Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.30.2 (endonuclease)
18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasmids in five strains of Salmonella typhimurium resistant to ampicillin, chloramphenicol, gentamicin, neomycin/kanamycin, streptomycin, sulphonamides, tetracyclines and trimethoprim (ACGKSSuTTm), CGKSSuTTm, ACSSuT or CSSuT which had been isolated from poultry in the first 3 months of 1989 have been characterized and compared with plasmids in two strains of R-types ACGKSSuTTm and ASSuTTm isolated from two patients later in the year. With the exception of the human isolate of R-type ASSuTTm, all strains carried two non-conjugative plasmids, one coding for SSu and belonging to incompatibility group Q, and a second coding for multiple resistance and belonging to the FIme incompatibility group. The human isolate of R-type ASSuTTm did not carry the IncQ SSu plasmid but like the poultry isolates, carried a non-conjugative FIme plasmid. Restriction endonuclease digestion with the enzymes EcoR I, Pst I and Hind III demonstrated that the FIme plasmids from strains of different R-types showed a high degree of homology but exhibited numerous fragment size polymorphisms. The restriction digest fingerprint of plasmids in the human isolate of R-type ACGKSSuTTm was indistinguishable from a poultry isolate of the same R-type. Analysis of segregants of one of the poultry isolates of R-type ACGKSSuTTm demonstrated that resistance determinants could be rapidly lost from the FIme plasmid to give rise to a number of R-types and fingerprint patterns. Loss of tetracycline resistance from this plasmid appeared to be correlated with the integration of other plasmid-mediated resistances into the bacterial chromosome. Evidence is presented for the rapid loss of antimicrobial resistance determinants from a multiple resistance plasmid of the FIme incompatibility group in response to withdrawal of antibiotic selective pressure.
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PMID:Instability of multiple drug resistance plasmids in Salmonella typhimurium isolated from poultry. 201 96

pBR322 plasmid DNA, randomly substituted with arylamine moieties, was introduced into Escherichia coli Uvr endonuclease deficient strains. Plasmid survival was determined by selection in the presence of ampicillin. Modification of plasmid DNA with N-acetoxy-N-trifluoroacetylaminobiphenyl yielded primarily N-(deoxyguanosin-8-yl)-4-aminobiphenyl residues. Reaction of DNA with N-acetoxy-N-acetylaminobiphenyl produced only N-(deoxyguanosin-8-yl)-4-acetylaminobiphenyl adducts. The aminobiphenyl (ABP) and acetylaminobiphenyl adducts reduced the ability of the plasmid DNA to transform E. coli to approximately the same extent in a wild-type strain. In uvrA, uvrB and uvrC, i.e. Uvr endonuclease deficient strains, both adducts produced equivalent decreases in survival, however, the reduction in survival was much more pronounced in the uvr- cells than in the wild-type strain. A similar pattern of toxicity was observed with plasmids carrying N-(deoxyguanosin-8-yl)-2-acetylaminofluorene adducts, although the acetylaminofluorene adduct was approximately 5-fold more effective in reducing the biological activity of the plasmid. In contrast, the deacetylated aminofluorene (AF) lesion, N-(deoxyguanosin-8-yl-2-aminofluorene, exhibited relatively little effect on plasmid survival in uvrA and uvrB cells as compared to the wild-type strain, even though the survival of both ABP and AF adducts was essentially similar in the uvrC and wild-type strains. These data demonstrate that (i) both the deacetylated and acetylated lesions are subject to repair by the Uvr endonuclease complex, and (ii) the presence of the N-acetyl group is not the sole determinant of the differential effects of arylamine adducts in uvr cells. These observations provide indirect evidence that both the N-acetyl and aryl moieties of these adducts alter the conformation of DNA.
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PMID:Comparative survival of aminobiphenyl- and aminofluorene-substituted plasmid DNA in Escherichia coli Uvr endonuclease deficient strains. 218 16

One of a number of large nocardioform plasmids previously obtained by a primarily genetic approach was reduced in size to about approximately 11 kb. This smaller plasmid possessed determinants for resistance to sodium arsenate and sodium arsenite, as well as immunity to nocardiophage Q4. It was joined to an Escherichia coli-positive selection vector constructed by M. Zabeau and colleagues, which had the EcoR1 endonuclease gene placed under the control of the PR promoter of lambda as well as a bla determinant. The resulting shuttle vector of about 14.6 kb was maintained in E. coli and in several strains of Rhodococcus. The vector was efficient in cloning DNA without prior alkaline phosphatase treatment, as a result of the presence of the positive selection function. This function was not significantly expressed in Rhodococcus, and the presence of the nocardioform resistance determinants led to no increase in arsenate or arsenite resistance in E. coli. The presence of the bla gene resulted in an increase of about threefold in ampicillin resistance in Rhodococcus strains.
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PMID:Nocardioform arsenic resistance plasmids and construction of Rhodococcus cloning vectors. 221 74

A total of 163 strains of Pasteurella multocida isolated from swine were examined for drug resistance and R plasmids. Strains resistant to sulfadimethoxine (Sar), ampicillin (Apr), streptomycin (Smr), kanamycin (Kmr), and chloramphenicol (Cpr) were found in 93.9, 1.8, 16.6, 1.2, and 10.4%, respectively. There were two patterns of drug resistance (Sar and SarCpr) in isolates from nasal cavities, and five patterns (Sar, SarSmr, SarSmrCpr, SarSmrApr, and SarSmrKmrCpr) in isolates from pneumonic lung specimens. Two isolates studied were proved to carry a nonconjugative R plasmid pJY2 or pJY8 with other unidentified plasmids, respectively. pJY2 (3.6 megadaltons) encoding resistance to SarSmr had one cleavage site for EcoRI or HindIII endonuclease and two sites for PstI endonuclease. pJY8 (5.5 megadaltons) encoding resistance to Sar SmrKmrCpr had one EcoRI site and two PstI sites.
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PMID:Drug resistance and R plasmids in Pasteurella multocida isolates from swine. 228 54

M13B1 vector based on the filamentous phage M13 has been constructed. M13B1 phage carries the gene of resistance to ampicillin and contains the unique site of recognition for BamHI restriction endonuclease in gene VIII coding for the major coat protein. BamHI restriction site has been inserted into the gene of the major coat protein by means of oligonucleotide directed mutagenesis. The synthetic DNA fragment coding for the model peptides has been inserted through BamHI site into the M13B1 DNA. The possibility of inserting foreign peptides into the N-terminus at maintaining the viability of hybrid phages has been shown. The differences in specificity of the recombinant phage maturation have been determined by analysing the amino acid sequence of B-protein.
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PMID:[The use of filamentous phage M13 in protein engineering]. 236 94

EPEC adherence factor (EAF) plasmids from three strains of enteropathogenic Escherichia coli (EPEC) - E2347/69 (O127:H6), E20517 (O111:H2) and E24582 (O142:H6) - were examined. The EAF plasmids were all marked with ampicillin resistance by transposition of Tn801 to give pDEP1, pDEP2 and pDEP11, respectively. All three plasmids showed incompatibility with an FIme and an FIV plasmid and had some similarity in restriction enzyme digest patterns. Plasmid pDEP1 differed from pDEP2 and pDEP11 in being autotransferring and fertility-inhibition positive. An EAF probe consisting of a 1 kb BamHI-SalI restriction endonuclease fragment of the prototype EAF-associated plasmid pMAR2 hybridized to similar-sized SalI-BamHI fragments of pDEP1 and pDEP11 but to a different-sized fragment of plasmid pDEP2. Loss of the EAF plasmids from EPEC strains resulted in a marked reduction in the ability of these strains to adhere to HEp-2 cells. The EAF-plasmid-negative variants did not express a 94 kDa outer-membrane protein (OMP). When these EAF plasmids were reintroduced into EAF-plasmid-negative EPEC strains a high level of adherence equivalent to that of the parent EPEC strains was restored and a 94 kDa OMP was usually expressed. However, when EAF plasmids were transferred into E. coli K12 or non-EPEC E. coli the host strains either did not adhere or adhered poorly to the HEp-2 cells. These transconjugants did not express a 94 kDa OMP.
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PMID:Properties of adherence factor plasmids of enteropathogenic Escherichia coli and the effect of host strain on expression of adherence to HEp-2 cells. 257 33

From 1981 to 1984, 254 isolates of Salmonella krefeld were isolated from newborns and infants with acute gastroenteritis in southern Taiwan. All the crude enterotoxin preparations of S. krefeld caused the cytotoxic elongation reaction in Chinese hamster ovary K1 (CHO-K1) cells. Cytotoxic enterotoxin was also produced by S. krefeld inducing Vero cells to round up and appear partially detached from the culture plate. It was noted that S. krefeld showed internalization and multiplication in CHO-K1 cells. S. krefeld exhibited 12 different resistant patterns. And the predominant patterns were found to be resistant to kanamycin and ampicillin (Ka-Amr), and resistant to kanamycin, ampicillin, chloramphenicol and tetracycline (Ka-Am-Cm-Ter). It was found that two distinct plasmids of 34 megadalton (Md) and 120 Md were commonly present in these strains. S. krefeld haboured 34 Md and 120 Md R-plasmid, which conferred resistance to Ka-Amr and Ka-Am-Cm-Ter, respectively. From the resistance transferred patterns, Ka-Amr was the most common resistance among transconjugants. The frequency of transfer of the 34 Md R-plasmid (2.71 x 10(-3) transconjugants/donor cell) from S. krefeld to E. coli K-12 14R525 was 20 times higher than that of the 120 Md R-plasmid (1.48 x 10(-4) transconjugants/donor cell). In analysis of the restriction endonuclease digest of the 34 Md plasmid obtained from different bacterial sources, their specific identical DNA fragment pattern suggested that the outbreak infection due to S. krefeld had a common origin.
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PMID:Characterization of cytotoxicity and R-plasmid in Salmonella krefeld. 259 11

In 1983, a small outbreak of infections caused by a previously unrecognized multiply-drug-resistant Shigella flexneri 3a strain occurred on the Hopi Indian reservation. The index patient, a diabetic woman with recurrent Escherichia coli bacteriuria on prophylactic trimethoprim/sulfamethoxazole (TMP/SMZ) therapy, was hospitalized with concurrent E. coli urinary tract infection and shigellosis. Both E. coli isolated from her urine and S. flexneri isolated from her stool were resistant to ampicillin, carbenicillin, streptomycin, sulfisoxazole, tetracycline, and TMP/SMZ. Both isolates contained a 35-MDa plasmid transferrable to recipient E. coli, and transconjugates acquiring the plasmid from either donor strain also acquired resistance to the same agents. The number and size of fragments generated by plasmid digestion with DNA restriction endonuclease ClaI were similar. A review of clinical microbiology records showed that an E. coli strain isolated from the patient 3 w before the onset of shigellosis had identical antimicrobial resistance to the E. coli and Shigella isolated during the outbreak. These studies indicate that the index patient receiving prophylactic TMP/SMZ was the likely source of the R-plasmid for the outbreak strain of Shigella.
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PMID:Interspecies gene transfer in vivo producing an outbreak of multiply resistant shigellosis. 268 26

The number of copies of the genes leuB, nifH, nifD, and nifK per cell of Azotobacter vinelandii has been determined to be about 80. A beta-lactamase gene was integrated into the A. vinelandii chromosome by single-point crossover. Subsequently, we have been able to detect nearly 80 copies of this beta-lactamase gene per cell of A. vinelandii when cultured for a large number of generations in the presence of ampicillin. The multiple copies of the beta-lactamase gene do not seem to be present on a single chromosome, as evident from the fragment obtained by digestion of cellular DNA with the appropriate restriction endonuclease. The kinetics of renaturation of DNA of A. vinelandii is suggestive of complexity similar to that of Escherichia coli. The DNA content of A. vinelandii, however, is 40 times that of E. coli. All these indicate the presence of multiple chromosomes, possibly as many as 80, in A. vinelandii.
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PMID:Multiple chromosomes of Azotobacter vinelandii. 278 85

Antimicrobial resistance determinants and plasmids present in 10 multiply antibiotic-resistant strains of Hemophilus influenzae isolated from patients in different geographic regions of Spain were characterized. Conjugative plasmids with molecular sizes of 38-50 MDa encoded resistance to ampicillin, chloramphenicol, kanamycin, streptomycin, sulfamethoxazole, and tetracycline. Trimethoprim resistance was not linked to the other antibiotic resistance determinants and trimethoprim-resistant transconjugants and transformants lacked detectable plasmid DNA, suggesting that this determinant is chromosomal. Restriction endonuclease analysis revealed similarities among the plasmids, but several restriction patterns could be distinguished. Three hybridization patterns were found with DNA probes coding for H. parainfluenzae beta-lactamase and chloramphenicol-acetyltransferase. Resistance to kanamycin was due to drug modification by aminoglycoside-phosphotransferase (3')I. In Spain, it appears that multiple antibiotic resistance phenotypes in H. influenzae did not arise from acquisition of a single R plasmid; rather, both plasmid and chromosomal resistance evolved independently from several sources.
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PMID:Genetic relatedness of antibiotic resistance determinants in multiply resistant Hemophilus influenzae. 280 56


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