Effect of repair deficiency and R plasmids on spontaneous and radiation-induced mutability in Pseudomonas aeruginosa.
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The effect of R plasmids on spontaneous and radiation (ultraviolet and gamma)-induced mutability in Pseudomonas aeruginosa was studied in strains containing the radiation-sensitive markers polA3 or rec-2 and the revertable auxotrophic markers hisO27 and trpB1. In the absence of an R plasmid, the radiation-induced mutability was dependent on the recA+ genotype and independent of the polA+ genotype, whereas spontaneous mutability was similar in all genetic backgrounds. R plasmids pPL1, R2, and pMG15 increased the ultraviolet radiation survival and ultraviolet-induced mutability of wild-type and polA host cells but did not alter either effect in a recA mutant. These R plasmids also increased the gamma radiation survival and gamma-induced mutability of wild-type host cells bud pMG15 also enhanced the level of spontaneous mutagenesis in wild-type host cells but not in a polA or recA mutant. These data suggested that a common plasmid gene product(s) may participate in various recA-dependent, error-prone deoxyribonucleic acid repair pathways of P. aeruginosa. The properties of a mutant R plasmid, pPL2, originally selected because it lacked enhanced ultraviolet-induced mutability, supported this conclusion. (+info)
Activity of beta-lactam antibiotics against Pseudomonas aeruginosa carrying R plasmids determining different beta-lactamases.
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Azlocillin, carbenicillin, cefsulodin, mezlocillin, nocardicin A, piperacillin, pirbenicillin, sulbenicillin, and ticarcillin, but not HR756, showed reduced activity against Pseudomonas aeruginosa strains producing seven types of beta-lactamase. (+info)
Transfer of R factors to and between genetically marked sublines of Rhizobium japonicum.
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Plasmids R1822 and pRD1 of the P-1 incompatibility group, for which Rhizobium japonicum had not previously been shown to serve as host, were introduced into a strain of R. japonicum. Acquisition of R68 and R68.45 plasmids by this Rhizobium was equivocal. Transfer of R1822 from Pseudomonas aeruginosa and of pRD1 from Escherichia coli to R. japonicum was unambiguous, because the exconjugants subsequently cotransferred the three R-factor resistance determinants (kanamycin, tetracycline, and penicillin) between genetically marked sublines of strain I-110. Under optimal conditions the transfer of R1822 and pRD1 occurred at frequencies of approximately 10(-3) in plate matings of strains bearing as many as five dissimilar genetic markers. In matings with R1822 on membrane filters, recombinants were formed at incidences as high as 4%. (+info)
Nonenzymatic chloramphenicol resistance mediated by IncC plasmid R55 is encoded by a floR gene variant.
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The IncC plasmid R55, initially described in the 1970s and isolated from Klebsiella pneumoniae, confers nonenzymatic chloramphenicol resistance. The gene coding for this resistance was cloned and sequenced and shows 95 to 97% nucleotide identity with the recently reported floR gene from Salmonella enterica serovar Typhimurium DT104 and from Escherichia coli animal isolates, respectively, conferring cross-resistance to florfenicol. (+info)
Horizontal transfer of a multi-drug resistance plasmid between coliform bacteria of human and bovine origin in a farm environment.
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Multi-drug-resistant coliform bacteria were isolated from feces of cattle exposed to antimicrobial agents and humans associated with the animals. Isolates from both cattle and humans harbored an R plasmid of 65 kb (pTMS1) that may have been transferred between them due to selective antibiotic pressure in the farm environment. (+info)
Specialized transduction of kanamycin resistance in a Providence strain.
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Properties of a transducing system with a phage able to transduce a kanamycin-resistance marker of the T compatibility group plasmid R394 at a frequency of 2 times 10(-2)/plaque-forming unit adsorbed are described. The phage was detected in Providence strain P29 transduced to kanamycin resistance by Providence phage PL25 grown on this strain harbouring the R factor. Four P29 transductants, specially selected at the lowest multiplicities of infection of the high frequency transducing (HFT) phage, were defective lysogens. They plated PL25 with an efficiency of I and only one liberated low-titre phage spontaneously or on u.v. induction. The defect in maturation function could be corrected by introduction of a wild PL25 prophage. The transducing phage was serologically frequency was increased by the simultaneous presence of homologous non-transducing phage. Transductants did not transfer the kanamycin-resistance marker by conjugation, and produced kanamycin-sensitive segregants at a moderate rate. These segregants could be transduced to kanamycin resistance by the HFT phage. Irradiation of HFT lysates by u.v. produced an exponential fall in transduction frequency. It was concluded that the defective phage transduced by lysogenization. Kanamycin-resistant transductants could themselves be transduced by streptomycin resistance by PL25 reared on a streptomycin-resistant mutant. Lysogenic transductants produced by the HFT phage did not always liberate HFT phage on u.v. induction. Possible explantations are considered. (+info)
Characterization and comparison of chloramphenicol acetyltransferase variants.
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1. Variants of chloramphenicol acetyltransferase from a variety of bacterial species have been isolated and purified to homogeneity. They constitute a heterogeneous group of proteins as judged by analytical affinity and hydrophobic ('detergent') chromatography, native and sodium dodecyl sulfate electrophoresis, sensitivity to sulfhydryl specific reagents, steady state kinetic analysis, and reaction with antisera. 2. The most striking observation is that three variants of chloramphenicol acetyltransferase (R factor type III, Streptomyces acrimycini, and Agrobacterium tumefaciens) possess an apparent subunit molecular weight (24,500) which is significantly greater than that of all other variants examined (22,500). The three atypical variants are not identical since they show marked differences in a number of important parameters. 3. Although the fundamental mechanism of catalysis may prove to be identical for all chloramphenicol acetyltransferase variants, there is a wide range of sensitivity to thiol-directed inhibitors among the enzymes studied. 4. Amino acid sequence analysis of the N-termini of selected variants suggests that the qualitative differences among chloramphenicol acetyltransferase variants is a reflection of structural heterogeneity which is most marked in comparisons between variants from Gram-positive and Gram-negative species. (+info)
Formation of methyl mercury by bacteria.
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Twenty-three Hg2+-resistant cultures were isolated from sediment of the Savannah River in Georgia; of these, 14 were gram-negative short rods belonging to the genera Escherichia and Enterobacter, six were gram-positive cocci (three Staphylococcus sp. and three Streptococcus sp.) and three were Bacillus sp. All the Escherichia, Enterobacter, and the Bacillus strain were more resistant to Hg2+ than the strains of staphylococci and streptococci. Adaptation using serial dilutions and concentration gradient agar plate techniques showed that it was possible to select a Hg2+-resistant strain from a parent culture identified as Enterobacter aerogenes. This culture resisted 1,200 mug of Hg2+ per ml of medium and produced methyl mercury from HgCl2, but was unable to convert Hg2+ to volatile elemental mercury (Hg0). Under constant aeration (i.e., submerged culture), slightly more methyl mercury was formed than in the absence of aeration. Production of methyl mercury was cyclic in nature and slightly decreased if DL-homocysteine was present in media, but increased with methylcobalamine. It is concluded that the bacterial production of methyl mercury may be a means of resistance and detoxification against mercurials in which inorganic Hg2+ is converted to organic form and secreted into the environment. (+info)