to a reduction of supercoiling or catenation (linking) beyond equilibrium. The mechanism behind this effect is less clear. We review the energy coupling process in both classes of enzyme and describe recent mechanistic and structural work on gyrase that addresses the mechanism of energy coupling.
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48

SEKIGUCHI, JOANN M., and ERIC B. KMIEC. "An Analysis of Transcription Factor TFIIIA-Mediated DNA Supercoiling." DNA and Cell Biology 10, no. 3 (1991): 223–32. http://dx.doi.org/10.1089/dna.1991.10.223.

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49

Regairaz, Marie, Yong-Wei Zhang, Haiqing Fu, et al. "Mus81-mediated DNA cleavage resolves replication forks stalled by topoisomerase I–DNA complexes." Journal of Cell Biology 195, no. 5 (2011): 739–49. http://dx.doi.org/10.1083/jcb.201104003.

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Deoxyribonucleic acid (DNA) topoisomerases are essential for removing the supercoiling that normally builds up ahead of replication forks. The camptothecin (CPT) Top1 (topoisomerase I) inhibitors exert their anticancer activity by reversibly trapping Top1–DNA cleavage complexes (Top1cc’s) and inducing replication-associated DNA double-strand breaks (DSBs). In this paper, we propose a new mechanism by which cells avoid Top1-induced replication-dependent DNA damage. We show that the structure-specific endonuclease Mus81-Eme1 is responsible for generating DSBs in response to Top1 inhibition and for allowing cell survival. We provide evidence that Mus81 cleaves replication forks rather than excises Top1cc’s. DNA combing demonstrated that Mus81 also allows efficient replication fork progression after CPT treatment. We propose that Mus81 cleaves stalled replication forks, which allows dissipation of the excessive supercoiling resulting from Top1 inhibition, spontaneous reversal of Top1cc, and replication fork progression.
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50

Vlijm, Rifka, Jaco v.d. Torre, and Cees Dekker. "Counterintuitive DNA Sequence Dependence in Supercoiling-Induced DNA Melting." PLOS ONE 10, no. 10 (2015): e0141576. http://dx.doi.org/10.1371/journal.pone.0141576.

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