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Deficient dwarf colony (DDC) mutants of E. coli K 12, harboring or no resistance plasmids, were obtained in vitro. The R plasmids of parental strains and to DDC mutants were transfered by conjugation to normal colony, and to DDC mutants of E. coli K 12; the frequencies of transfer were similar for all strains studied.
The TOL catabolic plasmid was shown to be compatible with the R91 drug resistance plasmid. However, the TOL plasmid was extremely unstable in mutant PA03 of P. aeruginosa. By selecting for stabilization of the TOL plasmid in PA03 harbouring R91, it was possible to isolate a strain in which markers from both R91 and TOL appeared to exist in a single recombinant plasmid. This plasmid, pND3, encoded resistance to carbenicillin, was able to transfer at the same frequency as the R91 plasmid and encoded the ability to grow on m-toluate, p-toluate, m-xylene, p-xylene and toluene. In addition, it was shown to be incompatible with the NAH catabolic plasmid and it could be transferred by transduction. The TOL plasmid could stabilize in PA03 harbouring R91 without fusion with R91, and could stabilize in PA03 in the absence of R91. PA03 harbouring either the recombinant plasmid or the stable TOL plasmid in the absence of R91 could promote bacterial chromosome transfer between mutant derivatives of P. aeruginosa strain PA0.
The origin and direction of replication of the resistance plasmid R100.1 and its resistance transfer factor derivative, pAR132, were studied by electron microscopy autoradiography of partially denatured molecules and partial denaturation mapping of replicative intermediates. Results of these studies indicate the existence of an origin of replication at 8.8 kilobases on the R100 map. Replication from this origin in cultures synchronized for initiation of replication is predominantly unidirectional in a single direction.
Multiple drug resistance plasmid NR1 is shown to code for at least 10 low molecular weight RNAs. These species, ranging in size from 60 to 120 nucleotides, have been purified from minicells by two-dimensional gel electrophoresis and characterized by RNase T1 fingerprinting. Hybridization of purified RNAs to restriction endonuclease digests of NR1 DNA indicates that most are derived from the resistance transfer factor region of the plasmid genome. One RNA was found to be coded by the transposable tetracycline resistance element Tn10, and several are associated with DNA fragments that contain origins of replication.
The bacterial drug resistance plasmids R711b and R778b, at present classified in the X incompatibility group, determine pili (designated 711) that resemble F pili morphologically. Like F pili, 711 pili adsorb F-specific filamentous bacteriophages to their tips, though more often in pairs, than singly. However, F-specific RNA-containing bacteriophages are not adsorbed to their sides, and strains carrying the plasmids are resistant to these phages. Pili determined by the only IncFV plasmid Folac are similar to 711 pili in their phage adsorption properties, but they are serologically different, as are F pili. It is concluded that F, Folac and 711 pili have basic differences in spite of a morphological resemblance.
Resistance plasmids were transferred in urine from a multi-drug-resistant Serratia marcescens to Escherichia coli. Transfer of resistance to kanamycin, tetracycline, chloramphenicol, streptomycin, ampicillin, and carbenicillin occurred readily after 4 h of incubation at room temperature (25 degrees C). The urinary catheter collection bag is postulated as a potential site for extraintestinal resistance plasmid transfer in the Enterobacteriaceae, especially for pathogens such as Serratia, which do not frequently colonize the intestinal tract.
A possibility of transfer of chloramphenicol-resistance and penicillin-resistance plasmids from 4 different donor S. epidermidis strains to 2 S. aureus strains was demonstrated. Chloramphenocol-resistance plasmid was found in S. epidermidis 1065/77 which was not expressed in this strain but could be transferred to and was expressed in Staphylococcus aureus strains. Penicillin-resistance and chloramphenicol-resistance plasmids were transferred simultaneously in 40 per cent of the colonies.
Experiments on elimination and transfer of resistance-plasmids in S. aureus (controlling resistance to penicillin, chloramphenicol and oxytetracycline) show that these plasmids have no restricting influence on phages used for typing of staphylococci. Prophages in lysogenic strains control a mechanism of restriction and modification which is active on phages and on chromosomal markers. The resistance-plasmids used in these experiments are insensitive to prophage controlled restriction.
Several antiseptic and disinfectant compounds have been investigated for their minimal inhibitory concentration (MIC) against antibiotic multiresistant strains of S. wien and S. bredeney as well as S. typhi and S. typhimurium strains characterized by wide spectrum of antibiotic sensitivity. The MICs of AgNO3, merthiolate, NaN3, phenol, Zephiran and Desogen were not substantially different for the former and the latter strains; on the contrary, the HgCl2 minimal inhibitory concentration was significantly higher against S. wien and S. bredeney than against the other strains. The mercury resistance appeared plasmid controlled and transferable to E. coli K-12, always associated with antibiotic resistance. The findings, which confirm the results of other AA., seem unrestrictive of the use of HgCl2, because its not probable selective role in the hospital environment.
Detailed examination of the structure of cloned DNA fragments of the R6-5 antibiotic resistance plasmid has revealed a substantial degree of polynucleotide sequence heterogeneity and indicates that sequence rearrangements in plasmids and possible other replicons occur more frequently than has hitherto been appreciated. The sequences changes in cloned R6-5 fragments were shown in some instances to have occurred prior to cloning, i.e. existing in the original population of R6-5 molecules that was obtained from a single bacterial clone and by several different criteria judged to be homogeneous, and in others to have occurred either during the cloning procedure or during subsequent propagation of hybrid molecules. The molecular changes that are described involved insertion/deletion of the previously characterized IS2 insertion element, formation of a new inverted repeat structure probably by duplication of a preexisting R6-5 DNA sequence, sequence inversion, and loss and gain of restriction endonuclease cleavage sites.
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Hly plasmide of wild type and its derepressive (by transmission) mutant communicated to the E. coli cells an increased resistance to the action of ultraviolet rays. Hly plasmide failed to compensate the defects associated with the excision and postreplicative DNA reparation or the reparative DNA synthesis. Hly plasmide increased the resistance to the ultraviolet light in the lon--mutant in which the ultraviolet irradiation disturbed the process of cell division. It is supposed that the resistance to the ultraviolet light connected with Hly plasmide was caused by the influence of the plasmide on some stages of cell division following the ultraviolet irradiation.
The wide host-range antibiotic resistance plasmid RP1 was transferred from Pseudomonas aeruginosa via Escherichia coli into Pseudomonas glycinea. The plasmid was then acquired by Pseudomonas phaseolicla both in vitro and in planta in Phaseolus limensis leaves and pods. This was the first step in the design of a model system to determine the possible epidemiological significance of antibiotic resistance plasmids in the control of plant disease.
A possibility of conjugation transfer of the markers of the plasmid resistance to gentamicin and other antibiotics from 10 clinical strains of Ps. aeruginosa, isolated from burn patients to the recipient strain of Ps. aeruginosa PTO 629 Rfr was shown. The marker of gentamicin resistance was transferred to 100 out of 110 of the exconjugants, i.e. 86.2 per cent. The rate of the conjugation transfer in the crosses between the clincal strains of Ps. aeruginosa and the recipient strain PTO 629 Rfr with respect to the gentamicin marker was about 10--7. The plasmid resistance markers in the clincal strains Ps. aeruginosa were transferred in various combinations. Transfer of the markers of resistance to streptomycin, carbenicillin, neomycin and combinations Sm, Nm and Sm, Nm, Cm was not achieved.
Despite targeting by CRISPR-Cas system, antimicrobial resistance plasmids are prevalent in clinical isolates of carbapenem-resistant Klebsiella pneumoniae which represent a major public health threat. A stable co-existence of plasmids and CRISPR-Cas systems is mediated by anti-CRISPR (Acr) proteins. Here, we report that previously identified AcrIE10 encoded by a resistance plasmid combines two functions: it inhibits CRISPR immunity by directly binding Cas7* subunit through its Acr domain, and acts as an Acr-associated (Aca) protein that self-represses the transcription of Acr locus. AcrIE10 is an example of an Aca protein that utilizes N-terminal ribbon-helix-helix (RHH) domain to specifically recognize the inverted repeat (IR) region in its own promoter. Crucially, a dimerization of AcrIE10 dimers is required for the effective binding to the IR and self-repression, while stoichiometry-dependent interaction with Cas7* facilitates transition to de-repressed state. These findings elucidate molecular mechanisms by which AcrIE10 operates as a dual functionAcr-Aca protein to achieve a delicate balance between host CRISPR-Cas immunity and plasmid anti-defense.
Drug resistance in Staphylococcus aureus is frequently mediated by non-chromosomal DNA molecules referred to as R plasmids. So far, resistance to aminosidic antibiotics was observed with streptomycin [8] and kanamycin-neomycin [3]. Resistance to gentamycin has not been reported in a recent survey by Lacey [7]. In this paper, we describe a strain of S. aureus resistant to gentamycin-kanamycin-tobramycin-sisomycin, and experiments which suggest that the genetic determinant of these resistance characters is plasmid borne.
Antibiotic resistance plasmids from organisms that had caused serious epidemics, including those responsible for epidemics of chloramphenicol-resistant typhoid fever and dysentery in Central America, were transferred to a strain of Salmonella typhimurium and of Salmonella gallinarum. The virulence and infectivity of these R(+) forms were then compared with the R(-) parent forms in orally inoculated chickens.None of the R(+) forms were more virulent than their R(-) parent forms. The mortality rates they produced were either the same as or less than that of their R(-) parent forms. The mortality rates were not increased by feeding the chickens on diets containing antibiotics against which the plasmids provided resistance.The removal of the plasmids from some R(+) forms of decreased virulence was not accompanied by any alteration in virulence, indicating that they were less virulent mutants of the parent strain that had conjugated preferentially. In other cases their virulence was increased, indicating that the very possession of the plasmid was involved in their decreased virulence. Of four forms of the S. gallinarum strain harbouring the plasmid that had been incriminated in the Central American dysentery outbreak, one was as virulent as the parent R(-) form and the other three were less virulent. Preferential conjugation by an avirulent mutant was responsible for the lack of virulence of one of them but the very possession of the plasmid appeared responsible for the decreased virulence of the other two. The decreased virulence of de-repressed F(+) and I(+) forms of the S. typhimurium strain was increased to that of repressed F(+) form and of the parent form by plasmid removal.Organisms of the R(+) forms of the S. typhimurium strain were not excreted in larger amounts or for longer periods of time by infected chickens than organisms of the R(-) parent form were. Neither did organisms of the R(+) forms of this strain or the S. gallinarum strain spread more rapidly or more extensively from infected chickens to in-contact chickens than organisms of the R(-) parent forms did. When antibiotics against which the infecting R(+) organisms provided resistance were included in the diet of these chickens the R(+) organisms were usually excreted in greater amounts, for longer periods of time and spread more rapidly and more extensively from the infected chickens to the in-contact chickens.
A 2.1-kilobase segment of the antibiotic resistance plasmid R6K carries sufficient information to replicate as a plasmid in Escherichia coli. This segment contains a functional origin of replication and a structural gene for a protein, designated pi, that is required for the initiation of R6K replication. The nucleotide sequence of a 520-base-pair portion of this 2.1-kilobase segment that includes the functional origin of replication and the region adjacent to the start of the pi structural gene was determined. A striking feature of the sequence is the presence of seven 22-base-pair direct repeats joined in tandem in the region adjacent to the start of the pi gene. A possible role of the tandem repeats in the regulation of expression of the pi protein and the control of initiation of replication of the plasmid R6K is discussed.