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Journal articles on the topic 'Plasmid replication control'

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Published: 4 June 2021
Last updated: 8 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Villafane, R., D. H. Bechhofer, C. S. Narayanan, and D. Dubnau. "Replication control genes of plasmid pE194." Journal of Bacteriology 169, no. 10 (1987): 4822–29. http://dx.doi.org/10.1128/jb.169.10.4822-4829.1987.

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12

Qin, Zhongjun, Meijuan Shen, and Stanley N. Cohen. "Identification and Characterization of a pSLA2 Plasmid Locus Required for Linear DNA Replication and Circular Plasmid Stable Inheritance in Streptomyces lividans." Journal of Bacteriology 185, no. 22 (November 15, 2003): 6575–82. http://dx.doi.org/10.1128/jb.185.22.6575-6582.2003.

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ABSTRACT Streptomyces linear plasmids and linear chromosomes can replicate also in a circular form when their telomeres are deleted. The 17-kb linear plasmid pSLA2 has been a useful model in studies of such replicons. Here we report that the minimal origin initiating replication of pSLA2-derived plasmids as circular molecules cannot propagate these plasmids in a linear mode unless they also contain a novel plasmid-encoded locus, here named rlrA (required for linear replication). In contrast with the need for rlrA to accomplish replication of telomere-containing linear plasmids, expression of rlrA, which encodes two LuxR family regulatory domains, interferes with the establishment of pSLA2 in circular form in Streptomyces lividans transformants. The additional presence of an adjacent divergently transcribed locus, rorA (rlrA override), which strongly resembles the kor (kil override) transcription control genes identified previously on Streptomyces plasmids, reversed the detrimental effects of rlrA on plasmid establishment and additionally stabilized circular plasmid inheritance by spores during the S. lividans life cycle. While the effects of the rlrA/rorA locus of pSLA2 were seen also on linear plasmids derived from the unrelated SLP2 replicon, they did not extend to plasmids whose replication was initiated at a cloned chromosomal origin. Our results establish the existence of, and provide the initial description of, a novel plasmid-borne regulatory system that differentially affects the propagation of linear and circular plasmids in Streptomyces.
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13

Pickett, Mark A., J. Sylvia Everson, Patrick J. Pead, and Ian N. Clarke. "The plasmids of Chlamydia trachomatis and Chlamydophila pneumoniae (N16): accurate determination of copy number and the paradoxical effect of plasmid-curing agents." Microbiology 151, no. 3 (March 1, 2005): 893–903. http://dx.doi.org/10.1099/mic.0.27625-0.

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A 7·5 kbp cryptic plasmid is found in almost all isolates of Chlamydia trachomatis. Real-time PCR assays, using TaqMan chemistry, were set up to quantify accurately both the chlamydial plasmid and the single copy, chromosomal omcB gene in the infectious, elementary bodies (EBs) of C. trachomatis L1 440. Plasmid copy number was also determined in the EBs of six other lymphogranuloma venereum (LGV) isolates (serovars L1–L3), ten trachoma isolates (serovars A–C) and nine urogenital isolates (serovars D–J). The results indicated an average plasmid copy number of 4·0±0·8 (mean±95 % confidence interval) plasmids per chromosome. During the chlamydial developmental cycle, up to 7·6 plasmids per chromosome were detected, indicating an increased plasmid copy number in the actively replicating reticulate bodies. Attempts to eliminate the plasmid from strain L1 440 using the plasmid-curing agents ethidium bromide, acridine orange or imipramine/novobiocin led to a paradoxical increase in plasmid copy number. It is speculated that the stress induced by chemical curing agents may stimulate the activity of plasmid-encoded replication (Rep) proteins. In contrast to C. trachomatis, only a single isolate of Chlamydophila pneumoniae bears a plasmid. C. pneumoniae strain N16 supports a 7·4 kbp plasmid in which ORF1, encoding one of the putative Rep proteins, is disrupted by a deletion and split into two smaller ORFs. Similar assay techniques revealed 1·3±0·2 plasmids per chromosome (mean±95 % confidence interval) in EBs of this strain. These findings are in agreement with the hypothesis that the ORF1-encoded protein is involved in, but not essential for, plasmid replication and control of copy number.
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14

Abeles, Ann L., Lucretia D. Reaves, Brenda Youngren-Grimes, and Stuart J. Austin. "Control of P1 plasmid replication by iterons." Molecular Microbiology 18, no. 5 (December 1995): 903–12. http://dx.doi.org/10.1111/j.1365-2958.1995.18050903.x.

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15

WADA, Chieko. "Control of initiation of F plasmid replication." Seibutsu Butsuri 28, no. 5 (1988): 250–54. http://dx.doi.org/10.2142/biophys.28.250.

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16

Espinosa, Manuel, Gloria del Solar, Fernando Rojo, and Juan C. Alonso. "Plasmid rolling circle replication and its control." FEMS Microbiology Letters 130, no. 2-3 (August 1995): 111–20. http://dx.doi.org/10.1111/j.1574-6968.1995.tb07707.x.

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17

Malmgren, Charlotta, E. Gerhart H. Wagner, Chantal Ehresmann, Bernard Ehresmann, and Pascale Romby. "Antisense RNA Control of Plasmid R1 Replication." Journal of Biological Chemistry 272, no. 19 (May 9, 1997): 12508–12. http://dx.doi.org/10.1074/jbc.272.19.12508.

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18

Krysan, P. J., and M. P. Calos. "Replication initiates at multiple locations on an autonomously replicating plasmid in human cells." Molecular and Cellular Biology 11, no. 3 (March 1991): 1464–72. http://dx.doi.org/10.1128/mcb.11.3.1464.

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We have used a two-dimensional gel electrophoresis mapping technique to determine where DNA replication initiates on a plasmid which utilizes a fragment of human DNA to replicate autonomously in human cells. Replication was found to initiate at multiple locations on the plasmid carrying the human sequence, in contrast to the pattern seen for an Epstein-Barr virus vector which served as a control with a fixed origin. The family of repeats, a portion of the Epstein-Barr virus origin of replication which is present our plasmid, was shown to function as a replication fork barrier. The nature of the stalled replicative intermediates on the human DNA-based plasmid further indicated that replication did not initiate at a single fixed position each time the plasmid replicated. The results suggest that the replication apparatus used to duplicate DNA in human cells may not have precise sequence requirements which target initiation to specific locations.
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19

Krysan, P. J., and M. P. Calos. "Replication initiates at multiple locations on an autonomously replicating plasmid in human cells." Molecular and Cellular Biology 11, no. 3 (March 1991): 1464–72. http://dx.doi.org/10.1128/mcb.11.3.1464-1472.1991.

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We have used a two-dimensional gel electrophoresis mapping technique to determine where DNA replication initiates on a plasmid which utilizes a fragment of human DNA to replicate autonomously in human cells. Replication was found to initiate at multiple locations on the plasmid carrying the human sequence, in contrast to the pattern seen for an Epstein-Barr virus vector which served as a control with a fixed origin. The family of repeats, a portion of the Epstein-Barr virus origin of replication which is present our plasmid, was shown to function as a replication fork barrier. The nature of the stalled replicative intermediates on the human DNA-based plasmid further indicated that replication did not initiate at a single fixed position each time the plasmid replicated. The results suggest that the replication apparatus used to duplicate DNA in human cells may not have precise sequence requirements which target initiation to specific locations.
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20

Venkova-Canova, Tatiana, Miroslav Pátek, and Jan Nešvera. "Control of rep Gene Expression in Plasmid pGA1 from Corynebacteriumglutamicum." Journal of Bacteriology 185, no. 8 (April 15, 2003): 2402–9. http://dx.doi.org/10.1128/jb.185.8.2402-2409.2003.

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ABSTRACT The cryptic multicopy plasmid pGA1 (4,826 bp) from Corynebacterium glutamicum LP-6 belongs to the fifth group of rolling-circle-replicating plasmids. A determinant, which negatively controls pGA1 replication, was localized in the leader region of the rep gene coding for the initiator of plasmid replication. This region, when cloned into the compatible vector pEC6, was found to cause decrease of segregational stability of the pGA1 derivative pKG48. A promoter and a single transcriptional start site were found in the rep leader region in orientation opposite to the rep gene. These results suggest that a small countertranscribed RNA (ctRNA) (ca. 89 nucleotides in length), which might inhibit translation of pGA1 rep gene, is formed. Analysis of predicted secondary structure of the pGA1-encoded ctRNA revealed features common with the known ctRNAs in bacteria. Inactivation of the promoter P-ctRNA caused a dramatic increase of copies of the respective plasmid, which proved a negative role of the ctRNA in control of pGA1 copy number. A region between the promoters Prep and P-ctRNA with a potential to form secondary structures on both ctRNA and rep mRNA was found to cause low activity of the rep promoter even when promoter P-ctRNA was deleted. Thus, the sequence within the rep leader region itself seems to act, in addition to the ctRNA, as a second regulatory element of a novel type, negatively influencing expression of the pGA1 rep gene.
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21

Fong, Ryan, Zhihao Hu, C. Richard Hutchinson, Jianqiang Huang, Stanley Cohen, and Camilla Kao. "Characterization of a Large, Stable, High-Copy-Number Streptomyces Plasmid That Requires Stability and Transfer Functions for Heterologous Polyketide Overproduction." Applied and Environmental Microbiology 73, no. 4 (December 1, 2006): 1296–307. http://dx.doi.org/10.1128/aem.01888-06.

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ABSTRACT A major limitation to improving small-molecule pharmaceutical production in streptomycetes is the inability of high-copy-number plasmids to tolerate large biosynthetic gene cluster inserts. A recent finding has overcome this barrier. In 2003, Hu et al. discovered a stable, high-copy-number, 81-kb plasmid that significantly elevated production of the polyketide precursor to the antibiotic erythromycin in a heterologous Streptomyces host (J. Ind. Microbiol. Biotechnol. 30:516-522, 2003). Here, we have identified mechanisms by which this SCP2*-derived plasmid achieves increased levels of metabolite production and examined how the 45-bp deletion mutation in the plasmid replication origin increased plasmid copy number. A plasmid intramycelial transfer gene, spd, and a partition gene, parAB, enhance metabolite production by increasing the stable inheritance of large plasmids containing biosynthetic genes. Additionally, high product titers required both activator (actII-ORF4) and biosynthetic genes (eryA) at high copy numbers. DNA gel shift experiments revealed that the 45-bp deletion abolished replication protein (RepI) binding to a plasmid site which, in part, supports an iteron model for plasmid replication and copy number control. Using the new information, we constructed a large high-copy-number plasmid capable of overproducing the polyketide 6-deoxyerythronolide B. However, this plasmid was unstable over multiple culture generations, suggesting that other SCP2* genes may be required for long-term, stable plasmid inheritance.
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22

Berkner, Silvia, and Georg Lipps. "Characterization of the Transcriptional Activity of the Cryptic Plasmid pRN1 from Sulfolobus islandicus REN1H1 and Regulation of Its Replication Operon." Journal of Bacteriology 189, no. 5 (December 15, 2006): 1711–21. http://dx.doi.org/10.1128/jb.01586-06.

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ABSTRACT The plasmid pRN1 from Sulfolobus islandicus REN1H1 belongs to the crenarchaeal plasmid family pRN. The plasmids in this family encode three conserved proteins that participate in plasmid replication and copy number regulation, as suggested by biochemical characterization of the recombinant proteins. In order to deepen our understanding of the molecular biology of these plasmids, we investigated the transcriptional activity of the model plasmid pRN1. We detected five major transcripts present at about 2 to 15 copies per cell. One long transcriptional unit comprises the genes for the plasmid-copy-number control protein Orf56/CopG and the replication protein Orf904. A second transcript with a long 3′-untranslated region codes for the DNA binding protein Orf80. For both transcripts, we identified countertranscripts which could play a regulatory role. The function of the fifth transcript is unclear. For the five transcripts, we determined the start site, the transcript end, the stability, and the abundance in different growth phases. Reporter gene experiments demonstrated that the copy number control protein Orf56 represses transcription of the orf56-orf904 cotranscript in vivo.
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23

Thomas, Christopher M. "Recent studies on the control of plasmid replication." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 949, no. 3 (March 1988): 253–63. http://dx.doi.org/10.1016/0167-4781(88)90150-9.

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24

Cesareni, G. "Control of ColE1 plasmid replication by antisense RNA." Trends in Genetics 7, no. 1 (January 1991): 230–35. http://dx.doi.org/10.1016/0168-9525(91)90143-e.

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25

Cesareni, G., M. Helmer-Citterich, and L. Castagnoli. "Control of ColE1 plasmid replication by antisense RNA." Trends in Genetics 7, no. 7 (July 1991): 230–35. http://dx.doi.org/10.1016/0168-9525(91)90370-6.

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26

Nordström, Kurt, E. Gerhart H. Wagner, Christine Persson, Pontus Blomberg, and Marie Öhman. "Translational control by antisense RNA in control of plasmid replication." Gene 72, no. 1-2 (December 1988): 237–40. http://dx.doi.org/10.1016/0378-1119(88)90148-5.

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27

Hagege, Juliette M., Michael A. Brasch, and Stanley N. Cohen. "Regulation of Transfer Functions by theimp Locus of the Streptomyces coelicolorPlasmidogenic Element SLP1." Journal of Bacteriology 181, no. 19 (October 1, 1999): 5976–83. http://dx.doi.org/10.1128/jb.181.19.5976-5983.1999.

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ABSTRACT SLP1 int is a 17.2-kb genetic element that normally is integrated site specifically into the chromosome ofStreptomyces coelicolor A3(2). The imp operon within SLP1 int represses replication of both chromosomally integrated and extrachromosomal SLP1. During mating withS. lividans, SLP1 int can excise, delete part of imp, and form a family of autonomously replicating conjugative plasmids. Earlier work has shown thatimpA and impC gene products act in concert to control plasmid maintenance and regulate their own transcription. Here we report that these imp genes act also on a second promoter, Popimp (promoter oppositeimp), located adjacent to, and initiating transcription divergent from, imp to regulate loci involved in the intramycelial transfer of SLP1 plasmids. spdB1 andspdB2, two overlapping genes immediately 3′ to Popimp and directly regulated byimp, are shown by Tn5 mutagenesis to control transfer-associated growth inhibition (i.e., pocking). Additional genes resembling transfer genes of other Streptomyces spp. plasmids and required for SLP1 transfer and/or postconjugal intramycelial spread are located more distally to Popimp . Expression of impA andimpC in an otherwise competent recipient strain prevented SLP1-mediated gene transfer of chromosomal and plasmid genes but not plasmid-independent chromosome-mobilizing activity, suggesting that information transduced to recipients after the formation of mating pairs affects imp activity. Taken together with earlier evidence that the imp operon regulates SLP1 DNA replication, the results reported here implicate imp in the overall regulation of functions related to the extrachromosomal state of SLP1.
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28

Paulsson, Johan, and Måns Ehrenberg. "Noise in a minimal regulatory network: plasmid copy number control." Quarterly Reviews of Biophysics 34, no. 1 (February 2001): 1–59. http://dx.doi.org/10.1017/s0033583501003663.

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1. Introduction 22. Plasmid biology 32.1 What are plasmids? 32.2 Evolution of CNC: cost and benefit 42.3 Plasmids are semi-complete regulatory networks 62.4 The molecular mechanisms of CNC for plasmids ColE1 and R1 62.4.1 ColE1 72.4.2 R1 72.5 General simplifying assumptions and values of rate constants 93. Macroscopic analysis 113.1 Regulatory logic of inhibitor-dilution CNC 113.2 Sensitivity amplification 123.3 Plasmid control curves 133.4 Multistep control of plasmid ColE1: exponential control curves 143.5 Multistep control of plasmid R1: hyperbolic control curves 163.6 Time-delays, oscillations and critical damping 184. Mesoscopic analysis 204.1 The master equation approach 204.2 A random walker in a potential well 234.3 CNC as a stochastic process 244.4 Sensitivity amplification 264.4.1 Single-step hyperbolic control 264.4.2 ColE1 multistep control can eliminate plasmid copy number variation 284.4.3 Replication backup systems – the Rom protein of ColE1 and CopB of R1 294.5 Time-delays 304.5.1 Limited rate of inhibitor degradation 304.5.2 Precise delays – does unlimited sensitivity amplification always reduce plasmid losses? 324.6 Order and disorder in CNC 334.6.1 Disordered CNC 344.6.2 Ordered CNC: R1 multistep control gives narrowly distributed interreplication times 344.7 Noisy signalling – disorder and sensitivity amplification 374.7.1 Eliminating a fast but noisy variable 384.7.2 Conditional inhibitor distribution: Poisson 394.7.3 Increasing inhibitor variation I: transcription in bursts 404.7.4 Increasing inhibitor variation II: duplex formation 414.7.5 Exploiting fluctuations for sensitivity amplification: stochastic focusing 444.7.6 A kinetic uncertainty principle 454.7.7 Disorder and stochastic focusing 464.7.8 Do plasmids really use stochastic focusing? 474.8 Metabolic burdens and values of in vivo rate constants 485. Previous models of copy number control 495.1 General models of CNC 495.2 Modelling plasmid ColE1 CNC 495.3 Modelling plasmid R1 CNC 526. Summary and outlook: the plasmid paradigm 537. Acknowledgements 568. References 56This work is a theoretical analysis of random fluctuations and regulatory efficiency in genetic networks. As a model system we use inhibitor-dilution copy number control (CNC) of the bacterial plasmids ColE1 and R1. We chose these systems because they are simple and well-characterised but also because plasmids seem to be under an evolutionary pressure to reduce both average copy numbers and statistical copy number variation: internal noise.
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29

Nordström, Kurt. "Control of plasmid replication—How do DNA iterons set the replication frequency?" Cell 63, no. 6 (December 1990): 1121–24. http://dx.doi.org/10.1016/0092-8674(90)90405-4.

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30

Wilcks, Andrea, Lasse Smidt, Ole Andreas Økstad, Anne-Brit Kolstø, Jacques Mahillon, and Lars Andrup. "Replication Mechanism and Sequence Analysis of the Replicon of pAW63, a Conjugative Plasmid from Bacillus thuringiensis." Journal of Bacteriology 181, no. 10 (May 15, 1999): 3193–200. http://dx.doi.org/10.1128/jb.181.10.3193-3200.1999.

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ABSTRACT A 5.8-kb fragment of the large conjugative plasmid pAW63 fromBacillus thuringiensis subsp. kurstaki HD73 containing all the information for autonomous replication was cloned and sequenced. By deletion analysis, the pAW63 replicon was reduced to a 4.1-kb fragment harboring four open reading frames (ORFs). Rep63A (513 amino acids [aa]), encoded by the largest ORF, displayed strong similarity (40% identity) to the replication proteins from plasmids pAMβ1, pIP501, and pSM19035, indicating that the pAW63 replicon belongs to the pAMβ1 family of gram-positive theta-replicating plasmids. This was confirmed by the facts that no single-stranded DNA replication intermediates could be detected and that replication was found to be dependent on host-gene-encoded DNA polymerase I. An 85-bp region downstream of Rep63A was also shown to have strong similarity to the origins of replication of pAMβ1 and pIP501, and it is suggested that this region contains the bona fide pAW63 ori. The protein encoded by the second large ORF, Rep63B (308 aa), was shown to display similarity to RepB (34% identity over 281 aa) and PrgP (32% identity over 310 aa), involved in copy control of theEnterococcus faecalis plasmids pAD1 and pCF10, respectively. No significant similarity to known proteins or DNA sequences could be detected for the two smallest ORFs. However, the location, size, hydrophilicity, and orientation of ORF6 (107 codons) were analogous to those features of the putative genes repCand prgO, which encode stability functions on plasmids pAD1 and pCF10, respectively. The cloned replicon of plasmid pAW63 was stably maintained in Bacillus subtilis and B. thuringiensis and displayed incompatibility with the native pAW63. Hybridization experiments using the cloned replicon as a probe showed that pAW63 has similarity to large plasmids from other B. thuringiensis subsp. kurstaki strains and to a strain of B. thuringiensis subsp. alesti.
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31

Yu, G. L., and E. H. Blackburn. "Amplification of tandemly repeated origin control sequences confers a replication advantage on rDNA replicons in Tetrahymena thermophila." Molecular and Cellular Biology 10, no. 5 (May 1990): 2070–80. http://dx.doi.org/10.1128/mcb.10.5.2070.

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The macronuclear rRNA genes (rDNA) in the ciliate Tetrahymena thermophila are normally palindromic linear replicons, containing two copies of the replication origin region in inverted orientation. A circular plasmid containing a single Tetrahymena rRNA gene (one half palindrome) joined to a tandem repeat of a 1.9-kilobase (kb) rDNA segment encompassing the rDNA replication origin and known replication control elements was used to transform Tetrahymena macronuclei by microinjection. This plasmid was shown previously to have a replication advantage over the rDNA allele of the recipient cell strain (G.-L. Yu and E. H. Blackburn, Proc. Natl. Acad. Sci. USA 86:8487-8491, 1990). During vegetative cell divisions, the circular and palindromic rDNAs were rapidly replaced by novel, successively longer linear rDNAs that eventually contained up to 30 tandem 1.9-kb repeats, resulting from homologous but unequal crossovers between the 1.9-kb repeats. We present evidence to show that increasing the number of copies of the replication control regions increases the replicative advantage of the rDNA, the first such situation for a cellular nuclear replicon in a eucaryote.
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32

Yu, G. L., and E. H. Blackburn. "Amplification of tandemly repeated origin control sequences confers a replication advantage on rDNA replicons in Tetrahymena thermophila." Molecular and Cellular Biology 10, no. 5 (May 1990): 2070–80. http://dx.doi.org/10.1128/mcb.10.5.2070-2080.1990.

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The macronuclear rRNA genes (rDNA) in the ciliate Tetrahymena thermophila are normally palindromic linear replicons, containing two copies of the replication origin region in inverted orientation. A circular plasmid containing a single Tetrahymena rRNA gene (one half palindrome) joined to a tandem repeat of a 1.9-kilobase (kb) rDNA segment encompassing the rDNA replication origin and known replication control elements was used to transform Tetrahymena macronuclei by microinjection. This plasmid was shown previously to have a replication advantage over the rDNA allele of the recipient cell strain (G.-L. Yu and E. H. Blackburn, Proc. Natl. Acad. Sci. USA 86:8487-8491, 1990). During vegetative cell divisions, the circular and palindromic rDNAs were rapidly replaced by novel, successively longer linear rDNAs that eventually contained up to 30 tandem 1.9-kb repeats, resulting from homologous but unequal crossovers between the 1.9-kb repeats. We present evidence to show that increasing the number of copies of the replication control regions increases the replicative advantage of the rDNA, the first such situation for a cellular nuclear replicon in a eucaryote.
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33

Skilton, Rachel J., Colette O'Neill, Nicholas R. Thomson, David J. Lampe, and Ian N. Clarke. "Progress towards an inducible, replication-proficient transposon delivery vector for Chlamydia trachomatis." Wellcome Open Research 6 (April 13, 2021): 82. http://dx.doi.org/10.12688/wellcomeopenres.16665.1.

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Background Genetic systems have been developed for Chlamydia but the extremely low transformation frequency remains a significant bottleneck. Our goal is to develop a self-replicating transposon delivery vector for C. trachomatis which can be expanded prior to transposase induction. Methods We made E. coli/ C. trachomatis shuttle vectors bearing the Himar1 C9 transposase under control of the tet promoter and a novel rearrangement of the Himar1 transposon with the β-lactamase gene. Activity of the transposase was monitored by immunoblot and by DNA sequencing. Results We constructed pSW2-mCh-C9, a C. trachomatis plasmid designed to act as a self-replicating vector carrying both the Himar1 C9 transposase under tet promoter control and its transposon. However, we were unable to recover this plasmid in C. trachomatis following multiple attempts at transformation. Therefore, we assembled two new deletion plasmids pSW2-mCh-C9-ΔTpon carrying only the Himar1 C9 transposase (under tet promoter control) and a sister vector (same sequence backbone) pSW2-mCh-C9-ΔTpase carrying its cognate transposon. We demonstrated that the biological components that make up both pSW2-mCh-C9-ΔTpon and pSW2-mCh-C9-ΔTpase are active in E. coli. Both these plasmids could be independently recovered in C. trachomatis. We attempted to perform lateral gene transfer by transformation and mixed infection with C. trachomatis strains bearing pSW2-mCh-C9-ΔTpon and pSW2-RSGFP-Tpon (a green fluorescent version of pSW2-mCh-C9-ΔTpase). Despite success in achieving mixed infections, it was not possible to recover progeny bearing both versions of these plasmids. Conclusions We have designed a self-replicating plasmid vector pSW2-mCh-C9 for C. trachomatis carrying the Himar1 C9 transposase under tet promoter control. Whilst this can be transformed into E. coli it cannot be recovered in C. trachomatis. Based on selected deletions and phenotypic analyses we conclude that low level expression from the tet inducible promoter is responsible for premature transposition and hence plasmid loss early on in the transformation process.
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34

Okibe, Naoko, Nobuaki Suzuki, Masayuki Inui, and Hideaki Yukawa. "Antisense-RNA-mediated plasmid copy number control in pCG1-family plasmids, pCGR2 and pCG1, in Corynebacterium glutamicum." Microbiology 156, no. 12 (December 1, 2010): 3609–23. http://dx.doi.org/10.1099/mic.0.043745-0.

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pCGR2 and pCG1 belong to different subfamilies of the pCG1 family of Corynebacterium glutamicum plasmids. Nonetheless, they harbour homologous putative antisense RNA genes, crrI and cgrI, respectively. The genes in turn share identical positions complementary to the leader region of their respective repA (encoding plasmid replication initiator) genes. Determination of their precise transcriptional start- and end-points revealed the presence of short antisense RNA molecules (72 bp, CrrI; and 73 bp, CgrI). These short RNAs and their target mRNAs were predicted to form highly structured molecules comprising stem–loops with known U-turn motifs. Abolishing synthesis of CrrI and CgrI by promoter mutagenesis resulted in about sevenfold increase in plasmid copy number on top of an 11-fold (CrrI) and 32-fold (CgrI) increase in repA mRNA, suggesting that CrrI and CgrI negatively control plasmid replication. This control is accentuated by parB, a gene that encodes a small centromere-binding plasmid-partitioning protein, and is located upstream of repA. Simultaneous deactivation of CrrI and parB led to a drastic 87-fold increase in copy number of a pCGR2-derived shuttle vector. Moreover, the fact that changes in the structure of the terminal loops of CrrI and CgrI affected plasmid copy number buttressed the important role of the loop structure in formation of the initial interaction complexes between antisense RNAs and their target mRNAs. Similar antisense RNA control systems are likely to exist not only in the two C. glutamicum pCG1 subfamilies but also in related plasmids across Corynebacterium species.
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35

Yang, Jun, Hai-Hong Wang, Yaoyao Lu, Ling-Xian Yi, Yinyue Deng, Luchao Lv, Vincent Burrus, and Jian-Hua Liu. "A ProQ/FinO family protein involved in plasmid copy number control favours fitness of bacteria carrying mcr-1-bearing IncI2 plasmids." Nucleic Acids Research 49, no. 7 (March 15, 2021): 3981–96. http://dx.doi.org/10.1093/nar/gkab149.

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Abstract The plasmid-encoded colistin resistance gene mcr-1 challenges the use of polymyxins and poses a threat to public health. Although IncI2-type plasmids are the most common vector for spreading the mcr-1 gene, the mechanisms by which these plasmids adapt to host bacteria and maintain resistance genes remain unclear. Herein, we investigated the regulatory mechanism for controlling the fitness cost of an IncI2 plasmid carrying mcr-1. A putative ProQ/FinO family protein encoded by the IncI2 plasmid, designated as PcnR (plasmid copy number repressor), balances the mcr-1 expression and bacteria fitness by repressing the plasmid copy number. It binds to the first stem-loop structure of the repR mRNA to repress RepA expression, which differs from any other previously reported plasmid replication control mechanism. Plasmid invasion experiments revealed that pcnR is essential for the persistence of the mcr-1-bearing IncI2 plasmid in the bacterial populations. Additionally, single-copy mcr-1 gene still exerted a fitness cost to host bacteria, and negatively affected the persistence of the IncI2 plasmid in competitive co-cultures. These findings demonstrate that maintaining mcr-1 plasmid at a single copy is essential for its persistence, and explain the significantly reduced prevalence of mcr-1 following the ban of colistin as a growth promoter in China.
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36

Adamczyk, Małgorzata, and Grazyna Jagura-Burdzy. "Spread and survival of promiscuous IncP-1 plasmids." Acta Biochimica Polonica 50, no. 2 (June 30, 2003): 425–53. http://dx.doi.org/10.18388/abp.2003_3696.

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Plasmids classified to the IncP-1 incompatibility group belong to the most stably maintained mobile elements among low copy number plasmids known to date. The remarkable persistence is achieved by various tightly controlled stability mechanisms like active partitioning, efficient conjugative transfer system, killing of plasmid-free segregants and multimer resolution. The unique feature of IncP-1 plasmids is the central control operon coding for global regulators which control the expression of genes involved in vegetative replication, stable maintenance and conjugative transfer. The multivalent regulatory network provides means for coordinated expression of all plasmid functions. The current state of knowledge about two fully sequenced plasmids RK2 and R751, representatives of the IncP-1alpha and IncP-1beta subgroups, is presented.
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37

Val, Marie-Eve, Martial Marbouty, Francisco de Lemos Martins, Sean P. Kennedy, Harry Kemble, Michael J. Bland, Christophe Possoz, Romain Koszul, Ole Skovgaard, and Didier Mazel. "A checkpoint control orchestrates the replication of the two chromosomes of Vibrio cholerae." Science Advances 2, no. 4 (April 2016): e1501914. http://dx.doi.org/10.1126/sciadv.1501914.

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Bacteria with multiple chromosomes represent up to 10% of all bacterial species. Unlike eukaryotes, these bacteria use chromosome-specific initiators for their replication. In all cases investigated, the machineries for secondary chromosome replication initiation are of plasmid origin. One of the important differences between plasmids and chromosomes is that the latter replicate during a defined period of the cell cycle, ensuring a single round of replication per cell. Vibrio cholerae carries two circular chromosomes, Chr1 and Chr2, which are replicated in a well-orchestrated manner with the cell cycle and coordinated in such a way that replication termination occurs at the same time. However, the mechanism coordinating this synchrony remains speculative. We investigated this mechanism and revealed that initiation of Chr2 replication is triggered by the replication of a 150-bp locus positioned on Chr1, called crtS. This crtS replication–mediated Chr2 replication initiation mechanism explains how the two chromosomes communicate to coordinate their replication. Our study reveals a new checkpoint control mechanism in bacteria, and highlights possible functional interactions mediated by contacts between two chromosomes, an unprecedented observation in bacteria.
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38

Brantl, Sabine. "Antisense-RNA mediated control of plasmid replication – pIP501 revisited." Plasmid 78 (March 2015): 4–16. http://dx.doi.org/10.1016/j.plasmid.2014.07.004.

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39

Rosenfeld, R., and N. B. Grover. "Control of Mini-R1 Plasmid Replication: A Computer Simulation." Plasmid 29, no. 2 (March 1993): 94–116. http://dx.doi.org/10.1006/plas.1993.1012.

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40

Romanczuk, H., and W. M. Wormington. "Selective enhancement of bovine papillomavirus type 1 DNA replication in Xenopus laevis eggs by the E6 gene product." Molecular and Cellular Biology 9, no. 2 (February 1989): 406–14. http://dx.doi.org/10.1128/mcb.9.2.406.

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Genetic analyses of bovine papillomavirus type 1 (BPV-1) DNA in transformed mammalian cells have indicated that the E6 gene product is essential for the establishment and maintenance of a high plasmid copy number. In order to analyze the direct effect of the E6 protein on the replication of a BPV-1-derived plasmid, a cDNA containing the BPV-1 E6 open reading frame was subcloned into an SP6 vector for the in vitro synthesis of the corresponding mRNA. The SP6 E6 mRNA was injected into Xenopus laevis oocytes to determine the subcellular localization of the E6 gene product and to analyze the effect of the protein on BPV-1 DNA replication. SP6 E6 mRNA microinjected into stage VI oocytes was translated into a 15.5-kilodalton protein that was specifically immunoprecipitated by antibodies directed against the E6 gene product. The E6 protein preferentially accumulated in oocyte nuclei, a localization which is consistent with the replicative functions in which it has been implicated. The expression of E6 in replication-competent mature oocytes selectively enhanced the replication of a BPV-derived plasmid, indicating a direct role for this gene product in the control of BPV-1 DNA replication.
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41

Romanczuk, H., and W. M. Wormington. "Selective enhancement of bovine papillomavirus type 1 DNA replication in Xenopus laevis eggs by the E6 gene product." Molecular and Cellular Biology 9, no. 2 (February 1989): 406–14. http://dx.doi.org/10.1128/mcb.9.2.406-414.1989.

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Genetic analyses of bovine papillomavirus type 1 (BPV-1) DNA in transformed mammalian cells have indicated that the E6 gene product is essential for the establishment and maintenance of a high plasmid copy number. In order to analyze the direct effect of the E6 protein on the replication of a BPV-1-derived plasmid, a cDNA containing the BPV-1 E6 open reading frame was subcloned into an SP6 vector for the in vitro synthesis of the corresponding mRNA. The SP6 E6 mRNA was injected into Xenopus laevis oocytes to determine the subcellular localization of the E6 gene product and to analyze the effect of the protein on BPV-1 DNA replication. SP6 E6 mRNA microinjected into stage VI oocytes was translated into a 15.5-kilodalton protein that was specifically immunoprecipitated by antibodies directed against the E6 gene product. The E6 protein preferentially accumulated in oocyte nuclei, a localization which is consistent with the replicative functions in which it has been implicated. The expression of E6 in replication-competent mature oocytes selectively enhanced the replication of a BPV-derived plasmid, indicating a direct role for this gene product in the control of BPV-1 DNA replication.
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42

Kiely, Joan, S. B. Haase, Paul Russell, and Janet Leatherwood. "Functions of Fission Yeast Orp2 in DNA Replication and Checkpoint Control." Genetics 154, no. 2 (February 1, 2000): 599–607. http://dx.doi.org/10.1093/genetics/154.2.599.

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Abstract orp2 is an essential gene of the fission yeast Schizosaccharomyces pombe with 22% identity to budding yeast ORC2. We isolated temperature-sensitive alleles of orp2 using a novel plasmid shuffle based on selection against thymidine kinase. Cells bearing the temperature-sensitive allele orp2-2 fail to complete DNA replication at a restrictive temperature and undergo cell cycle arrest. Cell cycle arrest depends on the checkpoint genes rad1 and rad3. Even when checkpoint functions are wild type, the orp2-2 mutation causes high rates of chromosome and plasmid loss. These phenotypes support the idea that Orp2 is a replication initiation factor. Selective spore germination allowed analysis of orp2 deletion mutants. These experiments showed that in the absence of orp2 function, cells proceed into mitosis despite a lack of DNA replication. This suggests either that the Orp2 protein is a part of the checkpoint machinery or more likely that DNA replication initiation is required to induce the replication checkpoint signal.
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43

Tang, Qiyi, Peter Bell, Peter Tegtmeyer, and Gerd G. Maul. "Replication but Not Transcription of Simian Virus 40 DNA Is Dependent on Nuclear Domain 10." Journal of Virology 74, no. 20 (October 15, 2000): 9694–700. http://dx.doi.org/10.1128/jvi.74.20.9694-9700.2000.

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ABSTRACT DNA viruses from several families including herpes simplex virus type 1, adenovirus type 5, and simian virus 40 (SV40), start their transcription and replication adjacent to a specific nuclear domain, ND10. We asked whether a specific viral DNA sequence determines the location of these synthetic activities at such restricted nuclear sites. Partial and overlapping SV40 sequences were introduced into a β-galactosidase expression vector, and the β-galactosidase transcripts were localized by in situ hybridization. Transcripts derived from control plasmids were found throughout the nucleus and at highly concentrated sites but not at ND10. SV40 genomic segments supported ND10-associated transcription only when the origin and the coding sequence for the large T antigen were present. When the large T-antigen coding sequence was eliminated but the T antigen was constitutively expressed in COS-7 cells, the viral origin was sufficient to localize transcription and replication to ND10. Deletion analysis showed that only the large T-antigen binding site II (the core origin) was required but the T antigen was needed for detectable transcription at ND10. Large T antigen expressed from plasmids without the viral core origin did not bind or localize to ND10. Blocking of DNA replication prevented the accumulation of transcripts at ND10, indicating that only sites with replicating templates accumulated transcripts. Transcription at ND10 did not enhance total protein synthesis of plasmid transcripts. These findings suggest that viral transcription at ND10 may only be a consequence of viral genomes directed to ND10 for replication. Although plasmid transcription can take place anywhere in the nucleus, T-antigen-directed replication is apparently restricted to ND10.
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44

Tanaka, Teruo, Hirofumi Ishida, and Tomoko Maehara. "Characterization of the Replication Region of Plasmid pLS32 from the Natto Strain of Bacillus subtilis." Journal of Bacteriology 187, no. 13 (July 1, 2005): 4315–26. http://dx.doi.org/10.1128/jb.187.13.4315-4326.2005.

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ABSTRACT Plasmid pL32 from the Natto strain of Bacillus subtilis belongs to a group of low-copy-number plasmids in gram-positive bacteria that replicate via a theta mechanism of replication. We studied the DNA region encoding the replication protein, RepN, of pLS32, and obtained the following results. Transcription of the repN gene starts 167 nucleotides upstream from the translational start site of repN. The copy number of repN-coding plasmid pHDCS2, in which the repN gene was placed downstream of the IPTG (isopropyl-1-thio-β-d-galactopyranoside)-inducible Pspac promoter, was increased 100 fold by the addition of IPTG. Histidine-tagged RepN bound to a specific region in the repN gene containing five 22-bp tandem repeats (iterons) with partial mismatches, as shown by gel retardation and foot printing analyses. Sequence alterations in the first three iterons resulted in an increase in plasmid copy number, whereas those in either the forth or fifth iteron resulted in the failure of plasmid replication. The iterons expressed various degrees of incompatibility with an incoming repN-driven replicon pSEQ243, with the first three showing the strongest incompatibility. Finally, by using a plasmid, pHDMAEC21, carrying the sequence alterations in all the five iterons in repN and thus unable to replicate but encoding intact RepN, the region necessary for replication was confined to a 96-bp sequence spanning the 3′-terminal half of the fourth iteron to an A+T-rich region located downstream of the fifth iteron. From these results, we conclude that the iterons in repN are involved in both the control of plasmid copy number and incompatibility, and we suggest that the binding of RepN to the last two iterons triggers replication by melting the A+T-rich DNA sequence.
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45

McEachern, M. J., M. A. Bott, P. A. Tooker, and D. R. Helinski. "Negative control of plasmid R6K replication: possible role of intermolecular coupling of replication origins." Proceedings of the National Academy of Sciences 86, no. 20 (October 1, 1989): 7942–46. http://dx.doi.org/10.1073/pnas.86.20.7942.

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46

Chattoraj, Dhruba K. "Control of plasmid DNA replication by iterons: no longer paradoxical." Molecular Microbiology 37, no. 3 (January 18, 2002): 467–76. http://dx.doi.org/10.1046/j.1365-2958.2000.01986.x.

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47

Das, N., M. Valjavec-Gratian, A. N. Basuray, R. A. Fekete, P. P. Papp, J. Paulsson, and D. K. Chattoraj. "Multiple homeostatic mechanisms in the control of P1 plasmid replication." Proceedings of the National Academy of Sciences 102, no. 8 (February 11, 2005): 2856–61. http://dx.doi.org/10.1073/pnas.0409790102.

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48

Hama, C., T. Takizawa, H. Moriwaki, Y. Urasaki, and K. Mizobuchi. "Organization of the replication control region of plasmid ColIb-P9." Journal of Bacteriology 172, no. 4 (1990): 1983–91. http://dx.doi.org/10.1128/jb.172.4.1983-1991.1990.

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49

Wagner, E. Gerhart H., and Sabine Brantl. "Kissing and RNA stability in antisense control of plasmid replication." Trends in Biochemical Sciences 23, no. 12 (December 1998): 451–54. http://dx.doi.org/10.1016/s0968-0004(98)01322-x.

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50

Abhyankar, Mayuresh M., Jagan M. Reddy, Rahul Sharma, Erika Büllesbach, and Deepak Bastia. "Biochemical Investigations of Control of Replication Initiation of Plasmid R6K." Journal of Biological Chemistry 279, no. 8 (December 9, 2003): 6711–19. http://dx.doi.org/10.1074/jbc.m312052200.

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