# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 431 | 0 | 1.0000 | Nucleotide sequence analysis of the complement resistance gene from plasmid R100. The multiple antibiotic resistance plasmid R100 renders Escherichia coli resistant to the bactericidal action of serum complement. We constructed a plasmid (pOW3) consisting of a 1,900-base-pair-long restriction fragment from R100 joined to a 2,900-base-pair-long fragment of pBR322 carrying ampicillin resistance. E. coli strains carrying pOW3 or R100 were up to 10,000-fold less sensitive to killing by serum complement than were plasmid-free bacteria or bacteria carrying pBR322. Nucleotide sequencing revealed that 875 of the 1,900 bases from R100 correspond exactly to part of the bacterial insertion sequence IS2. The remaining 1,075 bases contained only one sizeable open reading frame; it covered 729 base pairs (243 amino acids) and was preceded by nucleotide sequences characteristic of bacterial promoters and ribosome binding sites. The first 20 amino acids of the predicted protein showed features characteristic of a signal sequence. The remainder of the predicted protein showed an amino acid composition almost identical with that determined for the traT protein from the E. coli F factor. Southern blot analysis showed that the resistance gene from R100 does not hybridize to the serum resistance gene from ColV,I-K94 isolated by Binns et al.; we concluded that these genes are distinct. | 1982 | 6284713 |
| 422 | 1 | 0.9995 | Further characterization of complement resistance conferred on Escherichia coli by the plasmid genes traT of R100 and iss of ColV,I-K94. We have shown that the traT gene product was responsible for the complement resistance of the R100 plasmid. We compared this resistance with that specified by the iss gene of the ColV,I-K94 plasmid. The levels of resistance specified by the two genes were similar, and there was no additive effect on resistance when both genes were present together. Under conditions in which traT and iss conferred at least a 50- and 10-fold increase in survival, respectively, the consumption of C6, C7, C8, and C9 was the same for bacteria with and without the plasmid genes. This result indicated that it was the action of the terminal complex, not its formation, which was blocked by traT and iss. | 1982 | 7035371 |
| 3052 | 2 | 0.9995 | Expression of antibiotic resistance genes from Escherichia coli in Bacillus subtilis. Bifunctional recombinant plasmids were constructed, comprised of the E. coli vectors pBR322, pBR325 and pACYC184 and different plasmids from Gram-positive bacteria, e.g. pBSU161-1 of B. subtilis and pUB110 and pC221 of S. aureus. The beta-lactamase (bla) gene and the chloramphenicol acetyltransferase (cat) gene from the E. coli plasmids were not transcribed and therefore not expressed in B. subtilis. However, tetracycline resistance from the E. coli plasmids was expressed in B. subtilis. Transcription of the tetracycline resistance gene(s) started in B. subtilis at or near the original E. coli promoter, the sequence of which is almost identical with the sequence recognized by sigma 55 of B. subtilis RNA polymerase. | 1983 | 6410152 |
| 441 | 3 | 0.9994 | Preparation of a DNA gene probe for detection of mercury resistance genes in gram-negative bacterial communities. A DNA gene probe was prepared to study genetic change mechanisms responsible for adaptation to mercury in natural bacterial communities. The probe was constructed from a 2.6-kilobase NcoI-EcoRI DNA restriction fragment which spans the majority of the mercury resistance operon (mer) in the R-factor R100. The range of specificity of this gene probe was defined by hybridization to the DNA of a wide variety of mercury-resistant bacteria previously shown to possess the mercuric reductase enzyme. All of the tested gram-negative bacteria had DNA sequences homologous to the mer probe, whereas no such homologies were detected in DNA of the gram-positive strains. Thus, the mer probe can be utilized to study gene flow processes in gram-negative bacterial communities. | 1985 | 3994373 |
| 434 | 4 | 0.9994 | Homologous Streptomycin Resistance Gene Present among Diverse Gram-Negative Bacteria in New York State Apple Orchards. The streptomycin resistance gene of Pseudomonas syringae pv. papulans Psp36 was cloned into Escherichia coli and used to develop a 500-bp DNA probe that is specific for streptomycin resistance in P. syringae pv. papulans. The probe is a portion of a 1-kb region shared by three different DNA clones of the resistance gene. In Southern hybridizations, the probe hybridized only with DNA isolated from streptomycin-resistant strains of P. syringae pv. papulans and not with the DNA of streptomycin-sensitive strains. Transposon insertions within the region of DNA shared by the three clones resulted in loss of resistance to streptomycin. Colony hybridization of bacteria isolated from apple leaves and orchard soil indicated that 39% of 398 streptomycin-resistant bacteria contained DNA that hybridized to the probe. These included all strains of P. syringae pv. papulans and some other fluorescent pseudomonads and nonfluorescent gram-negative bacteria, but none of the gram-positive bacteria. The same-size restriction fragments hybridized to the probe in P. syringae pv. papulans. Restriction fragment length polymorphism of this region was occasionally observed in strains of other taxonomic groups of bacteria. In bacteria other than P. syringae pv. papulans, the streptomycin resistance probe hybridized to different-sized plasmids and no relationship between plasmid size and taxonomic group or between plasmid size and orchard type, soil association, or leaf association could be detected. | 1991 | 16348415 |
| 432 | 5 | 0.9993 | Repressor gene finO in plasmids R100 and F: constitutive transfer of plasmid F is caused by insertion of IS3 into F finO. Fertility factor F confers bacterial conjugation, a process which involves at least 20 tra genes. Resistance plasmids such as R100, R6-5, and R1 have homology with F in the tra region. Conjugal transfer of these plasmids is, however, repressed, while transfer of F is constitutive. Repression of R transfer is due to the existence of the two genes, called finO and finP; constitutive transfer of F is believed to be due to a lack of finO in F. In this paper, we report the identification and DNA sequence of the finO gene of R100, encoding a protein of 21,265 daltons. We show that F does actually encode finO, but the gene has been inactivated by insertion of IS3. Lederberg and Tatum (Nature [London] 158:558, 1946), who discovered sexuality in bacteria, may have had an Escherichia coli K-12 strain harboring such an finO F factor, which facilitated the generation of recombinant progeny useful for genetic analysis of bacteria and established the foundation for molecular genetics. | 1987 | 3027040 |
| 3046 | 6 | 0.9993 | Presence of STRA-STRB linked streptomycin-resistance genes in clinical isolate of Escherichia coil 2418. The streptomycin resistance of Escherichia coli 2418 strain has been shown to be associated with a 1.2-kb DNA fragment found in the naturally occurring plasmid R2418S. Here, nucleotide sequence analysis of the 1.2-kb DNA fragment revealed the presence of the strB gene which is located immediately downstream of the strA gene. Both sequences are identical to those of strA and strB genes in plasmid RSF1010. Thus, the observed resistance in the clinical isolate is due to the presence of strA-strB genes encoding streptomycin-modifying enzymes. The sequence downstream of strB gene showed a perfect homology with that of RSF1010. In addition, it contained the right inverted repeat of the transposon Tn5393 that has been suggested to be a relic of this transposon found in DNA plasmids isolated from human- and animal-associated bacteria. | 2010 | 21598829 |
| 3044 | 7 | 0.9993 | RSF1010 and a conjugative plasmid contain sulII, one of two known genes for plasmid-borne sulfonamide resistance dihydropteroate synthase. The nucleotide sequence of the type II sulfonamide resistance dihydropteroate synthase (sulII) gene was determined. The molecular weight determined by maxicells was 30,000, and the predicted molecular weight for the polypeptide was 28,469. Comparison with the sulI gene encoded by Tn21 showed 57% DNA similarity. The sulII-encoded polypeptide has 138 of 271 amino acids in common with the polypeptide encoded by sulI. The sulII gene is located on various IncQ (broad-host-range) plasmids and other small nonconjugative resistance plasmids. Detailed restriction maps were constructed to compare the different plasmids in which sulII is found. The large conjugative plasmid pGS05 and the IncQ plasmid RSF1010 contained identical nucleotide sequences for the sulII gene. This type of sulfonamide resistance is very frequently found among gram-negative bacteria because of its efficient spread to various plasmids. | 1988 | 3075438 |
| 430 | 8 | 0.9993 | Cloning and characterization of EcoRI and HindIII restriction endonuclease-generated fragments of antibiotic resistance plasmids R6-5 and R6. DNA fragments generated by the EcoRI of HindIII endonucleases from the low copy number antibiotic resistance plasmids R6 and R6-5 were separately cloned using the high copy number ColE1 or pML21 plasmid vectors and the insertional inactivation procedure. The hybrid plasmids that were obtained were used to determine the location of the EcoRI and HindIII cleavage sites on the parent plasmid genomes by means of electron microscope heteroduplex analysis and agarose gel electrophoresis. Ultracentrifugation of the cloned fragments in caesium chloride gradients localized the high buoyant density regions of R6-5 to fragments that carry the genes for resistance to streptomycin-spectinomycin, sulfonamide, and mercury and a low buoyant density region to fragments that carry the tetracycline resistance determinant. Functional analysis of hybrid plasmids localized a number of plasmid properties such as resistances to antibiotics and mercury and several replication functions to specific regions of the R6-5 genome. Precise localisation of the genes for resistance to chloramphenicol, kanamycin, fusidic acid and tetracycline was possible due to the presence of identified restriction endonuclease cleavage sites within these determinants. Only one region competent for autonomous replication was identified on the R6-5 plasmid genome and this was localized to EcoRI fragment 2 and HindIII fragment 1. However, two additional regions of replication activity designated RepB and RepC, themselves incapable of autonomous replication but capable supporting replication of a linked ColE1 plasmid in polA- bacteria, were also identified. | 1978 | 672900 |
| 379 | 9 | 0.9993 | Broad host range DNA cloning system for gram-negative bacteria: construction of a gene bank of Rhizobium meliloti. A broad host range cloning vehicle that can be mobilized at high frequency into Gram-negative bacteria has been constructed from the naturally occurring antibiotic resistance plasmid RK2. The vehicle is 20 kilobase pairs in size, encodes tetracycline resistance, and contains two single restriction enzyme sites suitable for cloning. Mobilization is effected by a helper plasmid consisting of the RK2 transfer genes linked to a ColE1 replicon. By use of this plasmid vehicle, a gene bank of the DNA from a wild-type strain of Rhizobium meliloti has been constructed and established in Escherichia coli. One of the hybrid plasmids in the bank contains a DNA insert of approximately 26 kilobase pairs which has homology to the nitrogenase structural gene region of Klebsiella pneumoniae. | 1980 | 7012838 |
| 3053 | 10 | 0.9993 | Expression in Escherichia coli of cryptic tetracycline resistance genes from bacteroides R plasmids. The putative clindamycin resistance region of the Bacteroides fragilis R plasmid pBF4 was cloned in the vector R300B in Escherichia coli. This 3.8-kb EcoRI D fragment from pBF4 expressed noninducible tetracycline resistance in E. coli under aerobic but not anaerobic growth conditions. The fragment does not express tetracycline resistance in Bacteroides, a strict anaerobe. The separate tetracycline resistance transfer system in the Bacteroides host strain V479-1 has no homology to the cryptic determinant on pBF4. In addition, this aerobic tetracycline resistance determinant is not homologous to the three major plasmid mediated tetracycline resistance regions found in facultative gram-negative bacteria, represented by R100, RK2, and pBR322. A similar cryptic tetracycline resistance fragment was cloned from pCP1, a separate clindamycin resistance plasmid from Bacteroides that shares homology with the EcoRI D fragment of pBF4. This study identifies cryptic drug resistance determinants in Bacteroides that are expressed when inserted into an aerobically growing organism. | 1984 | 6379711 |
| 426 | 11 | 0.9993 | Plasmid-determined resistance to serum bactericidal activity: a major outer membrane protein, the traT gene product, is responsible for plasmid-specified serum resistance in Escherichia coli. Resistance to the bactericidal activity of serum appears to be an important virulence property of invasive bacteria. The conjugative multiple-antibiotic-resistance plasmid R6-5 was found to confer upon Escherichia coli host bacteria increased resistance against rabbit serum. Gene-cloning techniques were used to localize the serum resistance determinant of R6-5 to a segment of the plasmid that encodes conjugal transfer functions, and a pACYC184 hybrid plasmid, designated pKT107, that contains this segment was constructed. The generation and analysis of deletion and insertion mutant derivatives of the pKT107 plasmid that no longer specify serum resistance permitted precise localization of the serum-resistance cistron on the R6-5 map and demonstrated that this locus is coincident with that of traT, one of the two surface exclusion genes of R6-5. Examination of the proteins synthesized in E. coli minicells of pKT107 and its serum-sensitive mutant derivative plasmids confirmed that the serum-resistance gene product of R6-5 is the traT protein and showed that this protein is a major structural component (about 21,000 copies per cell) of the bacterial outer membrane. | 1980 | 6995306 |
| 457 | 12 | 0.9993 | Molecular characterization of the genes encoding DNA gyrase and topoisomerase IV of Listeria monocytogenes. The genes encoding subunits A and B of DNA gyrase and subunits C and E of topoisomerase IV of Listeria monocytogenes, gyrA, gyrB, parC and parE, respectively, were cloned and sequenced. Compared with the sequences of quinolone-susceptible bacteria, such as Escherichia coli and Bacillus subtilis, the quinolone resistance-determining region (QRDR) of DNA gyrase subunit A was altered; the deduced amino acid sequences revealed the substitutions Ser-84-->Thr and Asp/Glu-88-->Phe, two amino acid variations at hot spots, commonly associated with resistance to quinolones. No relevant divergences from QRDR consensus sequences were observed in GyrB or both topoisomerase IV subunits. Thus, it could be argued that the amino acid substitutions in GyrA would explain the intrinsic resistance of L. monocytogenes to nalidixic acid. In order to analyse the actual role of the GyrA alterations, a plasmid-encoded gyrA allele was mutated and transformed into L. monocytogenes. However, these heterodiploid strains were not affected in their resistance to nalidixic acid. The effects of the mutant plasmids on ciprofloxacin and sparfloxacin susceptibility were only modest. | 2002 | 12039883 |
| 3045 | 13 | 0.9993 | Plasmid-borne sulfonamide resistance determinants studied by restriction enzyme analysis. The relationship between sulfonamide resistance genes carried on different plasmids was investigated by restriction enzyme analysis and DNA-DNA hybridization. The results showed that sulfonamide resistance mediated by different plasmids is determined by the production of at least two different types of drug-resistant dihydropteroate synthase. Plasmids pGS01, pGS02, and R22259, found in bacteria isolated from patients in Swedish hospitals, contained identical sulfonamide resistance genes, which were also identical to those of plasmids R1, R100, R6, and R388. These latter plasmids, which have been well studied in different laboratories, were originally from clinical isolates from different parts of the world. Two other clinically isolated plasmids, pGS04 and pGS05, were shown to contain sulfonamide resistance determinants of a completely different type. | 1983 | 6298179 |
| 428 | 14 | 0.9992 | Identification and analysis of genes for tetracycline resistance and replication functions in the broad-host-range plasmid pLS1. The streptococcal plasmid pMV158 and its derivative pLS1 are able to replicate and confer tetracycline resistance in both Gram-positive and Gram-negative bacteria. Copy numbers of pLS1 were 24, 4 and 4 molecules per genome in Streptococcus pneumoniae, Bacillus subtilis and Escherichia coli, respectively. Replication of the streptococcal plasmids in E. coli required functional polA and recA genes. A copy-number mutation corresponding to a 332 base-pair deletion of pLS1 doubled the plasmid copy number in all three species. Determination of the complete DNA sequence of pLS1 revealed transcriptional and translational signals and four open reading frames. A putative inhibitory RNA was encoded in the region deleted by the copy-control mutation. Two putative mRNA transcripts encoded proteins for replication functions and tetracycline resistance, respectively. The repB gene encoded a trans-acting, 23,000 Mr protein necessary for replication, and the tet gene encoded a very hydrophobic, 50,000 Mr protein required for tetracycline resistance. The polypeptides corresponding to these proteins were identified by specific labeling of plasmid-encoded products. The tet gene of pLS1 was highly homologous to tet genes in two other plasmids of Gram-positive origin but different in both sequence and mode of regulation from tet genes of Gram-negative origin. | 1986 | 2438417 |
| 3050 | 15 | 0.9992 | The type VII dihydrofolate reductase: a novel plasmid-encoded trimethoprim-resistant enzyme from gram-negative bacteria isolated in Britain. Plasmid pUN835 was identified in an Escherichia coli strain isolated from an outbreak of porcine diarrhoea on a farm near Nottingham, UK. The trimethoprim resistance gene did not hybridize with any of the gene probes derived from known plasmid-encoded trimethoprim resistance genes. The trimethoprim resistance gene of pUN835 was shown to encode the production of a dihydrofolate reductase which confers high-level resistance on its host. This enzyme was smaller than most plasmid-encoded dihydrofolate reductases (molecular mass = 11,500) and was labile to heat. It had relatively low affinity for the substrate dihydrofolate (Km = 20 microM) and it was resistant to competitive inhibition by trimethoprim (Ki = 7.0 microM). We classify this novel enzyme as type VII. | 1989 | 2676936 |
| 4499 | 16 | 0.9992 | Organization of two sulfonamide resistance genes on plasmids of gram-negative bacteria. The organization of two widely distributed sulfonamide resistance genes has been studied. The type I gene was linked to other resistance genes, like streptomycin resistance in R100 and trimethoprim resistance in R388 and other recently isolated plasmids from Sri Lanka. In R388, the sulfonamide resistance gene was transcribed from a promoter of its own, but in all other studied plasmids the linked genes were transcribed from a common promoter. This was especially established with a clone derived from plasmid R6-5, in which transposon mutagenesis showed that expression of sulfonamide resistance was completely dependent on the linked streptomycin resistance gene. The type II sulfonamide resistance gene was independently transcribed and found on two kinds of small resistance plasmids and also on large plasmids isolated from clinical material. | 1987 | 3032095 |
| 3043 | 17 | 0.9992 | The role of insertions, deletions, and substitutions in the evolution of R6 related plasmids encoding aminoglycoside transferase ANT-(2"). In 7% of gram-negative bacteria resistance to gentamicin is mainly mediated by plasmid-encoded aminoglycoside transferase ANT-(2"). The genome organization of 15 aadB plasmids (42-110 kb) was analyzed by restriction and hybridization techniques. They appeared to be IncFII-like replicons but were distinct from R6 by virtue of small substitutions in the transfer region. Aminoglycoside resistance genes aadB and aadA were located on Tn21 related elements. Only one of them was able to transpose its resistance genes mer sul aadA and aadB ( Tn4000 ), the other elements were naturally occurring defective transposons. In some of these structures deletions were identified at the termini, at sul, aadA , mer or transposition function--insertions adjacent to aadA or mer. The mode of these rearrangements and their site-specificity were considered with respect to the evolution of the Tn21 transposon family. | 1984 | 6328217 |
| 435 | 18 | 0.9992 | Molecular analysis of closely related copper- and streptomycin-resistance plasmids in Pseudomonas syringae pv. syringae. The genetic relationship of a group of copper (Cur) and streptomycin (Smr) resistance plasmids and their Pseudomonas syringae pv. syringae hosts was examined. Each of these plasmids contained sequences homologous to the oriV and par sequences from pOSU900, a cryptic P. syringae pv. syringae plasmid. Analysis of restriction digest patterns of plasmid DNA indicated that the plasmids could be clustered into four groups; two of the groups contained multiple members which differed by only a few fragments. An analysis of the host P. syringae genotypes using the arbitrarily primed PCR technique and genomic DNA indicated that the host strains could be placed in groups similar to those resulting from analysis of plasmid DNA. Southern hybridization analyses of plasmid DNA indicated that each Smr plasmid contained sequences homologous to probes specific for the strA-strB Smr genes and the transposase and resolvase genes from Tn5393. All plasmids hybridized to two additional probes derived from P. syringae plasmid DNA, but none of the plasmids contained IS51 or IS801 sequences. Furthermore, Tn5393 was mobilized, presumably by transposition, between the incompatible plasmids pPSR5 and pPSR4 in P. syringae pv. syringae FF5. The variation in molecular structure of the closely related plasmids in this study is similar to that observed with antibiotic-resistance plasmids from clinical bacteria. | 1996 | 8700971 |
| 5851 | 19 | 0.9992 | Arsenic resistance determinants from environmental bacteria. Arsenic resistance determinants from 42 environmental bacterial isolates (32 Gram negative) were analyzed by DNA: DNA hybridization using probes derived from Escherichia coli and Staphylococcus plasmid or chromosomal arsenic resistance (ars) genes. In colony hybridization assays, 11 and 1 Gram negative strains hybridized with the E. coli chromosome and plasmid probes, respectively. No hybridization was detected using a probe containing only the arsA (ATPase) gene from E. coli plasmid or with a Staphylococcus plasmid ars probe. From Southern hybridization tests of some of the positive strains it was concluded that homology to ars chromosomal genes occurred within chromosome regions, except in an E. coli isolate where hybridization occurred in both the chromosome and a 130-kb plasmid. Our results show that DNA sequences homologous to E. coli ars chromosomal genes are commonly present in the chromosomes of environmental arsenic-resistant Gram negative isolates. | 1998 | 10932734 |