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PubMed1975

A plasmid involved in chloramphenicol production in Streptomyces venezuelae: evidence from genetic mapping.

To test the hypothesis that chloramphenicol production in Streptomyces venezuelae depends on the presence of a plasmid, mapping analysis was carried out by using eight markers in addition to chloramphenicol production and melanoid pigment formation. The sequence of the eight markers was determined on a circular linkage map as follows: -his-ade-str-leu-lys-met-ilv-pro-(his-). This sequence resulted in the frequency of quadruple crossover (q.c.o.) recombinants having the lowest value, 3-2 to 4-9%. However, the character of chloramphenicol non-production, which was obtained by incubating mycelia with acriflavin, was not required to explain the results. From these results and other tests, it is concluded that chloramphenicol production is controlled by a plasmid. This plasmid appeared to be non-transferable in conjugation.

Acriflavine↗
PubMed1975

Effect of inorganic phosphate on acridine inhibition and plasmid curing in Escherichia coli.

Some mutants and stock strains of Escherichia coli K12 were sensitive to acriflavine in the presence of inorganic phosphate but were resistant to acriflavine in its absence. They mutated spontaneously to resistance to acriflavine plus phosphate. The synergistic effect of phosphate on acriflavine sensitivity was increased at high pH values. Genetic analysis suggested that the mutations occurred in the gene acrA. Electron microscopic observation suggested that the presence of acriflavine plus phosphate affected the structure of the plasma membrane and the cytoplasm under it. This structural alteration was not caused by acriflavine alone. Acridine orange plus phosphate can more effectively eliminate the plasmid F8-gal+ than acridine orange alone.

Acridines↗
PubMed1976

The elimination of urease activity in Streptococcus faecium as evidence for plasmid-coded urease.

A strain of Streptococcus faecium from the sheep rumen showed spontaneous loss of urease activity when subcultured at the normal rumen temperature of 38 degrees C, although in mixed cultures in vivo or in vitro loss of urease was not apparent. The rate of loss of urease in pure cultures was increased at incubation temperatures above 38 degrees C, but loss was never complete. However, at temperatures below 38 degrees C loss was greater, and at 22 or 18 degrees C the urease was completely eliminated. Incubation with sodium dodecyl sulphate (0-002%) or ethidium bromide (2-5 X 10(-5)M) caused complete loss of urease activity. The urease activity was also eliminated when the streptococcus was grown aerobically, and this loss of activity was irreversible. It is suggested that the urease activity is controlled by a plasmid gene and that aeration, low growth temperature and chemical agents 'cure' the streptococcus of the plasmid. Attempts to demonstrate the presence of covalently closed circular extrachromosomal DNA by caesium chloride-ethidium bromide equilibrium density-gradient centrifugation were unsuccessful.

Aerobiosis↗
PubMed1976

Further observations on the association of the colicine V plasmid of Escherichia coli with pathogenicity and with survival in the alimentary tract.

A high proportion of invasive strains of Escherichia coli produced colicine V. This property was easily eliminated from 20 of 21 of these strains by 'curing' agents, especially sodium lauryl sulphate, indicating that the genes determining it were located on a plasmid (ColV) which was transmitted from ten of the strains by conjugation. Inoculated intramuscularly, the ColV- forms of all 17 strains tested were less pathogenic for chickens than the corresponding ColV+ forms. The pathogenicity of the ColV- forms of four strains was increased, usually to that of the ColV+ form from which they were derived, by implanting other ColV determinants in them. Much higher concentrations of organisms were found in the blood and liver of chickens infected with ColV+ forms than in chickens infected with ColV- forms. Inoculated intraperitoneally, the ColV+ form of one of the strains, BI88, was more pathogenic for mice than the ColV- form; much higher concentrations of organisms were found in the peritoneal fluid and blood of ColV+-inoculated mice than of ColV--inoculated mice. Inoculated orally and intravenously, ColV+ forms were more pathogenic for colostrum-deprived calves than the corresponding ColV- forms. After mixtures of ColV+ and ColV- organisms of the same strain in ratios of 1:10,1:100 or 1:1000 were given orally, they were found in a similar ratio in the contents of the alimentary tract 1 to 2 days later, when the calves were near to death. Many more ColV+ than ColV- organisms were found in the mesenteric lymph nodes, the deeper tissues and the blood; in the urinary and gall bladders, locations remote from the defence mechanisms of the body, the numbers of ColV- organisms sometimes exceeded those of ColV+ organisms. Colicine V, although demonstrated in the blood at death, did not appear adversely to influence the concentration of ColV- organisms in these calves. Several days after mixtures of ColV+ and ColV- organisms of strain BI88 were taken orally by two human beings, the ColV+ organisms became much more numerous in their faeces than the ColV- ones. Similar results were obtained when colVr organisms of BI88 were included in the inoculum or when a strain whose ColV- form was completely colicine V-resistant was studied. A ColE+ form of BI88 ColV- was no more pathogenic for chickens, mice or colostrum-deprived calves than was a ColE- form of this strain, and it did not persist in the faeces of the two human beings for longer than the ColE- form.

Animals↗
PubMed1976

Extrachromosomal DNA in chloramphenicol resistant myxococcus strains.

The presence of extrachromosomal DNA in strains of Myxococcus xanthus and M fulvus was examined by rate-zonal centrifugation of radioactively-labelled DNA in 'cleared lysates'. All the strains examined contained extrachromosomal DNA, with the exception of M. xanthus FBt. Chloramphenicol resistance is inducible in M. xanthus FBt. A peak of extrachromosomal DNA, containing covalently closed molecules, was found in one of the induced strains, implying that induction of chloramphenicol resistance is associated with the production of a plasmid. By incubating R+ strains of Escherichia coli with myxococci, R factor-mediated chloramphenicol resistance can be introduced into the latter. Evidence of extra chromosomal DNA in a derivative of M. xanthus with chloramphenicol resistance from R factor RI. 19 unique to the chloramphenicol strain, was obtained. By using a double-labelling technique, several chloramphenicol-resistant strains of M. fulvus M were examined. Evidence for a peak, unique for the chloramphenicol-resistant strain, was found in a strain with resistance derived from the R factor, S-a, but not from comparable strains with resistance derived from R factors R57b, R1. 19 and R478.

Chloramphenicol↗
PubMed1976

Genetic studies on SCP1-prime strains of Streptomyces coelicolor A3(2).

SCP1'-cysB carries a short chromosomal insertion: cysB was the only chromosomal locus identified on this plasmid; the plasmid was seldom lost; and a comparatively low frequency of crossing-over between the exo- and endogenote in a cysB+/cysB+ heterozygote. SCP1'-argA, uraB carries a longer chromosomal insertion: five chromosomal loci have been detected on the plasmid; it was very often lost; and there was frequent crossing-over between exo- and endogenote in heterozygous strains. Both SCP1' plasmids gave rise to plasmids closely resembling, or perhaps identical with, the original SCP1 by deletion of the chromosomal insertion. Markers argA and uraB were always deleted together from SCP1'-argA, uraB, whereas random deletion should more often have removed uraB alone. This suggests that special DNA sequences are involved in SCP1' formation. An analysis of recombination between exo- and endogenote within a double heterozygote for argA and uraB supports the hypothesis that single copies of plasmid and chromosome assort from a pool of interacting molecules at, or immediately before, spore formation. A strain carrying the SCP1'-cysB plasmid gave rise to a 'bidirectional' donor of chromosomal markers in which the plasmid had apparently integrated into the chromosome at or close to the cysB locus.

Anti-Bacterial Agents↗
PubMed1976

The formation of a dissociable plasmid cointegrate from the Flac factor and the resident plasmid of Salmonella typhimurium LT2.

The Flac factor showed unstable maintenance in Salmonella typhimurium dnaC MP10LT2. The properties of a more stable lac+ derivate (SD-1) are described. SD-1 was ts and carried the fi+ property and the ability to transfer the lac+ character. It contained a large plasmid of molecular weight about 129 X 10(6) DALTONS. The properties of SD-1 and its derivatives suggested that the large plasmid was a cointegate of Flac and the MP10lt2 plasmid. Lac+ transfer was efficient from SD-1 to M799 MP10LT2 and one lac+ exconjugant contained the intact cointegrate. The cointegrate was not successfully transferred to strains lacking MP10LT2. It dissociated into apparently unaltered Flac and MP10LT2 plasmids, but the deletion of small parts of one or both plasmids during cointegrate formation could not be ruled out. Cointegrate dissociation was more marked in M799 than in SD-1 especially during growth in glucose-Casamino acids minimal medium. In the presence of R1drd19, the cointegrate (like the MP10LT2 plasmid) was stable maintained in the dnaC strain; maintenance of Flac was, however, unstable. It seems likely that replication of the cointegrate was controlled by the MP10LT2 plasmid constitutent.

Conjugation, Genetic↗
PubMed1976

Mechanisms of resistance to fusidic acid in Staphylococcus aureus.

The biochemical mechanisms of resistance to fusidic acid in Staphylococcus aureus were investigated. Organisms possessing plasmid genes for resistance showed a high basal level of resistance, but could be induced to higher levels after pre-incubation with fusidic acid. This induction occurred rapidly and probably did not depend on gene dosage effects. Mutants resistant to fusidic acid, obtained from plasmid-negative cultures, expressed resistance constitutively. Protein synthesis in cell-free extracts from staphylococci with plasmid-mediated resistance to fusidic acid was as sensitive to fusidic acid as was synthesis in preparations from sensitive organisms; whereas protein synthesis in preparations from a spontaneous fusidic acid resistant mutant was resistant to the antibiotic. None of the resistant strains caused detectable inactivation of fusidic acid and no new derivative of fusidic acid was found in culture extracts of plasmid-possessing organisms grown in the presence of radioactive antibiotic. Expression of plasmid-mediated resistance to fusidic acid was associated with a decrease in the molar ratio of phosphatidylglycerol to lysylphosphatidylglycerol, but the cardiolipin content remained constant.

Bacterial Proteins↗
PubMed1977

Genetic determination of methylenomycin synthesis by the SCP1 plasmid of Streptomyces coelicolor A3(2).

Evidence is presented that genes determining the pathway of methylenomycin A synthesis are carried on the SCP1 plasmid. All 16 mutations (mmy) leading to lack of antibiotic synthesis were SCP1-linked. Phenotypic classification, by co-synthesis and other criteria, suggested that they fell into at least five classes. When the wild-type SCP1 plasmid was transferred to Streptomyces lividans or Streptomyces parvulus, material that was chromatographically and biologically indistinguishable from methylenomycin A was produced. Recombination between some pairs of mmy mutations was detected. In crosses of mmy mutants of NF (integrated SCP1 donor) strains with SCP1-, a very high frequency of chromosomal recombination occurred; thus methylenomycin production appears not to be an important cause of the ultra-fertility normally associated with NF X SCP1- crosses.

Anti-Bacterial Agents↗
PubMed1977

Chloramphenicol acetylransferase-independent chloramphenicol resistance in Streptomyces coelicolor A3(2).

Streptomyces coelicolor A3(2) and S. lividans 66, which lack chloramphenicol acetyltraferase, gave rise to vhloramphenicol-sensitive (CmlS) variants spontaneously at frequencies of 0-5 to 2%. The fertility type of S. coelicolor in respect of the SCPI plasmid (SCPI+, SCPI- or NF) had no effect on chloramphenicol sensitivity or on the frequency at which CmlS variants arose. CmlS isolates spontaneously reverted to CmlR at frequencies one to three orders of magnitude lower than the frequency with which CmlS strains arose from CmlR. CmlR revertants obtained spontaneously from CmlS clones again produced CmlS isolates at the normal frequency of several per cent. Therefore, CmlS and CmlR are reversible phenotypes. In crosses between marked CmlR and CmlS S. coelicolor strains, transfer of chloramphenicol resistance into the sensitive strain apparently occurred independently of chromosomal recombination. Mapping experiments excluded the possibility that segregation of a chromosomal locus determines CmlR versus CmlS phenotype. In crosses between SCPI- strains, fertility was not significantly different in CmlR x CmlS, CmlR x CmlR and CmlS x CmlS combinations. Covalently closed circular DNA from CmlS and CmlR strains of S. coelicolor was indistinguishable in molecular weight and restriction endonuclease cleavage pattern. It is suggested that chloramphenicol resistance in S. coelicolor A3(2) is affected by some kind of transposable genetic element that may be capable of extra-chromosomal existence.

Acetyltransferases↗
PubMed1977

Transfer and expression of pseudomonas plasmid RP1 in Caulobacter.

This study demonstrates that the host range of Pseudomonas plasmid RP1 includes the genus Caulobacter. Caulobacter was shown to acquire three antibiotic resistance markers located in RP1. A fourth plasmid marker, susceptibility to an RNA bacteriophage, was not expressed, but could be transferred from Caulobacter to Escherichia coli. The lack of phenotypic expression of the phage marker was manifested by the inability of the phage to adsorb or to produce plaques on Caulobacter transcipients. Matings of Pseudomonas aeruginosa and Caulobacter vibrioides CV6 were carried out in the presence of bacteriophage phi6, a DNA phage that infects and kills only swarmer cells of Caulobacter. No decrease in plasmid transfer in the presence of phage phi6 was detected, suggesting that stalked cells, and not swarmer cells, serve as recipients. Our evidence suggests that transfer of chromosomal segments from Caulobacter may be mediated by plasmid RP1; such segments are not stably maintained.

Anti-Bacterial Agents↗