Relevant bibliographies by topics / Plasmid replication control

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  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Plasmid replication control'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Plasmid replication control"

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del Solar, Gloria, Rafael Giraldo, María Jesús Ruiz-Echevarría, Manuel Espinosa, and Ramón Díaz-Orejas. "Replication and Control of Circular Bacterial Plasmids." Microbiology and Molecular Biology Reviews 62, no. 2 (June 1, 1998): 434–64. http://dx.doi.org/10.1128/mmbr.62.2.434-464.1998.

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SUMMARY An essential feature of bacterial plasmids is their ability to replicate as autonomous genetic elements in a controlled way within the host. Therefore, they can be used to explore the mechanisms involved in DNA replication and to analyze the different strategies that couple DNA replication to other critical events in the cell cycle. In this review, we focus on replication and its control in circular plasmids. Plasmid replication can be conveniently divided into three stages: initiation, elongation, and termination. The inability of DNA polymerases to initiate de novo replication makes necessary the independent generation of a primer. This is solved, in circular plasmids, by two main strategies: (i) opening of the strands followed by RNA priming (theta and strand displacement replication) or (ii) cleavage of one of the DNA strands to generate a 3′-OH end (rolling-circle replication). Initiation is catalyzed most frequently by one or a few plasmid-encoded initiation proteins that recognize plasmid-specific DNA sequences and determine the point from which replication starts (the origin of replication). In some cases, these proteins also participate directly in the generation of the primer. These initiators can also play the role of pilot proteins that guide the assembly of the host replisome at the plasmid origin. Elongation of plasmid replication is carried out basically by DNA polymerase III holoenzyme (and, in some cases, by DNA polymerase I at an early stage), with the participation of other host proteins that form the replisome. Termination of replication has specific requirements and implications for reinitiation, studies of which have started. The initiation stage plays an additional role: it is the stage at which mechanisms controlling replication operate. The objective of this control is to maintain a fixed concentration of plasmid molecules in a growing bacterial population (duplication of the plasmid pool paced with duplication of the bacterial population). The molecules involved directly in this control can be (i) RNA (antisense RNA), (ii) DNA sequences (iterons), or (iii) antisense RNA and proteins acting in concert. The control elements maintain an average frequency of one plasmid replication per plasmid copy per cell cycle and can “sense” and correct deviations from this average. Most of the current knowledge on plasmid replication and its control is based on the results of analyses performed with pure cultures under steady-state growth conditions. This knowledge sets important parameters needed to understand the maintenance of these genetic elements in mixed populations and under environmental conditions.
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Rakowski, Sheryl A., and Marcin Filutowicz. "Plasmid R6K replication control." Plasmid 69, no. 3 (May 2013): 231–42. http://dx.doi.org/10.1016/j.plasmid.2013.02.003.

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TERAWAKI, YOSHIRO. "Control of plasmid replication." Nippon Saikingaku Zasshi 41, no. 2 (1986): 513–25. http://dx.doi.org/10.3412/jsb.41.513.

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Paulsson, Johan. "Multileveled Selection on Plasmid Replication." Genetics 161, no. 4 (August 1, 2002): 1373–84. http://dx.doi.org/10.1093/genetics/161.4.1373.

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Abstract The replication control genes of bacterial plasmids face selection at two conflicting levels. Plasmid copies that systematically overreplicate relative to their cell mates have a higher chance of fixing in descendant cells, but these cells typically have a lower chance of fixing in the population. Apart from identifying the conflict, this mathematical discussion characterizes the efficiency of the selection levels and suggests how they drive the evolution of kinetic mechanisms. In particular it is hypothesized that: (1) tighter replication control is more vulnerable to selfishness; (2) cis-acting replication activators are relics of a conflict where a plasmid outreplicated its intracellular competitors by monopolizing activators; (3) high-copy plasmids with sloppy replication control arise because intracellular selection favors overreplication, thereby relieving intercellular selection for lower loss rates; (4) the excessive synthesis of cis-acting replication activators and trans-acting inhibitors is the result of an arms race between cis selfishness and trans retaliations; (5) site-specific recombination of plasmid dimers is equivalent to self-policing; and (6) plasmids modify their horizontal transfer to spread without promoting selfishness. It is also discussed how replication control may be subject to a third level of selection acting on the entire population of plasmid-containing cells.
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Abeles, A. L., and S. J. Austin. "Antiparallel plasmid-plasmid pairing may control P1 plasmid replication." Proceedings of the National Academy of Sciences 88, no. 20 (October 15, 1991): 9011–15. http://dx.doi.org/10.1073/pnas.88.20.9011.

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Tomizawa, Jun-ichi. "Control of ColE1 Plasmid replication." Journal of Molecular Biology 212, no. 4 (April 1990): 695–708. http://dx.doi.org/10.1016/0022-2836(90)90231-a.

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Tomizawa, Jun-ichi. "Control of colE1 plasmid replication." Journal of Molecular Biology 212, no. 4 (April 1990): 683–94. http://dx.doi.org/10.1016/0022-2836(90)90230-j.

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Thomas, C. M. "Transcription regulatory circuits in bacterial plasmids." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1072–74. http://dx.doi.org/10.1042/bst0341072.

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Gene regulation circuits control all aspects of the life of plasmids. This review gives an overview of the current orchestration of the circuits that control plasmid replication, plasmid transfer, plasmid segregation and plasmid maintenance.
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Verma, Subhash C., Tathagata Choudhuri, and Erle S. Robertson. "The Minimal Replicator Element of the Kaposi's Sarcoma-Associated Herpesvirus Terminal Repeat Supports Replication in a Semiconservative and Cell-Cycle-Dependent Manner." Journal of Virology 81, no. 7 (December 6, 2006): 3402–13. http://dx.doi.org/10.1128/jvi.01607-06.

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ABSTRACT Kaposi's sarcoma-associated herpesvirus (KSHV) persists as episomes in infected cells by circularizing at the terminal repeats (TRs). The KSHV episome carries multiple reiterated copies of the terminal repeat, and each copy is capable of supporting replication. Expression of the latency-associated nuclear antigen (LANA) is critical for the replication of TR-containing plasmids. A 32-bp sequence upstream of LANA binding site 1 (LBS1), referred to as RE (replication element), along with LANA binding sites 1 and 2 (RE-LBS1/2), is sufficient to support replication (J. Hu and R. Renne, J. Virol. 79:2637-2642, 2005). In this report we demonstrate that the minimal replicator element (RE-LBS1/2) replicates in synchrony with the host cellular DNA, and only once, in a cell-cycle-dependent manner. Overexpression of the mammalian replication inhibitor geminin blocked replication of the plasmid containing the minimal replicator element, confirming the involvement of the host cellular replication control mechanism, and prevented rereplication of the plasmid in the same cell cycle. Overexpression of Cdt1 also rescued the replicative ability of the RE-LBS1/2-containing plasmids. A chromatin immunoprecipitation assay performed using anti-origin recognition complex 2 (α-ORC2) and α-LANA antibodies from cells transfected with RE-LBS1/2, RE-LBS1, LBS1, or RE showed the association of ORC2 with the RE region. Expression of LANA increased the number of copies of chromatin-bound DNA of replication elements, suggesting that LANA is important for the recruitment of ORCs and may contribute to the stabilization of the replication protein complexes at the RE site.
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Nordström, Kurt. "Plasmid R1—Replication and its control." Plasmid 55, no. 1 (January 2006): 1–26. http://dx.doi.org/10.1016/j.plasmid.2005.07.002.

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Dissertations / Theses on the topic "Plasmid replication control"

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Hamoudi, Haider Ibraheem. "Incompatibility and multimerization of plasmid NTP16." Thesis, University of London, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333554.

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Olsson, Jan. "Control of Chromosome and Plasmid Replication in Escherichia coli." Doctoral thesis, Uppsala universitet, Institutionen för cell- och molekylärbiologi, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3471.

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Life is cellular. Cells grow and divide to give two new cells; this process is called the cell cycle. The chromosome in a bacterium is replicated into two identical copies before the cell divides. DNA replication is a fundamental process common to all forms of life. In my thesis, I have studied control of chromosome and plasmid replication in Escherichia coli, a rod-shaped bacterium. Plasmids are extrachromosomal autonomously replicating DNA molecules. I have combined the classical Meselson-Stahl density-shift and DNA hybridisation with theoretical analysis of DNA replication. The minimal time between two successive replications of the same molecule, the eclipse, was determined for both plasmid and chromosome. The aim was to investigate the processes ensuring the precise timing of chromosome replication in the cell cycle. In wild-type strains, the chromosomal eclipse was long. Mutations affecting the so-called sequestration process, the superhelicity of the DNA, and the initiation protein, DnaA, reduced the eclipse. Fast-growing E. coli has overlapping replicative phases with synchronous initiation from multiple initiation sites, oriC. I have investigated the complex interplay between different control processes by measuring the length of the eclipse and the degree of asynchronous initiation in various mutants. I have measured the eclipse period of plasmid R1 during up- and down-shifts in plasmid copy number. The length of the eclipse was found to be determined by structural events as well as by the properties of the copy-number-control system. During downshift from very high copy numbers, the rate of plasmid replication started very slowly and gradually increased until the normal copy number was achieved, in accordance with the +n model. The CopB system of plasmid R1 was shown to be a rescue system preventing cells with few plasmid copies from losing the plasmid in some of the daughter cells.
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Perry, Clarice Lorraine. "Specialized Replication Operons Control Rhizobial Plasmid Copy Number in Developing Symbiotic Cells." BYU ScholarsArchive, 2015. https://scholarsarchive.byu.edu/etd/6167.

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The rhizobium – legume symbiosis is a complex process that involves genetic cooperation from both bacteria and plants. Previously, our lab described naturally occurring accessory plasmids in rhizobia that inhibit this cooperation. A transposon mutagenesis was performed on the plasmids to detect the genetic factor that blocked nitrogen fixation. Several of the plasmids were found to possess a replication operon that when disrupted by transposon insertion, restored symbiotic function. This study describes an in-depth investigation into one of those plasmids, pHRC377, and into its replication operon. The operon, which we have called repA2C2, comes from the repABC family of replication and partitioning systems commonly found in alphaproteobacteria. In this study we show that this operon is not necessary for pHRC377 replication in LB culture or free living cells, but is necessary for plasmid amplification in the plant, specifically during rhizobial differentiation into nitrogen fixing bacteroids. We also show how the other repABC type operons on pHRC377 function in relation to plasmid maintenance and copy number during endoreduplication and how they do not have the same phenotypic effect as repA2C2.
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Utter, Bryan David. "PHEROMONE-INTERACTING REPLICATION PROTEIN CONTROLS ENTEROCOCCAL CONJUGATIVE PLASMID HOST RANGE AND STABILITY THROUGH DISULFIDE BONDS." Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/211277.

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Microbiology and Immunology
Ph.D.
Enterococci are found in soil, sewage, food, water, and are commensal to the gastrointestinal tracts of mammals, insects, and birds. Enterococci often become nosocomial pathogens that cause a wide variety of diseases including urinary tract infections, endocarditis, and septicemia. These infections are often difficult to treat with antibiotics because most of the nosocomial strains are multi-drug resistant. Enterococcal plasmids function as reservoirs for resistance genes because they are extremely stable, allow for specific and efficient transfer, and can acquire resistance determinants from the chromosome and other plasmids. Additionally, enterococcal plasmids transfer across species boundaries transferring resistance genes like vancomycin to species like Staphylococcus aureus. There are two types of enterococcal plasmids, pheromone-responsive and broad host range. Pheromone-responsive plasmids are extremely stable, have a limited host range, and are primarily found in Enterococcus faecalis. Broad host range plasmids of E. faecalis and Enterococcus faecium are less stable than pheromone-responsive plasmids, but have an expanded host range into other Gram-positive species. E. faecalis has at least 25 known pheromone-responsive conjugative plasmids. One of the most extensively studied pheromone-responsive conjugative plasmids, pCF10. Conjugation of pCF10 from donor to recipient cell is induced by pheromone cCF10. cCF10 is contained within n the lipoprotein signal sequence encoded by the E. faecalis chromosomal gene ccfA. The lipoprotein signal sequence is processed by a series of proteolytic cleavage events to produce mature cCF10. Maturation of pheromone cCF10 produces three peptides: pre-cCF10 (CcfA1-22), cCF10 (CcfA13-19), and CcfA1-12. Cells containing pCF10 continue to produce cell membrane associated precursor pheromone of cCF10 (pre-cCF10), as well as, secreted and cell wall-associated cCF10. The presence of cCF10 does not self-induce conjugation by the donor cell because of two inhibitory molecules, PrgY and iCF10. Transmembrane protein PrgY is encoded by pCF10 and reduces cell wall associated cCF10, iCF10 is a pCF10 encoded inhibitory peptide (AITLIFI) that binds to PrgX, preventing cCF10 binding. While cCF10 controls pCF10 conjugation, pre-cCF10 controls host range of pCF10 by interacting with pCF10 replication initiation protein PrgW. cCF10 can initiate conjugation and mobilize the transfer of plasmids into other species, including Lactococcus lactis, but pCF10 cannot be maintained within the cell. However, if L. lactis is engineered to produce pre-cCF10, pCF10 can be maintained. The pre-cCF10 involvement in the establishment of pCF10 into other species might be related to the observation that it binds to the pCF10 replication initiation protein PrgW. By in vitro affinity chromatography experiments, interaction of cCF10 and pre-cCF10 with PrgW induced changes in PrgW mobility in gel electrophoresis that caused by formation of doublets and formation of aggregates which were thought to be mediated by disulfide bonds. Initial evidence of regulation of PrgW conformation by disulfide bonds was seen in Western blots of E. faecalis whole cell lysates where PrgW migration is sensitive to reduction. Sequence alignment comparisons between PrgW and a group of 54 of 59 known RepA_N superfamily proteins in E. faecalis revealed three highly conserved cysteines; these RepA_N proteins had a limited host range to E. faecalis. To study the importance of theses cysteines in pCF10 maintenance and host range limitation, prgW single, double, and triple cysteine to alanine (C to A) substitutions were generated. The cysteine mutant prgW was cloned into a plasmid functioning as either a contained the prgW alone (pORI10), or containing prgW with genes necessary for efficient pCF10 maintenance (pMSP6050). While all cysteine mutant plasmids of pORI10 and pMSP6050 were still capable of replicating in E. faecalis, the plasmid stability and copy number decreased, providing evidence that the cysteines were important to PrgW function. Additionally, Western blot analysis revealed PrgW C to A substitutions decreased PrgW aggregation. Mutations of PrgW cysteines reduced pMSP6050 stability and aggregation, but increased host range to L. lactis. Both L. lactis engineered to produce pre-cCF10 and the mutation of the conserved cysteines of PrgW extended host range of pMSP6050 into L. lactis. These data taken together with the observations that pre-cCF10 induced PrgW aggregation suggested that pre-cCF10 regulated the activity of the PrgW replication initiation protein through disulfide bonds. While the conserved cysteines of RepA_N proteins are found only in E. faecalis, phylogenetic analysis revealed that RepA_N homologs lacking the three cysteines are also found in E. faecium or S. aureus, suggesting that the host range of multiple plasmids might be affected by cysteine bond formation. Phylogenetic analysis also showed that the RepA_N proteins of enterococci and staphylococci appear to have evolved to determine host range based on the presence of two of the three conserved cysteines. Modular evolution of E. faecalis plasmids, like pCF10, that contained RepA_N proteins with three conserved cysteines, might have determined the fate of the plasmid as a limited host range, stable reservoir for antibiotic resistance.
Temple University--Theses
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LE, CHATELIER EMMANUELLE. "Initiation et controle de la replication du plasmide pam-beta-1 chez bacillus subtilis." Paris 11, 1994. http://www.theses.fr/1994PA112141.

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Pam-beta-1 est un grand plasmide isole d'enterococcus faecalis qui se replique par un mecanisme theta dans un grand nombre de bacteries a gram positif incluant bacillus subtilis. Deux aspects de sa replication ont ete abordes dans ce travail. Le premier concerne le mecanisme d'initiation. Les observations suivantes ont conduit a la proposition que pam-beta-1 se replique par un mecanisme original: (i) sa replication depend de l'adn polymerase i de l'hote et de deux elements plasmidiques, une proteine d'initiation (repe) et un fragment origine, et (ii) aucune homologie n'est trouvee entre pam-beta-1 et les replicons des bacteries a gram negatif. Le deuxieme aspect concerne la regulation de la replication. Celle-ci est realisee essentiellement en modulant la transcription du gene repe. Deux niveaux de controle independants et additifs ont ete detectes: un systeme d'attenuation transcriptionnelle regule par un arn antisens qui provoque une terminaison prematuree de 90% des transcrits, et un represseur proteique qui diminue d'un facteur 10 la transcription initiee au niveau de ce promoteur
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Kolb, Fabrice. "ROLE DE DEUX ARN DANS LE CONTROLE DE L'EXPRESSION DES GENES: REGULATIONS DE LA REPLICATION DU PLASMIDE R1 PAR UN ARN ANTISENS ET DES GENES DE VIRULENCE DE STAPHYLOCOCCUS AUREUS PAR L'ARN-III." Phd thesis, Université Louis Pasteur - Strasbourg I, 2001. http://tel.archives-ouvertes.fr/tel-00002806.

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L'ARN antisens CopA régule le taux de réplication du plasmide bactérien R1 en contrôlant la synthèse de la protéine initiatrice de la réplication, RepA. CopA se fixe à sa séquence complémentaire (CopT) dans la région 5' non traduite de l'ARNm repA. Cette interaction induit principalement une inhibition de la traduction de l'ARNm repA et favorise sa dégradation par la RNase III. L'efficacité du contrôle est directement reliée à la vitesse de formation du complexe CopA-CopT. Nous avons montré que les deux ARN interagissent via une interaction de type boucle-boucle, mais que celle-ci doit être rapidement convertie pour former un complexe irréversible et fonctionnel. Celui-ci n'est pas un duplexe étendu mais contient une jonction à quatre hélices stabilisée par une longue hélice intermoléculaire. Plusieurs intermédiaires réactionnels menant au complexe stable ont été caractérisés, ainsi que les déterminants structuraux de CopA et de CopT nécessaires à cette conversion qui est essentielle au contrôle. Ainsi, nous proposons un mécanisme de formation du complexe stable qui implique plusieurs étapes dans un ordre hiérarchique. Ce mode d'appariement ARN-ARN insoupçonné apparaît être une règle plutôt qu'une exception. En effet, nous avons montré qu'il est conservé dans de nombreux plasmides homologues à R1. L'ARN-III contrôle l'expression des gènes de virulence chez Staphylococcus aureus. Cette deuxième partie de mon travail de thèse a eu pour but de déterminer la structure secondaire de cet ARN en solution et in vivo, et de définir des domaines fonctionnels. En combinant différentes approches in vitro, nous avons établi que l'ARN-III contient 14 structures en tige-boucle et trois interactions à longue distance. Nous avons également identifié un sous domaine fonctionnel impliqué dans le contrôle de la synthèse de la protéine A.
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Bowers, Lisa. "Elements of plasmid R6K replication control." 2007. http://www.library.wisc.edu/databases/connect/dissertations.html.

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Book chapters on the topic "Plasmid replication control"

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Brantl, Sabine. "Plasmid Replication Control by Antisense RNAs." In Plasmid Biology, 47–62. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817732.ch3.

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Kittell, Barbara Lewis, and Donald R. Helinski. "Plasmid Incompatibility and Replication Control." In Bacterial Conjugation, 223–42. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9357-4_8.

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Brantl, Sabine. "Plasmid Replication Control by Antisense RNAs." In Plasmids, 83–103. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818982.ch6.

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Rownd, Robert H., David D. Womble, Xin-nian Dong, Verne A. Luckow, and Ru Ping Wu. "Incompatibility and INCFII Plasmid Replication Control." In Plasmids in Bacteria, 335–54. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2447-8_26.

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Novick, Richard P., Steven J. Projan, C. Chandra Kumar, Stephen Carleton, Alexandra Gruss, Sarah K. Highlander, and John Kornblum. "Replication Control for PT181, an Indirectly Regulated Plasmid." In Plasmids in Bacteria, 299–320. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2447-8_24.

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Nordström, Kurt. "Control of Plasmid Replication: Theoretical Considerations and Practical Solutions." In Plasmids in Bacteria, 189–214. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2447-8_17.

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Meyer, Richard J., Lung-Shen Lin, Kyunghoon Kim, and Michael A. Brasch. "Broad Host-Range Plasmid R1162: Replication, Incompatibility, and Copy-Number Control." In Plasmids in Bacteria, 173–88. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2447-8_16.

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Nijkamp, H. John J., Bob van Gemen, Marcel J. J. Hakkaart, Arnold J. van Putten, and Eduard Veltkamp. "Stable Maintenance of Plasmid CLO DF13: Structural and Functional Relationships Between Replication Control, Partitioning, and Incompatibility." In Plasmids in Bacteria, 283–98. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2447-8_23.

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Pritchard, R. H. "Control of Chromosome Replication in Bacteria." In Plasmids in Bacteria, 277–82. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2447-8_22.

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Pritchard, R. H. "Control of Replication of Genetic Material in Bacteria." In Ciba Foundation Symposium - Bacterial Episomes and Plasmids, 65–80. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470715345.ch5.

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