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At least 19 recordsLinked to original sources
PubMed1976

Acceptance and transfer of R-factor RP1 by members of the "herbicola" group of the genus Erwinia.

The R-factor RP1 was transferred by conjugation from Pseudomonas aeruginosa PAO12r(RPI) to various strains of Erwinia herbicola and to one strain of Erwinia stewartii. The exconjugate strains had minimum inhibitory concentration values for carbenicillin, kanamycin, neomycin, and tetracycline somewhat lower than the corresponding values for the pseudomonad RP1 donor strain. The biochemical characteristics of the exconjugant strains displayed minor variation in some instances from those of the corresponding R- strains. Sensitivity of the RP1+ strains to the RP1-specific bacteriophages PRD1 and PRR1 varied from an efficiency of plating [compared with P. aeruginosa PA067(RP1)] of 0 [E. herbicola Y46(RP1)] to 133 [E. herbicola Y190(RP1)] and 148 [E. stewartii SS104R(RP1)] for PRD1, and from 0 [E. herbicola Y46(RP1)] to 0.0002 [E. herbicola Y185(RP1)] and 18.4 [E. stewartii SS104R(RP1)] for PRR1. The phage-resistant strain E. herbicola Y46(RP1), would donate, by conjugation, the R-factor to E. herbicola Y46rifr, P, aeruginosa PAT900, or Escherichia coli UB1005 only at extremely low frequencies, if at all. Transformation of E. coli JC7620 by covalently closed circular DNA from E. herbicola Y46(RP1) gave and E. coli R+ strain exhibiting the expected antibiotic resistance pattern and having the ability to donate RP1 by conjugation. It is suggested (i) that some strains of E. herbicola RP1 either do not produce RP1 pili or produce defective pili, and (ii) that sensitivity to the bacteriophages PRD1 and PRR1 is not a suitable means of diagnosing the presence RP1 in E. herbicola strains.

Bacteriophages↗
PubMed1978

Influence of R-plasmid RP1 of Pseudomonas aeruginosa on cell wall composition, drug resistance, and sensitivity to cold shock.

R-plasmid RP1 was transferred to Pseudomonas aeruginosa cells, as indicated by their resistance to carbenicillin, ampicillin, cephaloridine, kanamycin, and tetracycline, and by the presence of a periplasmic beta-lactamase. The wild-type cells (RP1-) were lysed by ethylenediaminetetraacetic acid but not by ethylene-glycol-bis(2-aminoethyl ether)-N,N-tetraacetic acid, whereas cells carrying the plasmid (RP1+) were resistant to both these chelating agents. RP1+ and RP1- strains were both sensitive to the lytic action of polymyxin B and the lethal action of cold shock, but the effect was less marked in the RP1+ cultures. A proportion of the RP1+ cells surviving cold shock lost resistance to carbenicillin, tetracycline, and kanamycin. The chemical composition of whole cells and cell walls of RP1+ differed from that RP1- in the content of cation, phospholipid, and markers for lipopolysaccharide and peptidoglycan. Differences in cell wall composition, response to ethylenediaminetetraacetic acid and polymyxin B, and the effects of cold shock are all compatible with the hypothesis that RP1 confers changes in the cell envelope, probably in the outer membrane, of P. aeruginosa.

Ampicillin↗
PubMed1976

The properties of hybrids formed between the P-group plasmid RP1 and various plasmids from Pseudomonas aeruginosa.

R38, R931-1, and R933 are conjugative plasmids derived from strains of Pseudomonas aeruginosa. They confer resistance to mercuric ions (Hg-r), and do not tranfer from P. aeruginosa to Escherichia coli at detectable frequencies. Hybrids between each of these plasmids and the P-group plasmid, RP1, have been detected among the rare Hg-r transconjugants arising from matings of P. aeruginosa PAO donors (RP1 + R+) and E. coli K12 recipients. Two independently isolated hybrid plasmids from each of the three mating combinations have been studied. All were found to confer the entire marker phenotype of RP1, but only the Hg-r phenotype of their second parent. Moreover, all were larger than RP1 but comprised only two groups of sizes; those increased by about 14 x 10(6) daltons (the RP1/R38 hybrids), and those increased by about 30 x 10(6) daltons (the RP1/R931-1 and RP1/R933 hybrids). The hybrid plasmids were all too large to be transduced intact by phage F116L, but tranduction of fragments was possible. Thus, the determinants for both carbenicillin-resistance (Cb-r) (from RP1) and mercuric-ion-resistance could be "rescued" by recipients that already carried an RP1-like plasmid and were recombination-proficient. A molecular analysis of the plasmids recovered from such transductants suggested that each of the parental hybrids was comprised of an entire RP1 genome into which a fragment of heterologous DNA had been inserted. In similar experiments in which the recipient carried a derivative of R931-1, the Hg-r but not the Cb-r determinant could be rescued. This suggested that R38, R931-1, and R933 shared sufficient homology in the region of the mer gene for recombination to occur between them. The reason for the inability to rescue the Cb-r determinant was also investigated.

Chromosome Mapping↗
PubMed1977

Transposition of a beta-lactamase locus from RP1 into Pseudomonas putida degradative plasmids.

The beta-lactamase gene from the RP1 plasmid transposes into at least two Pseudomonas putida degradative plasmids. Donor strains that carry RP1 (bla+ tet+ aphA+) and a degradative plasmid yield transconjugants that have only the bla+ marker of RP1. This occurs in up to 80% of all bla+ transconjugants. Segregation of the bla+ marker requires the presence of a degradative plasmid in the donor and is only observed in transconjugants that have received degradative markers. The bla+ tet aphA transconjugants show 100% linkage of bla+ to degradative markers in conjugation,transduction, and transformation crosses. A transduction cross of an (RP1), (SAL) donor shows that 8% of all SAL plasmids also carry the transposed bla+ marker. Tn401 is the name we assign to the bla+ transposon from RP1 observed in Pseudomonas. Its identity with the RP1 bla+ transposon observed in Escherichia coli is not known. In four cases, Tn401 has inserted into the camphor genes of the CAM-OCT plasmid.

Alkanes↗
PubMed2025

Exome sequencing identifies a homozygous splice site variant in RP1 as the underlying cause of autosomal recessive retinitis pigmentosa in a Pakistani family.

BACKGROUND: Mutations in RP1 gene are the third leading cause of inherited retinal dystrophies (IRDs) in Pakistani families. PATIENTS: A two-generation consanguineous Pakistani family underwent both clinical and genetic analyses. Clinical examinations included visual acuity test, visual field, fundoscopy, and ocular coherence tomography (OCT). Whole exome sequencing (WES) was performed on the proband's DNA, and Sanger sequencing was performed to validate the WES findings. Splicing prediction tools such as Human Splicing Finder (HSF), NNSplice predictor, SpliceAI, MaxENTScan, and SpliceRover were used. RESULTS: A nuclear family of seven children, comprising five affected individuals (four males and one female) and two healthy siblings, was recruited from northwestern Pakistan. The proband was a 49-years old male who was presented with complaints of decreased visual acuity and night blindness since early childhood. Upon clinical evaluation, the proband appeared to have severely reduced visual acuity of hand movement (HM), bilateral visual field constriction, a waxy pale disc with vascular attenuation, pigmentary bone spicules at the periphery associated with chorioretinal degeneration, diffuse macular atrophy, and horizontal nystagmus in both of his eyes. Exome sequencing (ES) in the proband identified a homozygous splice site variant (NM_006269.2: c.615 + 1G > A) in RP1 gene. In-silico analysis, genotype-phenotype co-segregation study, and literature survey strongly supported the causality of the detected variant. CONCLUSIONS: We report a previously known pathogenic splice site variant of RP1 as the underlying cause of early-onset autosomal recessive retinitis pigmentosa (arRP) in a Pakistani family. We contemplate that the detected allele might constitute a mutational hotspot in RP1.

Humans↗
PubMed1979

Relationship of group P1 plasmids revealed by heteroduplex experiments: RP1, RP4, R68 and RK2 are identical.

The molecular relationships of the IncP1 plasmids RP1, RP4, R68 and RK2 were tested by electron microscopic examination of heteroduplexes. In several hybridization experiments molecules were detected which had a 7.8% portion of incomplete reannealing. This 'heterologous region' could be explained by the typical renaturation behaviour of the transposon Tn1. The identity of the Tn1 transposon present in RP1 and RP4 was proved by heteroduplex experiments with lambda phage DNA containing this transposon. These results indicated that the plasmids RP1 and RP4 are identical. Additional heteroduplex experiments between plasmids R68.45 and RP8 and between R68.45 and RK2 were performed. R68.45, a derivative of R68, has a small DNA insertion and RP8 can be regarded as a large insertion mutant of RP4; both insertions were used as single-stranded hybridization markers. From the hybrid molecules formed, it was deduced that R68 and RK2 are identical with RP1 and RP4 as far as molecular structure is revealed by the technique used.

Ampicillin↗
PubMed1979

Sites of insertion of TnA and TnM in RP1 and its derivatives.

The sites of insertion of TnM into the plasmid RP1, into derivatives of RP1 lacking TnA, and into derivatives in which the location of TnA within RP1 has been altered, were determined. Similarly, the sites of insertion of TnA into derivatives of RP1 from which TnA had been deleted, both with and without copies of TnM, have been examined. These studies show the presence in the plasmids of 'hot-spots' for TnA and TnM insertion. It is clear from the observations, however, that a particular DNA sequence in the recipient replicon is not sufficient to definite a 'hot-spot' since particular sequences sometimes do, and sometimes do not, contain many sites of insertion for a given transposon.

Base Sequence↗
PubMed1979

Host dependence of RP1-specified resistance to ampicillin: differential expression in Escherichia coli and Rhizobium leguminosarum.

Rhizobium leguminosarum L4 is able to serve as a host for the plasmid RP1. Properties of R. leguminosarum [RP1] plasmid carrier suggest that the expression of RP1-coded Apr gene(s) is inhibited in this host, although the determinants of transfer and resistance to kanamycin and tetracycline are expressed. This system exemplifies a differential expression of plasmid genes in a new host.

Ampicillin↗
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↗
PubMed1977

Properties of derivatives of the Pseudomonas plasmid pVS1 that have inherited carbenicillin resistance from RP1.

A procedure is described for the isolation, in Pseudomonas aeruginosa PAO, of bacteria carrying derivatives of pVS1 that inherited the carbenicillin-resistance determinant from RP1 either alone or together with that for aeruginocin resistance. Such bacteria occur among the transconjugant progeny from both recombination-proficient or -deficient pVS1+ RP1+ donors, suggesting that the formation of these plasmids is due to the translocation of TnA from RP1 into pVS1. It is possible, therefore, that the aeruginocin-resistance determinant is part of TnA or is closely linked to it. Unexpectedly, none of these plasmids showed the 3 x 10(6)- to 4 x 10(6)-dalton increase in size predicted for TnA+ derivatives of PVS1. It is suggested that an interaction between TnA and the Tn501 translocation unit in pVS1 could account for this result.

Anti-Bacterial Agents↗
PubMed1977

[Transgenosis with participation of plasmid RP1; indications of the presence of a "composit plasmid" in an interspecies hybrid of Escherichia coli].

One of the transconjugants (1-7) obtained by the authors earlier in the conjugation of Escherichia coli J-62 with Pseudomonas aeruginosa 1822, besides the plasmic RP1 has acquired the ability to grow without proline and tryptophan. The detailed analysis has shown that in the conjugation of the transconjugant 1-7 with different strains of E. coli the plasmic RP1 and chromosomal genes were transmitted together, but in transduction--by means of bacteriophage P1, independently of each other. The fertility was found only in the transductants carrying the plasmid RP1. This suggests that in the intergeneric conjugations the transmission of chromosomal genes may occur without any firm link with the plasmid (as in the case of "aggregated plasmids"). In E. coli cells these chromosomal fragments of Ps. aeruginosa apparently formed small nontransmissible replicons.

Chromosomes, Bacterial↗
PubMed1978

Regional preference of insertion of Tn501 and Tn802 into RP1 and its derivatives.

The sites of insertion of Tn501 into RP1 and into derivatives of this plasmid that either lack the Tn801 (TnA) element or contain it in a different location have been determined. Similarly, the sites of insertion of Tn802 into a derivative of RP1 that lacks the Tn801 element and into recombinants of this plasmid with Tn501 were determined. 'Hot spots' for insertion were observed with both transposons; but it is clear that a particular DNA sequence is not sufficient to define a 'hot spot', since a particular region does contain many insertions when present in one plasmid but does not do so when part of another.

Base Sequence↗
PubMed1978

Effect of R-plasmid RP1 and nutrient depletion on the gross cellular composition of Escherichia coli and its resistance to some uncoupling phenols.

The resistance of Escherichia coli batch cultures depleted of carbon (C-dep), magnesium (Mg-dep), or phosphate (P-dep) against low concentrations of 3-chlorophenol, 4-chlorophenol, or 2-phenoxyethanol varied. C-dep cultures were always significantly more sensitive than Mg-dep or P-dep cultures. The presence of R-plasmid RP1 increased the sensitivity of C-dep cultures to 3- and 4-chlorophenol, yet had little effect on those cultured depleted in magnesium or phosphate ions. Cultures with R-plasmid RP1 had increased levels of beta-polyhydroxybutyrate irrespective of the nature of the depleting nutrient. P-dep bacteria had less than one-third of the phospholipid of other cell types, this deficiency being compensated for by increases in fatty acid and neutral lipid content. The reduction in phospholipid content of P-dep cultures was entirely accounted for by decreased diphosphatidylglycerol and phosphatidylethanolamine levels in these cells.

Carbon↗
PubMed1975

Transfer of antibiotic resistance plasmid RP1 into Pseudomonas glycinea and Pseudomonas phaseolicola in vitro and in planta.

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.

Acridines↗
PubMed1976

[Conjugational transfer of R factor RP1 in Ps. aeruginosa and the possibility of inhibiting this process with a series of substances].

It was shown that the conjugation system of Ps. aeruginosa PAO 2604 X PTO 629 rifr used for transfer of the plasmid markers of R-factor RPI was a convenient model for a number of genetic investigations (the rate of transfer of the antibiotic resistance markers was 2.2 X 10(-3) to 8.8 X 10(-5). 80.7 per cent of the exconjugants obtained from this crossing acquired all 3 resistance plasmid markers (carbenicillin tetracycline, neomycin). In 12 per cent of R+-exconjugants transfer of 2 or 1 resistance determinant of R-factor was observed. The use of the above conjugation system revealed the inhibitory effect of bonafton (an antiviral drug), acridine dyes (acrichin, metachrome orange), ethidium bromide and rifampicin. A possibility of intraspecies transfer of resistance plasmid markers was found in crosses Ps. aeruginosa PAO 2604 X X E. coli CSH--2 rifr and Ps. aeruginosa PAO 2604 X E. coli C600 rifr. Transfer of the resistance markers was observed in combinations of carbenicillin, tetracycline, neomycin (Cb, Tc, Nm), tetracycline (Tc) and carbenicillin (Cb).

Anti-Bacterial Agents↗
PubMed1977

Transposition of TnA does not generate deletions.

We have examined the incidence of loss of the TnA unit, Tn801, from RP1 under conditions where transposition of Tn801 to another replicon. R388, was readily detected. We found that the frequency of transposition of Tn801 from RP1 to R388 exceeded, by at least a factor of one hundred, the frequency at which it was deleted from RP1. We conclude that, in general, transposition of Tn801 does not generate derivatives of the donor plasmid which specifically lack Tn801. The relevance of these findings to the mechanism of transposition is discussed.

Chromosome Aberrations↗
PubMed1976

Isolation and characterisation of deletion mutants involving the transfer genes of P-group plasmids in Pseudomonas aeruginosa.

The P-group plasmids RP1 and R26 are recovered at low frequency following conjugal transfer to B3-lysogens of P. aeruginosa PAO. The rare carbenicillin-resistant transcipients that do arise are usually transfer-defective (Tra-) and may show the loss of other plasmid borne functions, namely kanamycin-resistance (Kmr) and reduced plating of phage G101 (Spp+). The four phenotypic classes that occur among the Tra- derivatives are respectively, Tra- (69-81%), Tra- Spp- (12-30%), Tra- Kms and Tra- Kms Spp- (0.2-1%), of which the latter three are dut to plasmid deletions. This is seen from the sizes of the plasmids carried by these bacteria and from the transductional analysis of the R26-derivatives. Thus, although R26 (MW = 52 X 106 daltons) is too large to be transduced by phage F116L (MW = 40 X 106), this is possible for its Tra- Kms and Tra Kms Spp- derivatives. The phenotypes and frequencies of the various transcipient classes suggests that the gene order Km.. Tra.. Spp occurs in both RP1 and R26, and that Spp is more closely linked to Tra than is Km. These conclusions are supported by the sizes of the plasmid mutants since deletions spanning the loci Km Tra Spp, Km Tra, and Tra Spp involve the loss of DNA of MW 8-17 X 106, 5-13 X 106 AND 1-9 X 106 DALTONS RESPECTIVELY. Whilst all the transcipients displayed the incompatibility properties of the parent plasmids (Inc+), only some retanied plasmid surface exclusion (Sfx+). Moreover, a strict correlation existed between the Sfx and Spp phenotypes such that the transcipients were either wild type, Sfx- Spp-, or displayed an intermediate phenotype for both characters. Thir are different manifestations of the same gene function. The deletion map of these various markers in both RP1 and R26 therefore seems to be Km.. Tra.. Sfx/Spp.. Inc.

Bacteriophages↗