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Relevant bibliographies by topics / Bacteria; DNA replication

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Academic literature on the topic 'Bacteria; DNA replication'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Bacteria; DNA replication"

1

Skarstad, K., and T. Katayama. "Regulating DNA Replication in Bacteria." Cold Spring Harbor Perspectives in Biology 5, no. 4 (2013): a012922. http://dx.doi.org/10.1101/cshperspect.a012922.

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Majerník, A. I., E. R. Jenkinson, and J. P. J. Chong. "DNA replication in thermophiles." Biochemical Society Transactions 32, no. 2 (2004): 236–39. http://dx.doi.org/10.1042/bst0320236.

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DNA replication enzymes in the thermophilic Archaea have previously attracted attention due to their obvious use in methods such as PCR. The proofreading ability of the Pyrococcus furiosus DNA polymerase has resulted in a commercially successful product (Pfu polymerase). One of the many notable features of the Archaea is the fact that their DNA processing enzymes appear on the whole to be more like those found in eukaryotes than bacteria. These proteins also appear to be simpler versions of those found in eukaryotes. For these reasons, archaeal organisms make potentially interesting model systems to explore the molecular mechanisms of processes such as DNA replication, repair and recombination. Why archaeal DNA-manipulation systems were adopted over bacterial systems by eukaryotic cells remains a most interesting question that we suggest may be linked to thermophily.

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Greci, Mark D., and Stephen D. Bell. "Archaeal DNA Replication." Annual Review of Microbiology 74, no. 1 (2020): 65–80. http://dx.doi.org/10.1146/annurev-micro-020518-115443.

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It is now well recognized that the information processing machineries of archaea are far more closely related to those of eukaryotes than to those of their prokaryotic cousins, the bacteria. Extensive studies have been performed on the structure and function of the archaeal DNA replication origins, the proteins that define them, and the macromolecular assemblies that drive DNA unwinding and nascent strand synthesis. The results from various archaeal organisms across the archaeal domain of life show surprising levels of diversity at many levels—ranging from cell cycle organization to chromosome ploidy to replication mode and nature of the replicative polymerases. In the following, we describe recent advances in the field, highlighting conserved features and lineage-specific innovations.

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Marsin, Stéphanie, Yazid Adam, Claire Cargemel, et al. "Study of the DnaB:DciA interplay reveals insights into the primary mode of loading of the bacterial replicative helicase." Nucleic Acids Research 49, no. 11 (2021): 6569–86. http://dx.doi.org/10.1093/nar/gkab463.

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Abstract Replicative helicases are essential proteins that unwind DNA in front of replication forks. Their loading depends on accessory proteins and in bacteria, DnaC and DnaI are well characterized loaders. However, most bacteria do not express either of these two proteins. Instead, they are proposed to rely on DciA, an ancestral protein unrelated to DnaC/I. While the DciA structure from Vibrio cholerae shares no homology with DnaC, it reveals similarities with DnaA and DnaX, two proteins involved during replication initiation. As other bacterial replicative helicases, VcDnaB adopts a toroid-shaped homo-hexameric structure, but with a slightly open dynamic conformation in the free state. We show that VcDnaB can load itself on DNA in vitro and that VcDciA stimulates this function, resulting in an increased DNA unwinding. VcDciA interacts with VcDnaB with a 3/6 stoichiometry and we show that a determinant residue, which discriminates DciA- and DnaC/I-helicases, is critical in vivo. Our work is the first step toward the understanding of the ancestral mode of loading of bacterial replicative helicases on DNA. It sheds light on the strategy employed by phage helicase loaders to hijack bacterial replicative helicases and may explain the recurrent domestication of dnaC/I through evolution in bacteria.

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Bazin, Alexandre, Mickaël Cherrier, and Laurent Terradot. "Structural insights into DNA replication initiation in Helicobacter pylori." Acta Crystallographica Section A Foundations and Advances 70, a1 (2014): C1632. http://dx.doi.org/10.1107/s2053273314083673.

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In Gram-negative bacteria, opening of DNA double strand during replication is performed by the replicative helicase DnaB. This protein allows for replication fork elongation by unwinding DNA and interacting with DnaG primase. DnaB is composed of two domains: an N-terminal domain (NTD) and a C-terminal domain (CTD) connected by a flexible linker. The protein forms two-tiered hexamers composed of a NTD-ring and a CTD-ring. In Escherichia coli, the initiator protein DnaA binds to the origin of replication oriC and induces the opening of a AT-rich region. The replicative helicase DnaB is then loaded onto single stranded DNA by interacting with DnaA and with the AAA+ helicase loader DnaC. However, AAA+ loaders are absent in 80% of the bacterial genome, raising the question of how helicases are loaded in these bacteria [1]. In the genome of human pathogen Helicobacter pylori, no AAA+ loader has been identified. Moreover H. pylori DnaB (HpDnaB) has the ability to support replication of an otherwise unviable E. coli strain that bears a defective copy of DnaC by complementation [2]. In order to better understand the properties of HpDnaB we have first shown that HpDnaB forms double hexamers by negative stain electron microscopy [3]. Then, we have then solved the crystal structure of HpDnaB at a resolution of 6.7Å by X-ray crystallography with Rfree/Rfactor of 0.29/0.25. The structure reveals that the protein adopts a new dodecameric arrangement generated by crystallographic three fold symmetry. When compared to hexameric DnaBs, the hexamer of HpDnaB displays an original combination of NTD-ring and CTD-ring symmetries, intermediate between apo and ADP-bound structure. Biochemistry studies of HpDnaB interaction with HpDnaG-CTD and ssDNA provides mechanistic insights into the initial steps of DNA replication in H. pylori. Our results offer an alternative solution of helicase loading and DNA replication initiation in H. pylori and possibly other bacteria that do not employ helicase loaders.

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Sinha, Anurag Kumar, Christophe Possoz, and David R. F. Leach. "The Roles of Bacterial DNA Double-Strand Break Repair Proteins in Chromosomal DNA Replication." FEMS Microbiology Reviews 44, no. 3 (2020): 351–68. http://dx.doi.org/10.1093/femsre/fuaa009.

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ABSTRACT It is well established that DNA double-strand break (DSB) repair is required to underpin chromosomal DNA replication. Because DNA replication forks are prone to breakage, faithful DSB repair and correct replication fork restart are critically important. Cells, where the proteins required for DSB repair are absent or altered, display characteristic disturbances to genome replication. In this review, we analyze how bacterial DNA replication is perturbed in DSB repair mutant strains and explore the consequences of these perturbations for bacterial chromosome segregation and cell viability. Importantly, we look at how DNA replication and DSB repair processes are implicated in the striking recent observations of DNA amplification and DNA loss in the chromosome terminus of various mutant Escherichia coli strains. We also address the mutant conditions required for the remarkable ability to copy the entire E. coli genome, and to maintain cell viability, even in the absence of replication initiation from oriC, the unique origin of DNA replication in wild type cells. Furthermore, we discuss the models that have been proposed to explain these phenomena and assess how these models fit with the observed data, provide new insights and enhance our understanding of chromosomal replication and termination in bacteria.

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Cheung, Andrew K. "Rolling-Circle Replication of an Animal Circovirus Genome in a Theta-Replicating Bacterial Plasmid in Escherichia coli." Journal of Virology 80, no. 17 (2006): 8686–94. http://dx.doi.org/10.1128/jvi.00655-06.

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ABSTRACT A bacterial plasmid containing 1.75 copies of double-stranded porcine circovirus (PCV) DNA in tandem (0.8 copy of PCV type 1 [PCV1], 0.95 copy of PCV2) with two origins of DNA replication (Ori) yielded three different DNA species when transformed into Escherichia coli: the input construct, a unit-length chimeric PCV1Rep/PCV2Cap genome with a composite Ori but lacking the plasmid vector, and a molecule consisting of the remaining 0.75 copy PCV1Cap/PCV2Rep genome with a different composite Ori together with the bacterial plasmid. Replication of the input construct was presumably via the theta replication mechanism utilizing the ColE1 Ori, while characteristics of the other two DNA species, including a requirement of two PCV Oris and the virus-encoded replication initiator Rep protein, suggest they were generated via the rolling-circle copy-release mechanism. Interestingly, the PCV-encoded Rep′ protein essential for PCV DNA replication in mammalian cells was not required in bacteria. The fact that the Rep′ protein function(s) can be compensated by the bacterial replication machinery to support the PCV DNA replication process echoes previous suggestions that circular single-stranded DNA animal circoviruses, plant geminiviruses, and nanoviruses may have evolved from prokaryotic episomal replicons.

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Pelliciari, Simone, Mei-Jing Dong, Feng Gao, and Heath Murray. "Evidence for a chromosome origin unwinding system broadly conserved in bacteria." Nucleic Acids Research 49, no. 13 (2021): 7525–36. http://dx.doi.org/10.1093/nar/gkab560.

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Abstract Genome replication is a fundamental requirement for the proliferation of all cells. Throughout the domains of life, conserved DNA replication initiation proteins assemble at specific chromosomal loci termed replication origins and direct loading of replicative helicases (1). Despite decades of study on bacterial replication, the diversity of bacterial chromosome origin architecture has confounded the search for molecular mechanisms directing the initiation process. Recently a basal system for opening a bacterial chromosome origin (oriC) was proposed (2). In the model organism Bacillus subtilis, a pair of double-stranded DNA (dsDNA) binding sites (DnaA-boxes) guide the replication initiator DnaA onto adjacent single-stranded DNA (ssDNA) binding motifs (DnaA-trios) where the protein assembles into an oligomer that stretches DNA to promote origin unwinding. We report here that these core elements are predicted to be present in the majority of bacterial chromosome origins. Moreover, we find that the principle activities of the origin unwinding system are conserved in vitro and in vivo. The results suggest that this basal mechanism for oriC unwinding is broadly functionally conserved and therefore may represent an ancestral system to open bacterial chromosome origins.

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Mott, Melissa L., and James M. Berger. "DNA replication initiation: mechanisms and regulation in bacteria." Nature Reviews Microbiology 5, no. 5 (2007): 343–54. http://dx.doi.org/10.1038/nrmicro1640.

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Bartosik, Aneta A., and Grazyna Jagura-Burdzy. "Bacterial chromosome segregation." Acta Biochimica Polonica 52, no. 1 (2005): 1–34. http://dx.doi.org/10.18388/abp.2005_3481.

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In most bacteria two vital processes of the cell cycle: DNA replication and chromosome segregation overlap temporally. The action of replication machinery in a fixed location in the cell leads to the duplication of oriC regions, their rapid separation to the opposite halves of the cell and the duplicated chromosomes gradually moving to the same locations prior to cell division. Numerous proteins are implicated in co-replicational DNA segregation and they will be characterized in this review. The proteins SeqA, SMC/MukB, MinCDE, MreB/Mbl, RacA, FtsK/SpoIIIE playing different roles in bacterial cells are also involved in chromosome segregation. The chromosomally encoded ParAB homologs of active partitioning proteins of low-copy number plasmids are also players, not always indispensable, in the segregation of bacterial chromosomes.

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Dissertations / Theses on the topic "Bacteria; DNA replication"

1

Gibson, Roderick J. "Studies on DNA mismatch repair in Pseudomonas aeruginosa." Thesis, University of Kent, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262375.

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Marriott, Hannah. "Genome architecture and DNA replication in Haloferax volcanii." Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/50190/.

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The archaeon Haloferax volcanii is used to study DNA replication and repair, and it is unique amongst cellular organisms as it is able to grow in the absence of DNA replication origins. There are four DNA replication origins on the main circular chromosome (including the integrated mega-plasmid pHV4) and one on each of the other mega-plasmids pHV1 and pHV3. Replication origins are normally required for the initiation of DNA replication, however H. volcanii is able to grow faster when all chromosomal origins have been deleted. Therefore, H. volcanii must utilise other methods of DNA replication such as recombination-dependent replication. The origin found on pHV3 cannot be deleted from the episomal mega-plasmid, whereas the origin can be deleted from episomal pHV4. The pHV3 mega- plasmid can be integrated onto the main chromosome, which allows the pHV3 origin to be deleted from the chromosome. The pHV1 mega-plasmid origin can be deleted from the episomal mega-plasmid, and the entire mega-plasmid can be lost from the H. volcanii cell. This generates a viable, healthy strain, which shows that the pHV1 mega-plasmid is non- essential. It was also found that the pHV1 mega-plasmid exists in H. volcanii as a 6x concatemer which is ~510 kb in size, which may explain the reason for being able to delete the origin. To further investigate the mechanisms that recombination-dependent replication may use, replication machinery (MCM and GINS) were tagged and expressed. Due to time constraints, interactions were not seen. The mcm gene was put under the control of a tryptophan inducible promoter. A strain lacking chromosomal origins and therefore primarily using recombination-dependent replication was shown to require more MCM than a wild-type strain.

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Jenkins, Andrew John. "Aspects of the initiation of DNA replication in gram-negative bacteria." Thesis, University of Edinburgh, 1985. http://hdl.handle.net/1842/12288.

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Mirhabibollahi, B. "Influence of mode of DNA replication on the response of Salmonella typhimurium to physical stress." Thesis, University of Reading, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383460.

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Verma, Meera Mary. "On the effect of UV-irradiation on DNA replication in Escherichia coli." Title page, contents and summary only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phv522.pdf.

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Liébart, Jean-Claude. "Mecanisme d'integration de l'adn du bacteriophage mu dans le chromosome d'escherichia coli k12." Paris 6, 1987. http://www.theses.fr/1987PA066184.

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BEJAR, SAMIR. "Etudes de la region du terminus du chromosome d'escherichia coli k12 : replication et controle de la division cellulaire." Toulouse 3, 1986. http://www.theses.fr/1986TOU30190.

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Zhao, Gengjing. "Single-molecule studies of bacterial DNA replication and translesion synthesis." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/276234.

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Faithful replication of genomic DNA is crucial for the survival of a cell. In order to achieve high-level accuracy in copying its genome, all cells employ replicative DNA polymerases that have intrinsic high fidelity. When an error occurs on the template DNA strand, in the form of lesions caused by diverse chemicals, reactive oxygen species, or UV light, the high-fidelity replicative DNA polymerases are stalled. To bypass these replication blocks, cells harbor multiple specialized translesion DNA polymerases that are error-prone and therefore able to accommodate the lesions and continue DNA synthesis. As a result of their low fidelity, the translesion polymerases are associated with increased mutagenesis, drug resistance, and cancer. Therefore, the access of the translesion polymerases to DNA needs to be tightly controlled, but how this is achieved has been the subject of debate. This Thesis presents the development of a co-localization single-molecule spectroscopy (CoSMoS) method to directly visualize the loading of the Escherichia coli replicative polymerase on DNA, as well as the exchange between the replicative polymerase and the translesion polymerases Pol II and Pol IV. In contrast to the toolbelt model for the exchange between the polymerases, this work shows that the translesion polymerases Pol II and Pol IV do not form a stable complex with the replicative polymerase Pol IIIα on the β-clamp. Furthermore, we find that the sequential activities of the replication proteins: clamp loader, clamp, and Pol IIIα, are highly organized while the exchange with the translesion polymerases is disordered. This exchange is not determined by lesion-recognition but instead a concentration-dependent competition between the replicative and translesion polymerases for the hydrophobic groove on the surface of the β-clamp. Hence, our results provide a unique insight into the temporal organization of events in DNA replication and translesion synthesis.

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HODGES-GARCIA, YVONNE KATHLEEN. "PURIFICATION AND CHARACTERIZATION OF BACTERIAL PHAGE PHI29 GENE 6 PROTEIN." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183864.

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A DNA fragment containing the coding region for gene 6 of Bacterial phage ϕ29 was placed into an expression vector. The ϕ29 gene 6 protein was isolated in large amounts by chromatography on double-stranded DNA cellulose and DE52 cellulose. The ϕ29 gene 6 protein was determined to be greater 95% pure and has a molecular weight of approximately 16,000. The ϕ29 gene 6 protein is thought to be a dimer in its native form. The partial N-terminal amino acid sequence of the purified protein is identically to the inferred amino acid sequence from the nucleotide sequence of ϕ29 gene 6. Gene 6 protein of ϕ29 aggregates in a more purified state which suggest protein to protein interactions. Purified gene 6 protein did not stimulate the ϕ29 in vitro DNA replication system and may require binding with other replication proteins to enable it to function. Gene 6 protein binds weakly to double-stranded and single-strand DNA cellulose. There is segmental amino acid sequence and secondary structure homology with adenovirus DNA binding protein Antibody to gene 6 protein inhibits it from binding to ϕ29 DNA. The results presented in this dissertation suggest that ϕ29 gene 6 protein is a weak DNA bind protein and may not be required for the in vitro ϕ29 DNA replication system.

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Goranov, Alexi I. "Regulation of DNA replication and cellular responses to perturbations in replication in the bacterium Bacillus subtilis." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/37261.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2006.<br>"September 2006."<br>Includes bibliographical references.<br>When a cell grows and divides to give rise to genetically identical cells, the genome of the cell is duplicated prior to cell-division. The process of genomic duplication is called DNA replication, and is closely coordinated with other processes in the cell, such as growth rate, and cell division. The mechanisms that regulate when DNA replication initiates and how cells respond to perturbations in replication are not well understood. I used the gram-positive bacterium Bacillus subtilis to address these questions. My research showed that a conserved component of the DNA replication machinery, processivity u-clamp, regulates the initiation of replication. This regulation appears to affect the loading of helicase, a replication component that generates the single-strand DNA template for replication. My results indicate that the replication initiation protein DnaA is the likely target of P-clamp regulation. I also observed that in vivo, in B. subtilis, most of the DNA replication machinery, including P-clamp, can associate with the origin of replication before helicase. This is in stark contrast to in vitro studies in other bacteria. I also addressed the question of how B. subtilis responds to perturbations in DNA replication and DNA damage.<br>(cont.) My results demonstrate that the conserved recombination protein, RecA, mediates most of the transcriptional response under the tested conditions. More than 75% of the RecA-mediated transcriptional response is due to the expression of phage and mobile element genes and their indirect effects. Under conditions of replication elongation arrest, there is still a significant recA-independent response, at least part of which is mediated by the replication protein DnaA. The DnaA-mediated response appears to be conserved in other bacteria, as homologues if the affected genes also have DnaA binding sites in their promoter regions. Previously, one of the DnaA regulated genes, sda, has been shown to affect cell viability after perturbations in replication. Here I showed that another DnaA-regulated gene,ftsL, also affects cell survival after replication arrest by coordinating replication and cell-division. I believe that my results have furthered our understanding of how replication is coordinated with other cell-cycle processes, and have raised interesting questions for future investigation.<br>by Alexi I. Goranov.<br>Ph.D.

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Books on the topic "Bacteria; DNA replication"

1

Campisi, Judith. Perspectives in Cellular Regulation: Bacteria to Cancer. Wiley-Liss, 1991.

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1921-, Pardee Arthur B., and Campisi Judith, eds. Perspectives on cellular regulation: From bacteria to cancer : essays in honor of Arthur B. Pardee. Wiley-Liss, 1991.

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Money, Nicholas P. 4. Viruses. Oxford University Press, 2014. http://dx.doi.org/10.1093/actrade/9780199681686.003.0004.

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‘Viruses’ explains that millions of people die from interacting with viruses every year, but beyond the effects of viruses on human health, the lives of all organisms and the cycling of nutrients through the biosphere depend upon the activities of viruses. Viruses control populations of bacteria, archaea, and eukaryotes and this destructive power liberates massive quantities of nutrients in aquatic and terrestrial ecosystems. Viruses are organized into seven groups based upon the type of genome and its mechanism of replication. Viral genomes are encoded in single-stranded and double-stranded DNA and RNA molecules. The expression of viral genes occurs within infected cells utilizing the molecular machinery of the host.

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Role Of Bacterial Membrane In Chromosome Replication And Partition. Chapman & Hall, 1996.

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Book chapters on the topic "Bacteria; DNA replication"

1

Tsurimoto, Toshiki, Haruhiko Kouhara, and Kenichi Matsubara. "Origin and Initiation Sites of λdv DNA Replication In Vitro." In Plasmids in Bacteria. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2447-8_15.

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Bastia, D., C. Vocke, J. Germino, and J. Gray. "DNA-Protein Interaction at the Replication Origins of Plasmid Chromosomes." In Plasmids in Bacteria. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2447-8_29.

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Salas, Margarita, and Fernando Rojo. "Replication and Transcription of Bacteriophage ϕ29 DNA." In Bacillus subtilis and Other Gram-Positive Bacteria. ASM Press, 2014. http://dx.doi.org/10.1128/9781555818388.ch58.

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Wilkins, Brian, and Erich Lanka. "DNA Processing and Replication during Plasmid Transfer between Gram-Negative Bacteria." In Bacterial Conjugation. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9357-4_5.

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Kreuzer, Kenneth N., and Bénédicte Michel. "Reinitiation of DNA Replication." In The Bacterial Chromosome. ASM Press, 2014. http://dx.doi.org/10.1128/9781555817640.ch12.

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Birge, Edward A. "Replication and Analysis of DNA." In Bacterial and Bacteriophage Genetics. Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4757-2328-1_2.

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Birge, Edward A. "Replication and Analysis of DNA." In Bacterial and Bacteriophage Genetics. Springer New York, 2000. http://dx.doi.org/10.1007/978-1-4757-3258-0_2.

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Konieczny, Igor, and Maciej Zylicz. "Role of Bacterial Chaperones in DNA Replication." In Genetic Engineering. Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4707-5_6.

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Bodholdt, Brian, Bjarke B. Christensen, Jacob Engelbrecht, Erik Mosekilde, and Jeppe Sturis. "Modeling Control of DNA-Replication in Bacterial Cells." In Computer-Based Management of Complex Systems. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74946-9_25.

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Radman, M., I. Matic, J. A. Halliday, and F. Taddei. "Editing DNA replication and recombination by mismatch repair: from bacterial genetics to mechanisms of predisposition to cancer in humans." In DNA Repair and Recombination. Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0537-8_14.

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Conference papers on the topic "Bacteria; DNA replication"

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Bauer, Michael, Zuzana Nascakova, Anca Mihai, and Anne Müller. "Abstract B34: The ALPK1/TIFA/NF-kB axis links a bacterial carcinogen to replication stress and DNA damage." In Abstracts: AACR Special Conference on the Microbiome, Viruses, and Cancer; February 21-24, 2020; Orlando, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.mvc2020-b34.

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