Relevant bibliographies by topics / Plasmid pBS32

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Academic literature on the topic 'Plasmid pBS32'

Author: Grafiati
Published: 28 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Plasmid pBS32"

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Myagmarjav, B. E., M. A. Konkol, J. Ramsey, S. Mukhopadhyay, and D. B. Kearns. "ZpdN, a Plasmid-Encoded Sigma Factor Homolog, Induces pBS32-Dependent Cell Death in Bacillus subtilis." Journal of Bacteriology 198, no. 21 (August 22, 2016): 2975–84. http://dx.doi.org/10.1128/jb.00213-16.

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ABSTRACTThe ancestralBacillus subtilisstrain 3610 contains an 84-kb plasmid called pBS32 that was lost during domestication of commonly used laboratory derivatives. Here we demonstrate that pBS32, normally present at 1 or 2 copies per cell, increases in copy number nearly 100-fold when cells are treated with the DNA-damaging agent mitomycin C. Mitomycin C treatment also caused cell lysis dependent on pBS32-borne prophage genes. ZpdN, a sigma factor homolog encoded by pBS32, was required for the plasmid response to DNA damage, and artificial expression of ZpdN was sufficient to induce pBS32 hyperreplication and cell death. Plasmid DNA released by cell death was protected by the capsid protein ZpbH, suggesting that the plasmid was packaged into a phagelike particle. The putative particles were further indicated by CsCl sedimentation but were not observed by electron microscopy and were incapable of killingB. subtiliscells extracellularly. We hypothesize that pBS32-mediated cell death releases a phagelike particle that is defective and unstable.IMPORTANCEProphages are phage genomes stably integrated into the host bacterium's chromosome and less frequently are maintained as extrachromosomal plasmids. Here we report that the extrachromosomal plasmid pBS32 ofBacillus subtilisencodes a prophage that, when activated, kills the host. pBS32 also encodes both the sigma factor homolog ZpdN that is necessary and sufficient for prophage induction and the protein ComI, which is a potent inhibitor of DNA uptake by natural transformation. We provide evidence that the entire pBS32 sequence may be part of the prophage and thus that competence inhibition may be linked to lysogeny.
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Omer Bendori, Shira, Shaul Pollak, Dorit Hizi, and Avigdor Eldar. "The RapP-PhrP Quorum-Sensing System of Bacillus subtilis Strain NCIB3610 Affects Biofilm Formation through Multiple Targets, Due to an Atypical Signal-Insensitive Allele of RapP." Journal of Bacteriology 197, no. 3 (November 24, 2014): 592–602. http://dx.doi.org/10.1128/jb.02382-14.

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The genome ofBacillus subtilis168 encodes eightrap-phrquorum-sensing pairs. Rap proteins of all characterized Rap-Phr pairs inhibit the function of one or several important response regulators: ComA, Spo0F, or DegU. This inhibition is relieved upon binding of the peptide encoded by the cognatephrgene.Bacillus subtilisstrain NCIB3610, the biofilm-proficient ancestor of strain 168, encodes, in addition, therapP-phrPpair on the plasmid pBS32. RapP was shown to dephosphorylate Spo0F and to regulate biofilm formation, but unlike other Rap-Phr pairs, RapP does not interact with PhrP. In this work we extend the analysis of the RapP pathway by reexamining its transcriptional regulation, its effect on downstream targets, and its interaction with PhrP. At the transcriptional level, we show thatrapPandphrPregulation is similar to that of otherrap-phrpairs. We further find that RapP has an Spo0F-independent negative effect on biofilm-related genes, which is mediated by the response regulator ComA. Finally, we find that the insensitivity of RapP to PhrP is due to a substitution of a highly conserved residue in the peptide binding domain of therapPallele of strain NCIB3610. Reversing this substitution to the consensus amino acid restores the PhrP dependence of RapP activity and eliminates the effects of therapP-phrPlocus on ComA activity and biofilm formation. Taken together, our results suggest that RapP strongly represses biofilm formation through multiple targets and that PhrP does not counteract RapP due to a rare mutation inrapP.
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Titok, Marina, Catherine Suski, Bérengère Dalmais, S. Dusko Ehrlich, and Laurent Jannière. "The replicative polymerases PolC and DnaE are required for theta replication of the Bacillus subtilis plasmid pBS72." Microbiology 152, no. 5 (May 1, 2006): 1471–78. http://dx.doi.org/10.1099/mic.0.28693-0.

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Plasmids are the tools of choice for studying bacterial functions involved in DNA maintenance. Here a genetic study on the replication of a novel, low-copy-number, Bacillus subtilis plasmid, pBS72, is reported. The results show that two plasmid elements, the initiator protein RepA and an iteron-containing origin, and at least nine host-encoded replication proteins, the primosomal proteins DnaB, DnaC, DnaD, DnaG and DnaI, the DNA polymerases DnaE and PolC, and the polymerase cofactors DnaN and DnaX, are required for pBS72 replication. On the contrary, the cellular initiators DnaA and PriA, the helicase PcrA and DNA polymerase I are dispensable. From this, it is inferred that pBS72 replication is of the theta type and is initiated by an original mechanism. Indirect evidence suggests that during this process the DnaC helicase might be delivered to the plasmid origin by the weakly active DnaD pathway stimulated by a predicted interaction between DnaC and a domain of RepA homologous to the major DnaC-binding domain of the cellular initiator DnaA. The plasmid pBS72 replication fork appears to require the same functions as the bacterial chromosome and the unrelated plasmid pAMβ1. Most importantly, this replication machinery contains the two type C polymerases, PolC and DnaE. As the mechanism of initiation of the three genomes is substantially different, this suggests that both type C polymerases might be required in any Cairns replication in B. subtilis and presumably in other bacteria encoding PolC and DnaE.
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Lawrenz, Matthew B., Hiroki Kawabata, Joye E. Purser, and Steven J. Norris. "Decreased Electroporation Efficiency in Borrelia burgdorferi Containing Linear Plasmids lp25 and lp56: Impact on Transformation of Infectious B. burgdorferi." Infection and Immunity 70, no. 9 (September 2002): 4798–804. http://dx.doi.org/10.1128/iai.70.9.4798-4804.2002.

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ABSTRACT The presence of the linear plasmids lp25 and lp56 of Borrelia burgdorferi B31 was found to dramatically decrease the rate of transformation by electroporation with the shuttle vector pBSV2, an autonomously replicating plasmid that confers kanamycin resistance (P. E. Stewart, R. Thalken, J. L. Bono, and P. Rosa, Mol. Microbiol. 39:714-721, 2001). B. burgdorferi B31 clones had transformation efficiencies that were either low, intermediate, or high, and this phenotype correlated with the presence or absence of lp25 and lp56. Under the conditions utilized in this study, no transformants were detected in clones that contained both lp25 and lp56; the few kanamycin-resistant colonies isolated did not contain pBSV2, indicating that the resistance was due to mutation. Intermediate electroporation rates (10 to 200 colonies per μg of DNA) were obtained with B31 clones that were either lp25− and lp56+ or lp25+ and lp56−. Clones in this group that initially contained lp25 lacked this plasmid in pBSV2 transformants, a finding consistent with selective transformation of lp25− variants. High transformation rates (>1,000 colonies per μg of DNA) occurred in clones that lacked both lp25 and lp56. Sequence analysis indicated that lp25 and lp56 contain genes that may encode restriction and/or modification systems that could result in the low transformation rates obtained with strains containing these plasmids. The previously reported correlation between lp25 and infectivity in mice, coupled with the barrier lp25 presents to transformation, may explain the difficulty in obtaining virulent transformants of B. burgdorferi.
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Dam, Bomba, Michael Kube, Somasri Dam, Richard Reinhardt, and Werner Liesack. "Complete Sequence Analysis of Two Methanotroph-SpecificrepABC-Containing Plasmids from Methylocystis sp. Strain SC2." Applied and Environmental Microbiology 78, no. 12 (April 13, 2012): 4373–79. http://dx.doi.org/10.1128/aem.00628-12.

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ABSTRACTThe complete nucleotide sequences of two large, low-copy-number plasmids of 229.6 kb (pBSC2-1) and 143.5 kb (pBSC2-2) were determined during assembly of the whole-genome shotgun sequences of the methane-oxidizing bacteriumMethylocystissp. strain SC2. The physical existence of the two plasmids in strain SC2 was confirmed by pulsed-field gel electrophoresis followed by Southern hybridization. Both plasmids have a conserved replication module of therepABCsystem and carry genes involved in their faithful maintenance and conjugation. In addition, they contain genes that might be involved in essential metabolic processes. These include several heavy metal resistance genes and copper transport genes in pBSC2-1 and a complete nitrous oxide reductase operon and apmoCsingleton in pBSC2-2, the latter encoding the PmoC subunit of particulate methane monooxygenase.
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Frank, Kristi L., Sharyl F. Bundle, Michele E. Kresge, Christian H. Eggers, and D. Scott Samuels. "aadA Confers Streptomycin Resistance in Borrelia burgdorferi." Journal of Bacteriology 185, no. 22 (November 15, 2003): 6723–27. http://dx.doi.org/10.1128/jb.185.22.6723-6727.2003.

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ABSTRACT To enhance genetic manipulation of the Lyme disease spirochete Borrelia burgdorferi, we assayed the aadA gene for the ability to confer resistance to the antibiotics spectinomycin and streptomycin. Using the previously described pBSV2 as a backbone, a shuttle vector, termed pKFSS1, which carries the aadA open reading frame fused to the B. burgdorferi flgB promoter was constructed. The hybrid flgB promoter-aadA cassette confers resistance to spectinomycin and streptomycin in both B. burgdorferi and Escherichia coli. pKFSS1 has a replication origin derived from the 9-kb circular plasmid and can be comaintained in B. burgdorferi with extant shuttle vector pCE320, which has a replication origin derived from a 32-kb circular plasmid, or pBSV2, despite the fact that pKFSS1 and pBSV2 have the same replication origin. Our results demonstrate the availability of a new selectable marker and shuttle vector for genetically dissecting B. burgdorferi at the molecular level.
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Rekhter, Dmitrij, Daniel Lüdke, Yuli Ding, Kirstin Feussner, Krzysztof Zienkiewicz, Volker Lipka, Marcel Wiermer, Yuelin Zhang, and Ivo Feussner. "Isochorismate-derived biosynthesis of the plant stress hormone salicylic acid." Science 365, no. 6452 (August 1, 2019): 498–502. http://dx.doi.org/10.1126/science.aaw1720.

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The phytohormone salicylic acid (SA) controls biotic and abiotic plant stress responses. Plastid-produced chorismate is a branch-point metabolite for SA biosynthesis. Most pathogen-induced SA derives from isochorismate, which is generated from chorismate by the catalytic activity of ISOCHORISMATE SYNTHASE1. Here, we ask how and in which cellular compartment isochorismate is converted to SA. We show that in Arabidopsis, the pathway downstream of isochorismate requires only two additional proteins: ENHANCED DISEASE SUSCEPTIBILITY5, which exports isochorismate from the plastid to the cytosol, and the cytosolic amidotransferase avrPphB SUSCEPTIBLE3 (PBS3). PBS3 catalyzes the conjugation of glutamate to isochorismate to produce isochorismate-9-glutamate, which spontaneously decomposes into SA and 2-hydroxy-acryloyl-N-glutamate. The minimal requirement of three compartmentalized proteins controlling unidirectional forward flux may protect the pathway against evolutionary forces and pathogen perturbations.
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8

Jacobs, Mary B., Steven J. Norris, Kathrine M. Phillippi-Falkenstein, and Mario T. Philipp. "Infectivity of the Highly Transformable BBE02− lp56− Mutant of Borrelia burgdorferi, the Lyme Disease Spirochete, via Ticks." Infection and Immunity 74, no. 6 (June 2006): 3678–81. http://dx.doi.org/10.1128/iai.00043-06.

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ABSTRACT Infectious Borrelia burgdorferi strains that have increased transformability with the shuttle vector pBSV2 were recently constructed by inactivating the gene encoding BBE02, a putative restriction-modification gene product expressed by the linear plasmid lp25 (Kawabata et al., Infect. Immun. 72:7147-7154, 2004). The absence of the linear plasmid lp56, which carries another putative restriction-modification gene, further enhanced transformation rates. The infectivity of these mutants was assessed previously in mice that were inoculated with needle and syringe and was found to be equivalent to that of wild-type spirochetes. Here we examined the infectivity of spirochetes to ticks after capillary inoculation of Ixodes scapularis nymphs and the subsequent spirochetal infectivity to mice via ticks by using B. burgdorferi B31 clonal isolates lacking lp56 and/or BBE02. The absence of lp56 (but not BBE02) correlated with a lower number of spirochetes in ticks after feeding on mice; this plasmid thus may play a role, albeit not an essential one, in supporting spirochetal survival in the feeding tick. Importantly, however, the absence of lp56 and BBE02 did not detectably influence infectivity to mice via ticks.
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9

Gurinovich, A. S., and M. A. Titok. "Molecular Genetic and Functional Analysis of the PBS72 Plasmid from Bacillus subtilis Environmental Isolates." Microbiology 89, no. 6 (November 2020): 660–69. http://dx.doi.org/10.1134/s0026261720060065.

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Darabi, Ali, Raza Forough, Gabu Bhardwaj, Misako Watabe, Goodarz Goodarzi, Steven C. Gross, and Kounosuke Watabe. "Identification and nucleotide sequence of the minimal replicon of the low-copy-number plasmid pBS2." Plasmid 22, no. 3 (November 1989): 281–86. http://dx.doi.org/10.1016/0147-619x(89)90015-2.

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Dissertations / Theses on the topic "Plasmid pBS32"

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Kambová, Milada. "SigN z Bacillus subtilis: Funkční charakterizace." Master's thesis, 2021. http://www.nusl.cz/ntk/nusl-446423.

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Bacillus subtilis strain 3610 is an ancestral undomesticated strain. It diers from the laboratory strain 168 in many aspects. One dierence in strain 3610 is the presence of plasmid pBS32 encoding the sigma factor N (σN). This σ factor is activated when DNA damage occurs and induces the bacteria's cell death. The aim of the Thesis was a systematic characterisation of σN-dependent transcription. First, I showed that plasmid-borne but not chromosome-borne predicted σN-dependent promoters were ac- tive in transcription in vitro. Next, the anities of RNAP with σN for DNA, initiating NTP (iNTP) were determined for both relaxed and supercoiled DNA templates. Sur- prisingly, the activity of RNAP on relaxed σN-dependent promoters was higher than on their supercoiled versions, an opposite trend than displayed by RNAP associated with other σ factors. This property of σN-dependent promoters was not encoded by the core promoter sequence. In summary, this Thesis contributed to our understanding of the bacterial transcription apparatus. 1
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